Raras
Buscar doenças, sintomas, genes...
Lisencefalia
ORPHA:48471DOENÇA RARA

O termo lisencefalia abrange um grupo de malformações raras que compartilham a característica comum de anomalias no aparecimento de circunvoluções cerebrais (caracterizadas por simplificação ou ausência de dobramento) associadas à organização anormal das camadas corticais como resultado de defeitos de migração neuronal durante a embriogênese.

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Introdução

O que você precisa saber de cara

📋

O termo lisencefalia abrange um grupo de malformações raras que compartilham a característica comum de anomalias no aparecimento de circunvoluções cerebrais (caracterizadas por simplificação ou ausência de dobramento) associadas à organização anormal das camadas corticais como resultado de defeitos de migração neuronal durante a embriogênese.

Publicações científicas
1.651 artigos
Último publicado: 2026 Apr 14
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Sinais e sintomas

O que aparece no corpo e com que frequência cada sintoma acontece

Partes do corpo afetadas

🧠
Neurológico
94 sintomas
😀
Face
45 sintomas
🦴
Ossos e articulações
39 sintomas
👁️
Olhos
27 sintomas
📏
Crescimento
13 sintomas
❤️
Coração
12 sintomas

+ 181 sintomas em outras categorias

Características mais comuns

Atraso global do desenvolvimento
Crise tônico-clônica bilateral com início generalizado
Crise motora
Pneumonia
Dismielinização cerebral
Mielinização anormal
461sintomas
Sem dados (461)

Os sintomas variam de pessoa para pessoa. Abaixo estão as 461 características clínicas mais associadas, ordenadas por frequência.

Atraso global do desenvolvimentoGlobal developmental delay
Crise tônico-clônica bilateral com início generalizadoBilateral tonic-clonic seizure with generalized onset
Crise motoraMotor seizure
Pneumonia
Dismielinização cerebralCerebral dysmyelination

Linha do tempo da pesquisa

Publicações por ano — veja quando o interesse científico cresceu
Anos de pesquisa1desde 2026
Total histórico1.651PubMed
Últimos 10 anos200publicações
Pico202552 papers
Linha do tempo
2026Hoje · 2026🧪 1996Primeiro ensaio clínico📈 2025Ano de pico
Publicações por ano (últimos 10 anos)

Encontrou um erro ou informação desatualizada? Sugira uma correção →

Genética e causas

O que está alterado no DNA e como passa nas famílias

Genes associados

24 genes identificados com associação a esta condição.

PHGDHD-3-phosphoglycerate dehydrogenaseDisease-causing germline mutation(s) inTolerante
FUNÇÃO

Catalyzes the reversible oxidation of 3-phospho-D-glycerate to 3-phosphonooxypyruvate, the first step of the phosphorylated L-serine biosynthesis pathway. Also catalyzes the reversible oxidation of 2-hydroxyglutarate to 2-oxoglutarate and the reversible oxidation of (S)-malate to oxaloacetate

LOCALIZAÇÃO

VIAS BIOLÓGICAS (1)
Serine metabolism
MECANISMO DE DOENÇA

Phosphoglycerate dehydrogenase deficiency

An autosomal recessive inborn error of L-serine biosynthesis, clinically characterized by congenital microcephaly, psychomotor retardation, and seizures.

VIAS REACTOME (1)
EXPRESSÃO TECIDUAL(Ubíquo)
Fibroblastos
83.1 TPM
Brain Spinal cord cervical c-1
50.3 TPM
Skin Not Sun Exposed Suprapubic
50.0 TPM
Glândula salivar
47.9 TPM
Testículo
45.6 TPM
OUTRAS DOENÇAS (2)
Neu-Laxova syndrome 1PHGDH deficiency
HGNC:8923UniProt:O43175
DAG1Dystroglycan 1Candidate gene tested inAltamente restrito
FUNÇÃO

The dystroglycan complex is involved in a number of signaling events and processes including laminin deposition and extracellular matrix assembly, acetylcholine receptor clustering, sarcolemmal stability, cell survival, peripheral nerve myelination, nodal structure, cell migration, epithelial polarization, and epithelium branching morphogenesis (By similarity). Required for the formation of photoreceptor ribbon synapses, and long-term maintenance of inhibitory synapses in cerebellar Purkinje cel

LOCALIZAÇÃO

Secreted, extracellular spaceSecreted, extracellular space, extracellular matrix, basement membraneSynapseCell membraneCytoplasm, cytoskeletonNucleus, nucleoplasmCell membrane, sarcolemmaPostsynaptic cell membrane

VIAS BIOLÓGICAS (1)
Formation of the dystrophin-glycoprotein complex (DGC)
MECANISMO DE DOENÇA

Muscular dystrophy-dystroglycanopathy limb-girdle C9

An autosomal recessive muscular dystrophy showing onset in early childhood, and associated with intellectual disability without structural brain anomalies.

EXPRESSÃO TECIDUAL(Ubíquo)
Nervo tibial
118.7 TPM
Artéria tibial
71.1 TPM
Aorta
69.5 TPM
Esôfago - Muscular
66.9 TPM
Esôfago - Junção
64.7 TPM
OUTRAS DOENÇAS (5)
autosomal recessive limb-girdle muscular dystrophy type 2Pmuscular dystrophy-dystroglycanopathy (congenital with brain and eye anomalies), type A9isolated asymptomatic elevation of creatine phosphokinasemuscular dystrophy-dystroglycanopathy, type A
HGNC:2666UniProt:Q14118
YWHAE14-3-3 protein epsilonCandidate gene tested inAltamente restrito
FUNÇÃO

Adapter protein implicated in the regulation of a large spectrum of both general and specialized signaling pathways (PubMed:21189250). Binds to a large number of partners, usually by recognition of a phosphoserine or phosphothreonine motif (PubMed:35343654). Binding generally results in the modulation of the activity of the binding partner (By similarity). Positively regulates phosphorylated protein HSF1 nuclear export to the cytoplasm (PubMed:12917326). Plays a positive role in the antiviral si

LOCALIZAÇÃO

NucleusCytoplasmMelanosome

VIAS BIOLÓGICAS (10)
Recruitment of mitotic centrosome proteins and complexesLoss of proteins required for interphase microtubule organization from the centrosomeLoss of Nlp from mitotic centrosomesRegulation of PLK1 Activity at G2/M TransitionAURKA Activation by TPX2
EXPRESSÃO TECIDUAL(Ubíquo)
Cérebro - Hemisfério cerebelar
592.3 TPM
Brain Spinal cord cervical c-1
579.8 TPM
Brain Frontal Cortex BA9
577.0 TPM
Fibroblastos
492.8 TPM
Brain Anterior cingulate cortex BA24
483.1 TPM
OUTRAS DOENÇAS (5)
distal 17p13.3 microdeletion syndromeMiller-Dieker lissencephaly syndromechromosome 17p13.3 duplication syndromeclear cell sarcoma of kidney
HGNC:12851UniProt:P62258
HIC1Hypermethylated in cancer 1 proteinCandidate gene tested inRestrito
FUNÇÃO

Transcriptional repressor (PubMed:12052894, PubMed:15231840). Recognizes and binds to the consensus sequence '5-[CG]NG[CG]GGGCA[CA]CC-3' (PubMed:15231840). May act as a tumor suppressor (PubMed:20154726). Involved in development of head, face, limbs and ventral body wall (By similarity). Involved in down-regulation of SIRT1 and thereby is involved in regulation of p53/TP53-dependent apoptotic DNA-damage responses (PubMed:16269335). The specific target gene promoter association seems to be depend

LOCALIZAÇÃO

Nucleus

VIAS BIOLÓGICAS (1)
SUMOylation of transcription factors
EXPRESSÃO TECIDUAL(Ubíquo)
Ovário
30.1 TPM
Útero
28.4 TPM
Cervix Endocervix
25.2 TPM
Fallopian Tube
24.4 TPM
Cervix Ectocervix
21.2 TPM
OUTRAS DOENÇAS (1)
Miller-Dieker lissencephaly syndrome
HGNC:4909UniProt:Q14526
PSPHPhosphoserine phosphataseCandidate gene tested inTolerante
FUNÇÃO

Catalyzes the last irreversible step in the biosynthesis of L-serine from carbohydrates, the dephosphorylation of O-phospho-L-serine to L-serine (PubMed:12213811, PubMed:14673469, PubMed:15291819, PubMed:25080166, PubMed:9222972). L-serine can then be used in protein synthesis, to produce other amino acids, in nucleotide metabolism or in glutathione synthesis, or can be racemized to D-serine, a neuromodulator (PubMed:14673469). May also act on O-phospho-D-serine (Probable)

LOCALIZAÇÃO

Cytoplasm, cytosol

VIAS BIOLÓGICAS (1)
Serine metabolism
MECANISMO DE DOENÇA

Phosphoserine phosphatase deficiency

An autosomal recessive disorder that results in pre- and postnatal growth retardation, moderate psychomotor retardation and facial features suggestive of Williams syndrome.

VIAS REACTOME (1)
EXPRESSÃO TECIDUAL(Ubíquo)
Fibroblastos
27.3 TPM
Linfócitos
22.7 TPM
Pituitária
15.6 TPM
Testículo
15.5 TPM
Ovário
13.4 TPM
OUTRAS DOENÇAS (2)
PSPH deficiencyneu-laxova syndrome due to 3-phosphoserine phosphatase deficiency
HGNC:9577UniProt:P78330
TMTC3Protein O-mannosyl-transferase TMTC3Disease-causing germline mutation(s) inTolerante
FUNÇÃO

Transfers mannosyl residues to the hydroxyl group of serine or threonine residues. The 4 members of the TMTC family are O-mannosyl-transferases dedicated primarily to the cadherin superfamily, each member seems to have a distinct role in decorating the cadherin domains with O-linked mannose glycans at specific regions. Also acts as O-mannosyl-transferase on other proteins such as PDIA3 (PubMed:28973932). Involved in the positive regulation of proteasomal protein degradation in the endoplasmic re

LOCALIZAÇÃO

MembraneEndoplasmic reticulum

MECANISMO DE DOENÇA

Lissencephaly 8

A form of lissencephaly, a disorder of cortical development characterized by agyria or pachygyria and disorganization of the clear neuronal lamination of normal six-layered cortex. LIS8 patients manifest delayed psychomotor development, intellectual disability with poor or absent speech, early-onset refractory seizures, hypotonia, cortical gyral abnormalities, and hypoplasia of the corpus callosum, brainstem and cerebellum. LIS8 inheritance is autosomal recessive.

EXPRESSÃO TECIDUAL(Ubíquo)
Fibroblastos
21.6 TPM
Skin Sun Exposed Lower leg
13.9 TPM
Skin Not Sun Exposed Suprapubic
13.7 TPM
Vagina
10.3 TPM
Esôfago - Mucosa
10.1 TPM
OUTRAS DOENÇAS (3)
lissencephaly 8periventricular nodular heterotopiacobblestone lissencephaly without muscular or ocular involvement
HGNC:26899UniProt:Q6ZXV5
CDK5Cyclin-dependent kinase 5Disease-causing germline mutation(s) inRestrito
FUNÇÃO

Proline-directed serine/threonine-protein kinase essential for neuronal cell cycle arrest and differentiation and may be involved in apoptotic cell death in neuronal diseases by triggering abortive cell cycle re-entry. Interacts with D1 and D3-type G1 cyclins. Phosphorylates SRC, NOS3, VIM/vimentin, p35/CDK5R1, MEF2A, SIPA1L1, SH3GLB1, PXN, PAK1, MCAM/MUC18, SEPT5, SYN1, DNM1, AMPH, SYNJ1, CDK16, RAC1, RHOA, CDC42, TONEBP/NFAT5, MAPT/TAU, MAP1B, histone H1, p53/TP53, HDAC1, APEX1, PTK2/FAK1, hun

LOCALIZAÇÃO

CytoplasmNucleusCell membranePerikaryonCell projection, lamellipodiumCell projection, growth conePostsynaptic densitySynapse

VIAS BIOLÓGICAS (9)
Phosphorylation and nuclear translocation of BMAL1 (ARNTL) and CLOCKPhosphorylation and nuclear translocation of the CRY:PER:kinase complexCRMPs in Sema3A signalingActivated NTRK2 signals through CDK5NPAS4 regulates expression of target genes
MECANISMO DE DOENÇA

Lissencephaly 7, with cerebellar hypoplasia

A form of lissencephaly, a disorder of cortical development characterized by agyria or pachygyria and disorganization of the clear neuronal lamination of normal six-layered cortex. LIS7 patients manifest lack of psychomotor development, facial dysmorphism, arthrogryposis, and early-onset intractable seizures resulting in death in infancy.

OUTRAS DOENÇAS (1)
lissencephaly 7 with cerebellar hypoplasia
HGNC:HGNC:1774UniProt:Q00535
ACTG1Actin, cytoplasmic 2Disease-causing germline mutation(s) inModerado
FUNÇÃO

Actins are highly conserved proteins that are involved in various types of cell motility and are ubiquitously expressed in all eukaryotic cells. May play a role in the repair of noise-induced stereocilia gaps thereby maintains hearing sensitivity following loud noise damage (By similarity)

LOCALIZAÇÃO

Cytoplasm, cytoskeleton

VIAS BIOLÓGICAS (10)
Paradoxical activation of RAF signaling by kinase inactive BRAFSignaling by moderate kinase activity BRAF mutantsSignaling by high-kinase activity BRAF mutantsSignaling downstream of RAS mutantsMAP2K and MAPK activation
MECANISMO DE DOENÇA

Deafness, autosomal dominant, 20

A form of non-syndromic sensorineural hearing loss. Sensorineural deafness results from damage to the neural receptors of the inner ear, the nerve pathways to the brain, or the area of the brain that receives sound information.

OUTRAS DOENÇAS (6)
autosomal dominant nonsyndromic hearing loss 20Baraitser-winter syndrome 2Baraitser-Winter cerebrofrontofacial syndromecoloboma of iris
HGNC:144UniProt:P63261
ACTBActin, cytoplasmic 1Disease-causing germline mutation(s) inAltamente restrito
FUNÇÃO

Actin is a highly conserved protein that polymerizes to produce filaments that form cross-linked networks in the cytoplasm of cells (PubMed:25255767, PubMed:29581253). Actin exists in both monomeric (G-actin) and polymeric (F-actin) forms, both forms playing key functions, such as cell motility and contraction (PubMed:29581253). In addition to their role in the cytoplasmic cytoskeleton, G- and F-actin also localize in the nucleus, and regulate gene transcription and motility and repair of damage

LOCALIZAÇÃO

Cytoplasm, cytoskeletonNucleus

VIAS BIOLÓGICAS (10)
Paradoxical activation of RAF signaling by kinase inactive BRAFSignaling by moderate kinase activity BRAF mutantsSignaling by high-kinase activity BRAF mutantsSignaling downstream of RAS mutantsMAP2K and MAPK activation
MECANISMO DE DOENÇA

Dystonia-deafness syndrome 1

An autosomal dominant form of dystonia with juvenile onset, associated with congenital or childhood-onset sensorineural deafness. Dystonia is defined by the presence of sustained involuntary muscle contraction, often leading to abnormal postures. Some DDS1 patients have dysmorphic features, skeletal anomalies, and/or mild developmental delay with impaired intellectual development.

OUTRAS DOENÇAS (7)
developmental malformations-deafness-dystonia syndromecongenital smooth muscle hamartoma, with or without hemihypertrophyBaraitser-Winter syndrome 1Becker nevus syndrome
HGNC:132UniProt:P60709
RAB18Ras-related protein Rab-18Disease-causing germline mutation(s) inRestrito
FUNÇÃO

The small GTPases Rab are key regulators of intracellular membrane trafficking, from the formation of transport vesicles to their fusion with membranes (PubMed:24891604, PubMed:30970241). Rabs cycle between an inactive GDP-bound form and an active GTP-bound form that is able to recruit to membranes different sets of downstream effectors directly responsible for vesicle formation, movement, tethering and fusion (PubMed:24891604, PubMed:30970241). RAB18 is required for the localization of ZFYVE1 t

LOCALIZAÇÃO

Endoplasmic reticulum membraneGolgi apparatus, cis-Golgi network membraneLipid dropletApical cell membrane

VIAS BIOLÓGICAS (2)
RAB geranylgeranylationCOPI-independent Golgi-to-ER retrograde traffic
MECANISMO DE DOENÇA

Warburg micro syndrome 3

A rare syndrome characterized by microcephaly, microphthalmia, microcornia, congenital cataracts, optic atrophy, cortical dysplasia, in particular corpus callosum hypoplasia, severe intellectual disability, spastic diplegia, and hypogonadism.

EXPRESSÃO TECIDUAL(Ubíquo)
Cérebro - Hemisfério cerebelar
47.3 TPM
Artéria tibial
42.3 TPM
Glândula adrenal
41.9 TPM
Cervix Ectocervix
40.6 TPM
Vagina
40.5 TPM
OUTRAS DOENÇAS (2)
Warburg micro syndrome 3Warburg micro syndrome
HGNC:14244UniProt:Q9NP72
PSAT1Phosphoserine aminotransferaseDisease-causing germline mutation(s) inTolerante
FUNÇÃO

Involved in L-serine biosynthesis via the phosphorylated pathway, a three-step pathway converting the glycolytic intermediate 3-phospho-D-glycerate into L-serine (PubMed:36851825, PubMed:37627284). Catalyzes the second step, that is the pyridoxal 5'-phosphate-dependent transamination of 3-phosphohydroxypyruvate and L-glutamate to O-phosphoserine (OPS) and alpha-ketoglutarate (PubMed:36851825, PubMed:37627284). Acts as an inhibitor of ferroptosis in response to interferon-gamma (IFNG) by promotin

LOCALIZAÇÃO

VIAS BIOLÓGICAS (1)
Serine metabolism
MECANISMO DE DOENÇA

Phosphoserine aminotransferase deficiency

Characterized biochemically by low plasma and cerebrospinal fluid concentrations of serine and glycine and clinically by intractable seizures, acquired microcephaly, hypertonia, and psychomotor retardation.

VIAS REACTOME (1)
EXPRESSÃO TECIDUAL(Ubíquo)
Fibroblastos
212.8 TPM
Cérebro - Amígdala
147.1 TPM
Brain Spinal cord cervical c-1
141.2 TPM
Brain Anterior cingulate cortex BA24
119.5 TPM
Brain Caudate basal ganglia
117.0 TPM
OUTRAS DOENÇAS (2)
Neu-Laxova syndrome 2PSAT deficiency
HGNC:19129UniProt:Q9Y617
CEP85LCentrosomal protein of 85 kDa-likeDisease-causing germline mutation(s) inTolerante
FUNÇÃO

Plays an essential role in neuronal cell migration

LOCALIZAÇÃO

Cytoplasm, cytoskeleton, microtubule organizing center, centrosome

OUTRAS DOENÇAS (2)
lissencephaly 10lissencephaly 9 with complex brainstem malformation
HGNC:21638UniProt:Q5SZL2
TUBA1ATubulin alpha-1A chainDisease-causing germline mutation(s) inAltamente restrito
FUNÇÃO

Tubulin is the major constituent of microtubules, a cylinder consisting of laterally associated linear protofilaments composed of alpha- and beta-tubulin heterodimers. Microtubules grow by the addition of GTP-tubulin dimers to the microtubule end, where a stabilizing cap forms. Below the cap, tubulin dimers are in GDP-bound state, owing to GTPase activity of alpha-tubulin

LOCALIZAÇÃO

Cytoplasm, cytoskeletonCytoplasm, cytoskeleton, flagellum axoneme

VIAS BIOLÓGICAS (10)
HCMV Early EventsPKR-mediated signalingGap junction assemblyAggrephagyAssembly and cell surface presentation of NMDA receptors
MECANISMO DE DOENÇA

Lissencephaly 3

A classic type lissencephaly associated with psychomotor retardation and seizures. Features include agyria or pachygyria or laminar heterotopia, severe intellectual disability, motor delay, variable presence of seizures, and abnormalities of corpus callosum, hippocampus, cerebellar vermis and brainstem.

EXPRESSÃO TECIDUAL(Ubíquo)
Brain Spinal cord cervical c-1
1761.9 TPM
Hipotálamo
655.7 TPM
Substância negra
642.6 TPM
Cérebro - Hemisfério cerebelar
562.6 TPM
Cerebelo
519.9 TPM
OUTRAS DOENÇAS (4)
lissencephaly due to TUBA1A mutationfetal akinesia deformation sequence 1tubulinopathy-associated dysgyriacongenital fibrosis of extraocular muscles
HGNC:20766UniProt:Q71U36
RAB3GAP2Rab3 GTPase-activating protein non-catalytic subunitDisease-causing germline mutation(s) inRestrito
FUNÇÃO

Regulatory subunit of the Rab3 GTPase-activating (Rab3GAP) complex composed of RAB3GAP1 and RAB3GAP2, which accelerates the otherwise slow GTP hydrolysis catalyzed by Rab proteins (PubMed:9733780, PubMed:39779760). The complex has GTPase-activating protein (GAP) activity towards various Rab3 subfamily members (RAB3A, RAB3B, RAB3C and RAB3D), RAB5A and RAB43, and has guanine nucleotide exchange factor (GEF) activity towards RAB18 (PubMed:9733780, PubMed:39779760, PubMed:24891604). The Rab3GAP com

LOCALIZAÇÃO

CytoplasmEndoplasmic reticulum

VIAS BIOLÓGICAS (1)
RAB GEFs exchange GTP for GDP on RABs
MECANISMO DE DOENÇA

Martsolf syndrome 1

An autosomal recessive disease characterized by congenital cataracts, intellectual disability, and hypogonadism.

EXPRESSÃO TECIDUAL(Ubíquo)
Linfócitos
30.9 TPM
Fibroblastos
20.4 TPM
Nervo tibial
16.4 TPM
Cérebro - Hemisfério cerebelar
15.7 TPM
Artéria tibial
15.5 TPM
OUTRAS DOENÇAS (4)
Warburg micro syndrome 2Martsolf syndrome 1autosomal recessive spastic paraplegia type 69Warburg micro syndrome
HGNC:17168UniProt:Q9H2M9
KATNB1Katanin p80 WD40 repeat-containing subunit B1Disease-causing germline mutation(s) inTolerante
FUNÇÃO

Participates in a complex which severs microtubules in an ATP-dependent manner. May act to target the enzymatic subunit of this complex to sites of action such as the centrosome. Microtubule severing may promote rapid reorganization of cellular microtubule arrays and the release of microtubules from the centrosome following nucleation. Microtubule release from the mitotic spindle poles may allow depolymerization of the microtubule end proximal to the spindle pole, leading to poleward microtubule

LOCALIZAÇÃO

CytoplasmCytoplasm, cytoskeleton, microtubule organizing center, centrosomeCytoplasm, cytoskeleton, spindle poleCytoplasm, cytoskeletonCytoplasm, cytoskeleton, spindle

MECANISMO DE DOENÇA

Lissencephaly 6, with microcephaly

A form of lissencephaly, a disorder of cortical development characterized by agyria or pachygyria and disorganization of the clear neuronal lamination of normal six-layered cortex. LIS6 features include hypoplasia of the corpus callosum, severe microcephaly and developmental delay.

EXPRESSÃO TECIDUAL(Ubíquo)
Testículo
84.6 TPM
Córtex cerebral
54.6 TPM
Brain Frontal Cortex BA9
50.4 TPM
Skin Sun Exposed Lower leg
45.8 TPM
Cerebelo
39.1 TPM
OUTRAS DOENÇAS (2)
lissencephaly 6 with microcephalyNorman-Roberts syndrome
HGNC:6217UniProt:Q9BVA0
NDE1Nuclear distribution protein nudE homolog 1Disease-causing germline mutation(s) inTolerante
FUNÇÃO

Required for centrosome duplication and formation and function of the mitotic spindle. Essential for the development of the cerebral cortex. May regulate the production of neurons by controlling the orientation of the mitotic spindle during division of cortical neuronal progenitors of the proliferative ventricular zone of the brain. Orientation of the division plane perpendicular to the layers of the cortex gives rise to two proliferative neuronal progenitors whereas parallel orientation of the

LOCALIZAÇÃO

Cytoplasm, cytoskeletonCytoplasm, cytoskeleton, microtubule organizing center, centrosomeChromosome, centromere, kinetochoreCytoplasm, cytoskeleton, spindleCleavage furrowCytoplasmic vesicle membrane

VIAS BIOLÓGICAS (10)
Amplification of signal from unattached kinetochores via a MAD2 inhibitory signalRHO GTPases Activate ForminsMitotic PrometaphaseEML4 and NUDC in mitotic spindle formationResolution of Sister Chromatid Cohesion
MECANISMO DE DOENÇA

Lissencephaly 4 with microcephaly

A neurodevelopmental disorder characterized by lissencephaly, severe brain atrophy, extreme microcephaly, and profound intellectual disability.

EXPRESSÃO TECIDUAL(Ubíquo)
Linfócitos
54.8 TPM
Brain Spinal cord cervical c-1
24.3 TPM
Skin Sun Exposed Lower leg
21.6 TPM
Skin Not Sun Exposed Suprapubic
20.0 TPM
Vagina
17.1 TPM
OUTRAS DOENÇAS (4)
lissencephaly 4NDE1-related microhydranencephalyhydranencephalyNorman-Roberts syndrome
HGNC:17619UniProt:Q9NXR1
RAB3GAP1Rab3 GTPase-activating protein catalytic subunitDisease-causing germline mutation(s) inTolerante
FUNÇÃO

Catalytic subunit of the Rab3 GTPase-activating (Rab3GAP) complex composed of RAB3GAP1 and RAB3GAP2, which accelerates the otherwise slow GTP hydrolysis catalyzed by Rab proteins (PubMed:9030515, PubMed:10859313, PubMed:39779760). Has GTPase-activating protein (GAP) activity towards various Rab3 subfamily members (RAB3A, RAB3B, RAB3C and RAB3D), RAB5A and RAB43 (PubMed:10859313, PubMed:9030515, PubMed:39779760). Additionally, it has guanine nucleotide exchange factor (GEF) activity towards RAB18

LOCALIZAÇÃO

CytoplasmEndoplasmic reticulumGolgi apparatus, cis-Golgi network

VIAS BIOLÓGICAS (1)
RAB GEFs exchange GTP for GDP on RABs
MECANISMO DE DOENÇA

Warburg micro syndrome 1

A rare, autosomal recessive syndrome characterized by microcephaly, microphthalmia, microcornia, congenital cataracts, optic atrophy, cortical dysplasia, in particular corpus callosum hypoplasia, severe intellectual disability, spastic diplegia, and hypogonadism.

EXPRESSÃO TECIDUAL(Ubíquo)
Artéria tibial
52.2 TPM
Aorta
47.2 TPM
Fibroblastos
41.0 TPM
Cervix Ectocervix
40.4 TPM
Útero
39.8 TPM
OUTRAS DOENÇAS (4)
Martsolf syndrome 2Warburg micro syndrome 1Warburg micro syndromeMartsolf syndrome 1
HGNC:17063UniProt:Q15042
MACF1Microtubule-actin cross-linking factor 1, isoforms 1/2/3/4/5Disease-causing germline mutation(s) inAltamente restrito
FUNÇÃO

F-actin-binding protein which plays a role in cross-linking actin to other cytoskeletal proteins and also binds to microtubules (PubMed:15265687, PubMed:20937854). Plays an important role in ERBB2-dependent stabilization of microtubules at the cell cortex (PubMed:20937854). Acts as a positive regulator of Wnt receptor signaling pathway and is involved in the translocation of AXIN1 and its associated complex (composed of APC, CTNNB1 and GSK3B) from the cytoplasm to the cell membrane (By similarit

LOCALIZAÇÃO

Cytoplasm, cytoskeletonCytoplasmGolgi apparatusCell membraneCell projection, ruffle membrane

VIAS BIOLÓGICAS (1)
Signaling by BRAF and RAF1 fusions
MECANISMO DE DOENÇA

Lissencephaly 9 with complex brainstem malformation

A form of lissencephaly, a disorder of cortical development characterized by agyria or pachygyria and disorganization of the clear neuronal lamination of normal six-layered cortex. LIS9 is an autosomal dominant form clinically characterized by global developmental delay apparent since infancy, impaired intellectual development with poor or absent speech, and sometimes abnormal or involuntary movements. Brain imaging shows malformation of the brainstem, in addition to pachygyria and lissencephaly.

EXPRESSÃO TECIDUAL(Ubíquo)
Pulmão
65.0 TPM
Artéria tibial
50.4 TPM
Útero
49.0 TPM
Cólon sigmoide
43.1 TPM
Artéria coronária
42.8 TPM
OUTRAS DOENÇAS (1)
lissencephaly 9 with complex brainstem malformation
HGNC:13664UniProt:Q9UPN3
RELNReelinDisease-causing germline mutation(s) inAltamente restrito
FUNÇÃO

Extracellular matrix serine protease secreted by pioneer neurons that plays a role in layering of neurons in the cerebral cortex and cerebellum by coordinating cell positioning during neurodevelopment. Regulates microtubule function in neurons and neuronal migration. Binding to the extracellular domains of lipoprotein receptors VLDLR and LRP8/APOER2 induces tyrosine phosphorylation of DAB1 and modulation of TAU phosphorylation. Affects migration of sympathetic preganglionic neurons in the spinal

LOCALIZAÇÃO

Secreted, extracellular space, extracellular matrix

VIAS BIOLÓGICAS (1)
Reelin signalling pathway
MECANISMO DE DOENÇA

Lissencephaly 2

A classic type lissencephaly associated with ataxia, intellectual disability, seizures and abnormalities of the cerebellum, hippocampus and brainstem.

EXPRESSÃO TECIDUAL(Ubíquo)
Cérebro - Hemisfério cerebelar
161.3 TPM
Cerebelo
101.1 TPM
Nervo tibial
38.5 TPM
Tireoide
4.3 TPM
Hipotálamo
3.8 TPM
OUTRAS DOENÇAS (3)
Norman-Roberts syndromeautosomal dominant epilepsy with auditory featuresfamilial temporal lobe epilepsy 7
HGNC:9957UniProt:P78509
TBC1D20TBC1 domain family member 20Disease-causing germline mutation(s) inAltamente restrito
FUNÇÃO

GTPase-activating protein (GAP) specific for Rab1 and Rab2 small GTPase families for which it can accelerate the intrinsic GTP hydrolysis rate by more than five orders of magnitude (PubMed:23236136). Also shows GAP activity for RAB18 GTPase (PubMed:26063829). Promotes RAB18 dissociation from the endoplasmic reticulum (ER) membrane into the cytosol, probably through stimulating RAB18 GTP-hydrolysis (PubMed:26063829). Involved in maintaining endoplasmic reticulum structure (PubMed:24891604)

LOCALIZAÇÃO

Membrane

VIAS BIOLÓGICAS (2)
COPII-mediated vesicle transportTBC/RABGAPs
MECANISMO DE DOENÇA

Warburg micro syndrome 4

A form of Warburg micro syndrome, a rare syndrome characterized by microcephaly, microphthalmia, microcornia, congenital cataracts, optic atrophy, cortical dysplasia, in particular corpus callosum hypoplasia, severe intellectual disability, spastic diplegia, and hypogonadism.

EXPRESSÃO TECIDUAL(Ubíquo)
Cérebro - Hemisfério cerebelar
52.2 TPM
Cerebelo
52.0 TPM
Útero
49.2 TPM
Cervix Ectocervix
48.7 TPM
Cervix Endocervix
48.6 TPM
OUTRAS DOENÇAS (2)
Warburg micro syndrome 4Warburg micro syndrome
HGNC:16133UniProt:Q96BZ9
DCXNeuronal migration protein doublecortinDisease-causing germline mutation(s) inAltamente restrito
FUNÇÃO

Microtubule-associated protein required for initial steps of neuronal dispersion and cortex lamination during cerebral cortex development. May act by competing with the putative neuronal protein kinase DCLK1 in binding to a target protein. May in that way participate in a signaling pathway that is crucial for neuronal interaction before and during migration, possibly as part of a calcium ion-dependent signal transduction pathway. May be part with PAFAH1B1/LIS-1 of overlapping, but distinct, sign

LOCALIZAÇÃO

CytoplasmCell projection, neuron projection

VIAS BIOLÓGICAS (1)
Neurofascin interactions
MECANISMO DE DOENÇA

Lissencephaly, X-linked 1

A classic lissencephaly characterized by intellectual disability and seizures that are more severe in male patients. Affected boys show an abnormally thick cortex with absent or severely reduced gyri. Clinical manifestations include feeding problems, abnormal muscular tone, seizures and severe to profound psychomotor retardation. Female patients display a less severe phenotype referred to as 'doublecortex'.

VIAS REACTOME (1)
EXPRESSÃO TECIDUAL(Baixa expressão)
Brain Frontal Cortex BA9
2.7 TPM
Hipotálamo
2.2 TPM
Brain Anterior cingulate cortex BA24
2.1 TPM
Brain Nucleus accumbens basal ganglia
2.0 TPM
Córtex cerebral
2.0 TPM
OUTRAS DOENÇAS (2)
lissencephaly type 1 due to doublecortin gene mutationsubcortical band heterotopia
HGNC:2714UniProt:O43602
ARXHomeobox protein ARXDisease-causing germline mutation(s) inAltamente restrito
FUNÇÃO

Transcription factor (PubMed:22194193, PubMed:31691806). Binds to specific sequence motif 5'-TAATTA-3' in regulatory elements of target genes, such as histone demethylase KDM5C (PubMed:22194193, PubMed:31691806). Positively modulates transcription of KDM5C (PubMed:31691806). Activates expression of KDM5C synergistically with histone lysine demethylase PHF8 and perhaps in competition with transcription regulator ZNF711; synergy may be related to enrichment of histone H3K4me3 in regulatory element

LOCALIZAÇÃO

Nucleus

MECANISMO DE DOENÇA

Lissencephaly, X-linked 2

A classic type lissencephaly associated with abnormal genitalia. Patients have severe congenital or postnatal microcephaly, lissencephaly, agenesis of the corpus callosum, neonatal-onset intractable epilepsy, poor temperature regulation, chronic diarrhea, and ambiguous or underdeveloped genitalia.

OUTRAS DOENÇAS (9)
X-linked lissencephaly with abnormal genitaliaPartington syndromecorpus callosum agenesis-abnormal genitalia syndromedevelopmental and epileptic encephalopathy, 1
HGNC:18060UniProt:Q96QS3
PAFAH1B1Platelet-activating factor acetylhydrolase IB subunit betaDisease-causing germline mutation(s) inAltamente restrito
FUNÇÃO

Regulatory subunit (beta subunit) of the cytosolic type I platelet-activating factor (PAF) acetylhydrolase (PAF-AH (I)), an enzyme that catalyzes the hydrolyze of the acetyl group at the sn-2 position of PAF and its analogs and participates in PAF inactivation. Regulates the PAF-AH (I) activity in a catalytic dimer composition-dependent manner (By similarity). Required for proper activation of Rho GTPases and actin polymerization at the leading edge of locomoting cerebellar neurons and postmigra

LOCALIZAÇÃO

Cytoplasm, cytoskeletonCytoplasm, cytoskeleton, microtubule organizing center, centrosomeCytoplasm, cytoskeleton, spindleNucleus membrane

VIAS BIOLÓGICAS (10)
Amplification of signal from unattached kinetochores via a MAD2 inhibitory signalRHO GTPases Activate ForminsMitotic PrometaphaseEML4 and NUDC in mitotic spindle formationResolution of Sister Chromatid Cohesion
MECANISMO DE DOENÇA

Lissencephaly 1

A classical lissencephaly. It is characterized by agyria or pachygyria and disorganization of the clear neuronal lamination of normal six-layered cortex. The cortex is abnormally thick and poorly organized with 4 primitive layers. Associated with enlarged and dysmorphic ventricles and often hypoplasia of the corpus callosum.

EXPRESSÃO TECIDUAL(Ubíquo)
Cérebro - Hemisfério cerebelar
168.8 TPM
Cerebelo
131.0 TPM
Testículo
125.6 TPM
Brain Frontal Cortex BA9
94.1 TPM
Artéria tibial
93.4 TPM
OUTRAS DOENÇAS (4)
lissencephaly due to LIS1 mutationMiller-Dieker lissencephaly syndromesubcortical band heterotopiachromosome 17p13.3 duplication syndrome
HGNC:8574UniProt:P43034
LAMB1Laminin subunit beta-1Disease-causing germline mutation(s) inTolerante
FUNÇÃO

Binding to cells via a high affinity receptor, laminin is thought to mediate the attachment, migration and organization of cells into tissues during embryonic development by interacting with other extracellular matrix components. Involved in the organization of the laminar architecture of the cerebral cortex (PubMed:23472759). It is probably required for the integrity of the basement membrane/glia limitans that serves as an anchor point for the endfeet of radial glial cells and as a physical bar

LOCALIZAÇÃO

Secreted, extracellular space, extracellular matrix, basement membrane

VIAS BIOLÓGICAS (2)
Post-translational protein phosphorylationRegulation of Insulin-like Growth Factor (IGF) transport and uptake by Insulin-like Growth Factor Binding Proteins (IGFBPs)
MECANISMO DE DOENÇA

Lissencephaly 5

An autosomal recessive brain malformation characterized by cobblestone changes in the cortex, more severe in the posterior region, and subcortical band heterotopia. Affected individuals have hydrocephalus, seizures, and severely delayed psychomotor development.

EXPRESSÃO TECIDUAL(Ubíquo)
Fibroblastos
416.2 TPM
Nervo tibial
271.7 TPM
Adipose Visceral Omentum
245.7 TPM
Pulmão
216.7 TPM
Cólon sigmoide
161.6 TPM
OUTRAS DOENÇAS (1)
cobblestone lissencephaly without muscular or ocular involvement
HGNC:6486UniProt:P07942

Variantes genéticas (ClinVar)

375 variantes patogênicas registradas no ClinVar.

🧬 PHGDH: NM_006623.4(PHGDH):c.701G>T (p.Cys234Phe) ()
🧬 PHGDH: NM_006623.4(PHGDH):c.367C>T (p.Gln123Ter) ()
🧬 PHGDH: NM_006623.4(PHGDH):c.636del (p.Thr213fs) ()
🧬 PHGDH: NM_006623.4(PHGDH):c.510+1G>T ()
🧬 PHGDH: NM_006623.4(PHGDH):c.557T>A (p.Phe186Tyr) ()
Ver todas no ClinVar

Classificação de variantes (ClinVar)

Distribuição de 979 variantes classificadas pelo ClinVar.

587
343
49
Patogênica (60.0%)
VUS (35.0%)
Benigna (5.0%)
VARIANTES MAIS SIGNIFICATIVAS
MACF1: NM_001394062.1(MACF1):c.20288T>G (p.Phe6763Cys) [Likely pathogenic]
ARX: NM_139058.3(ARX):c.969dup (p.Leu324fs) [Pathogenic]
LAMB1: LAMB1, EX23-EX24DEL [Pathogenic]
LAMB1: LAMB1, NT5201_5224+28DEL [Pathogenic]
LAMB1: LAMB1, ASN788SER [Pathogenic]

Vias biológicas (Reactome)

120 vias biológicas associadas aos genes desta condição.

Serine metabolism Non-integrin membrane-ECM interactions ECM proteoglycans Defective POMGNT1 causes MDDGA3, MDDGB3 and MDDGC3 Defective POMT2 causes MDDGA2, MDDGB2 and MDDGC2 Defective POMT1 causes MDDGA1, MDDGB1 and MDDGC1 DAG1 core M2 glycosylations DAG1 core M3 glycosylations DAG1 core M1 glycosylations Regulation of expression of SLITs and ROBOs EGR2 and SOX10-mediated initiation of Schwann cell myelination Formation of the dystrophin-glycoprotein complex (DGC) Matriglycan biosynthesis on DAG1 Activation of BAD and translocation to mitochondria Translocation of SLC2A4 (GLUT4) to the plasma membrane Signaling by Hippo NADE modulates death signalling Regulation of PLK1 Activity at G2/M Transition Regulation of HSF1-mediated heat shock response HSF1 activation Loss of Nlp from mitotic centrosomes Recruitment of mitotic centrosome proteins and complexes Loss of proteins required for interphase microtubule organization from the centrosome Recruitment of NuMA to mitotic centrosomes Anchoring of the basal body to the plasma membrane RHO GTPases activate PKNs TP53 Regulates Metabolic Genes Chk1/Chk2(Cds1) mediated inactivation of Cyclin B:Cdk1 complex AURKA Activation by TPX2 Deregulated CDK5 triggers multiple neurodegenerative pathways in Alzheimer's disease models RAB GEFs exchange GTP for GDP on RABs SARS-CoV-1 targets host intracellular signalling and regulatory pathways SARS-CoV-2 targets host intracellular signalling and regulatory pathways Transcriptional and post-translational regulation of MITF-M expression and activity SUMOylation of transcription factors Regulation of CDH1 posttranslational processing and trafficking to plasma membrane DARPP-32 events CRMPs in Sema3A signaling Regulation of TP53 Activity through Phosphorylation NGF-stimulated transcription Activated NTRK2 signals through CDK5 NPAS4 regulates expression of target genes Factors involved in megakaryocyte development and platelet production MLL4 and MLL3 complexes regulate expression of PPARG target genes in adipogenesis and hepatic steatosis Phosphorylation and nuclear translocation of BMAL1 (ARNTL) and CLOCK Phosphorylation and nuclear translocation of the CRY:PER:kinase complex Gap junction degradation Formation of annular gap junctions Regulation of actin dynamics for phagocytic cup formation EPHB-mediated forward signaling EPH-ephrin mediated repulsion of cells Adherens junctions interactions Recycling pathway of L1 VEGFA-VEGFR2 Pathway Interaction between L1 and Ankyrins Cell-extracellular matrix interactions RHO GTPases activate IQGAPs RHO GTPases Activate WASPs and WAVEs RHO GTPases Activate Formins MAP2K and MAPK activation Signaling by moderate kinase activity BRAF mutants Signaling by high-kinase activity BRAF mutants Signaling by BRAF and RAF1 fusions Paradoxical activation of RAF signaling by kinase inactive BRAF Clathrin-mediated endocytosis RHOBTB2 GTPase cycle Signaling downstream of RAS mutants Signaling by RAF1 mutants Sensory processing of sound by inner hair cells of the cochlea Sensory processing of sound by outer hair cells of the cochlea FCGR3A-mediated phagocytosis Regulation of CDH1 Function GBP-mediated host defense HATs acetylate histones Prefoldin mediated transfer of substrate to CCT/TriC Folding of actin by CCT/TriC B-WICH complex positively regulates rRNA expression UCH proteinases DNA Damage Recognition in GG-NER RHOF GTPase cycle Neutrophil degranulation COPI-independent Golgi-to-ER retrograde traffic RAB geranylgeranylation Microtubule-dependent trafficking of connexons from Golgi to the plasma membrane Gap junction assembly MHC class II antigen presentation Separation of Sister Chromatids Resolution of Sister Chromatid Cohesion HSP90 chaperone cycle for steroid hormone receptors (SHR) in the presence of ligand Formation of tubulin folding intermediates by CCT/TriC Post-chaperonin tubulin folding pathway Hedgehog 'off' state Cargo trafficking to the periciliary membrane Intraflagellar transport COPI-mediated anterograde transport COPI-dependent Golgi-to-ER retrograde traffic Mitotic Prometaphase The role of GTSE1 in G2/M progression after G2 checkpoint Carboxyterminal post-translational modifications of tubulin HCMV Early Events Amplification of signal from unattached kinetochores via a MAD2 inhibitory signal EML4 and NUDC in mitotic spindle formation p-BRAF-MACF1 fusion dimer BRAF-MACF1 fusion dimer p-BRAF(1-380)-MACF1(600-7388) fusion BRAF(1-380)-MACF1(600-7388)fusion Reelin signalling pathway COPII-mediated vesicle transport TBC/RABGAPs Neurofascin interactions SLIT2 gene expression is stimulated by ISL1 Primary multipotent pancreatic progenitor cell produces trunk bipotent pancreatic progenitor cell Degradation of the extracellular matrix Laminin interactions L1CAM interactions Regulation of Insulin-like Growth Factor (IGF) transport and uptake by Insulin-like Growth Factor Binding Proteins (IGFBPs) MET activates PTK2 signaling Post-translational protein phosphorylation Attachment of bacteria to epithelial cells Developmental Lineage of Pancreatic Ductal Cells

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Publicações mais relevantes

Timeline de publicações
578 papers (10 anos)
#1

Genetic landscape and phenotypic correlations of lissencephaly: prenatal and postnatal insights.

Brain communications2026

Lissencephaly (LIS) is a spectrum of cortical malformations including agyria, pachygyria and subcortical band heterotopia, which arises from aberrant neuronal migration and is associated with severe neurodevelopmental impairments. Despite advancements in prenatal imaging, diagnosing LIS remains challenging. Genetic factors play a crucial role in LIS, involving multiple genes and signalling pathways, yet research on prenatal diagnosis and the genetic basis is still limited. This study aimed to assess the diagnostic yield of whole exome sequencing (WES) in LIS and to examine genotype-phenotype correlations, addressing the challenge of 'phenotype lag' in prenatal LIS diagnosis. This study included 20 fetuses with LIS suggested by prenatal imaging and 20 children with LIS diagnosed after birth; all cases were diagnosed by magnetic resonance imaging and underwent genetic testing. In addition, a literature review was conducted and 80 studies were included, of which 1 was used to compare detection efficacy and 79 studies totalling 210 cases were used to assess genotype-phenotype correlation. In the prenatal cohort, 85.0% (17/20) of cases exhibited concurrent anomalies, predominantly ventriculomegaly (50.0%) and microcephaly (25.0%). In the postnatal cohort, the most common phenotypes were epilepsy (80.0%, 16/20) and global developmental delay (65.0%, 13/20), with half of the cases (10/20) showing no abnormalities in the prenatal period. The diagnostic yields were 55.0% (11/20) and 65.0% (13/20), respectively, with PAFAH1B1 point mutations or 17p13.3 microdeletions being the predominant genetic variant in both cohorts, accounting for 31.3% (prenatal) and 25.5% (postnatal) of cases, respectively. DARS2 and NPRL3 were reported to be associated with LIS for the first time in this study. Literature synthesis revealed an overall diagnostic yield of 79.04%, dominated by PAFAH1B1 (26.3%), DYNC1H1 (11.9%), and DCX (10.2%). By reviewing the prenatal images, up to 48.05% (74/154) of the cases had no specific findings in the prenatal period, and the most common presentations were ventriculomegaly/hydrocephalus (52.63%) and head circumference anomalies (29.82%). This study highlights the significant genetic heterogeneity, phenotypic complexity and diagnostic challenges of LIS by integrating data from our cohort and the published literature. We developed a comprehensive genetic aetiology classification framework for LIS and identified novel associations with non-canonical genes such as NPRL3 and DARS2. With a high molecular diagnostic yield of 79.04%, we recommend WES as the first-line genetic test. Furthermore, the establishment of an integrated prenatal imaging-molecular diagnostic system, along with a postnatal multidisciplinary model, is crucial for improving prognosis assessment, clinical decision-making and genetic counselling.

#2

Bi-allelic variants in NRDC cause a neurodevelopmental disorder characterized by neonatal lethality, microcephaly, and brain abnormalities.

American journal of human genetics2026 Mar 05

Nardilysin (NRDC) plays a role in multiple cellular functions in diverse cellular compartments, including ectodomain shedding in the plasma membrane, as well as chaperoning a key Krebs cycle enzyme in mitochondria. We had previously reported limited clinical information from two individuals with homozygous frameshift variants in NRDC. With inclusion of previously published individuals, here we report 14 individuals (10 females, four males) from nine unrelated families carrying homozygous NRDC pathogenic variants. Common clinical features include severe to profound developmental delay/intellectual disability (12/12), microcephaly (13/13), prematurity (5/13), lethality in the first 3 years of life (9/14), seizures (7/11), joint contractures (4/8), eye/visual abnormalities (5/7), and abnormal brain imaging studies ranging from diffuse atrophy to lissencephaly (8/11). The identified variants include two splice, three frameshift, and three missense variants. RT-PCR from affected individual fibroblasts and a minigene assay in HEK293T cells demonstrate that the splice variants led to exon skipping of NRDC. To further investigate the pathogenicity of the variants in vivo, we used the Drosophila Nrdc (dNrdc) mutant model. dNrdc null mutants caused developmental lethality, which is fully rescued by wild-type human NRDC. Studies in the Drosophila dNrdc mutant models showed that both splice variants and frameshift variants cause severe loss of function, leading to lethality, whereas missense variants cause partial lethality and short lifespan, consistent with less severe phenotype. Our data establish that homozygous variants in NRDC are pathogenic, leading to highly lethal and severe neurodevelopmental disorder in humans.

#3

Roles of microtubules and LIS1 in dynein transport machinery assembly.

Nature2026 Feb 18

Cytoplasmic dynein-1, a microtubule (MT)-based motor protein, requires dynactin and a coiled-coil adaptor to form the processive dynein-dynactin-adaptor (DDA) complex1,2. The roles of MTs and dynein regulator lissencephaly-1 (LIS1) in DDA assembly have remained elusive. Here we use cryo-electron microscopy to determine the structural basis of MT- and LIS1-mediated DDA assembly. We show that an adaptor-independent dynein-dynactin complex spontaneously forms on MTs with an intrinsic 2:1 stoichiometry in a highly efficient manner, driven by parallel alignment of dynein tails upon MT binding. Adaptors can wedge into and exchange within the assembled MT-bound dynein-dynactin complex; these processes are enabled by relative rotations between dynein and dynactin and facilitated by the dynein light-intermediate chains that assist the adaptor 'search' mechanism. Although LIS1 is dispensable for efficient DD(A)-MT assembly, its presence expands the conformational landscape of DD(A) assemblies on MTs. Cryo-electron microscopy reveals that LIS1 bridges dynactin p150glued and dynein in both the closed Phi-like and open prepowerstroke states, stabilizing low-MT-affinity intermediates that tether dynein molecules in proximity to MTs and prime them for subsequent DD(A) assembly through alternative pathways. These findings demonstrate the dynamic adaptability of the dynein transport machinery and the coordinated roles of MTs and LIS1 in DDA assembly.

#4

Bi-allelic variants in neuronal adhesion molecule astrotactin 1 gene ASTN1 cause diverse neurodevelopmental disorders.

American journal of human genetics2026 Feb 05

ASTN1 encodes astrotactin 1, a neuronal-glial ligand in the developing brain that promotes neuronal migration along radial glia in brain structures with laminar organization, such as the cerebral cortex, hippocampus, and cerebellum. In mouse models, disruption of Astn1 results in neuronal migration deficits, a mild reduction in cerebellar volume, and balance and coordination deficits. In humans, bi-allelic ASTN1 variants have been identified in nine individuals with neurodevelopmental disorders (NDDs) with or without brain malformations. ASTN1 additionally interacts with astrotactin 2 (ASTN2) to implement neuronal migration; ASTN2 deletions associate with NDDs with reduced penetrance. Here, we describe eighteen individuals with NDDs from twelve unrelated families with bi-allelic, ultra-rare, predicted damaging variants in ASTN1 and one individual with heterozygous variants in both ASTN1 and ASTN2. We expand the clinical phenotypic descriptions of ASTN1-related NDDs, which range from mild to profound developmental delay or intellectual disability and can be associated with autism, attention-deficient hyperactivity disorder (ADHD), and epilepsy. Other recurrent abnormalities include dysmorphic facial features, hypotonia, spasticity, and ataxia. Additionally, we add to the neuroradiographic phenotype of this condition, which can be normal, mildly dysmorphic (a thin corpus callosum and cerebellar dysgenesis), or severely dysmorphic (polymicrogyria and lissencephaly). Remarkably, three genetic models of multilocus pathogenic variation (MPV), including tri-allelic, double heterozygous, and double homozygous due to distributive absence of heterozygosity (AOH), were observed. This ASTN1 allelic series characterizes the consequences of perturbations in radial-glia-guided neuronal migration in humans, the phenotypic spectrum of ASTN1-related NDDs, and the contribution of MPV to the genetic basis of NDDs.

#5

A rare complication of vagus nerve stimulation surgery: the Horner Syndrome. Case report and systematic review.

Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology2026 Jan 05

Vagus nerve stimulation (VNS) is a therapy used for drug-resistant epilepsy, refractory status epilepticus and treatment-resistant depression. VNS can reduce seizure severity and frequency, improving quality of life. It is generally well tolerated, with rare complications, which can be early (surgical) or late (device-related or stimulation-related). Common side effects include vocal cord issues, cough, and infections. We present Horner syndrome as a rare complication of VNS caused by damage to the sympathetic innervation of the ipsilateral eye and characterized by ptosis, miosis and rarely anhidrosis.  MATERIALS AND METHODS: This was a case report and systematic review of the available literature according to PRISMA guidelines. The examined databases are Medline/PubMed, Scopus and Web of Science.  RESULTS: A fourteen-year-old girl with drug-resistant epileptic encephalopathy and lissencephaly underwent VNS. Clinical signs of Horner syndrome appeared a few hours later. Our systematic review of the literature collected only three cases of Horner syndrome following VNS surgery out of 178 patients studied (one case report and two retrospective studies included in review).  CONCLUSION: We report the fourth case in the literature, a case of permanent Horner.

Publicações recentes

Ver todas no PubMed

📚 EuropePMC523 artigos no totalmostrando 197

2026

Genetic landscape and phenotypic correlations of lissencephaly: prenatal and postnatal insights.

Brain communications
2026

Bi-allelic variants in NRDC cause a neurodevelopmental disorder characterized by neonatal lethality, microcephaly, and brain abnormalities.

American journal of human genetics
2026

MRI-based spectral analysis of fetal brain gyrification in typical development and in lissencephaly and polymicrogyria.

Scientific reports
2026

Roles of microtubules and LIS1 in dynein transport machinery assembly.

Nature
2026

Biophysical modeling of anatomically realistic prenatal cortical folding development.

Research square
2026

Neonatal-onset epileptic encephalopathy with lissencephaly associated with a SCN3A variant: The first case in Korea and literature review.

Seizure
2026

Selective Lis1 inactivation disrupts migration and positioning of cortical somatostatin interneurons.

Scientific reports
2026

Neuro-ophthalmic disorders resulting from defects in the gamma tubulin ring complex: a clinically oriented review.

Ophthalmic genetics
2026

Bi-allelic variants in neuronal adhesion molecule astrotactin 1 gene ASTN1 cause diverse neurodevelopmental disorders.

American journal of human genetics
2026

Cobblestone lissencephaly in the setting of congenital cytomegalovirus infection: A case report and review of the literature.

Clinical neuropathology
2026

The Baraitser-Winter Cerebrofrontofacial Syndrome Recurrent R196H Variant in Cytoplasmic β-Actin Impairs Its Cellular Polymerization and Stability.

FASEB journal : official publication of the Federation of American Societies for Experimental Biology
2026

A rare complication of vagus nerve stimulation surgery: the Horner Syndrome. Case report and systematic review.

Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
2025

Rethinking fetal central nervous system anomalies: predicting central nervous system anomalies with corpus callosum to head circumference and occipitofrontal diameter ratios.

BMC pregnancy and childbirth
2025

Biophysical basis for brain folding and misfolding patterns in ferrets and humans.

eLife
2026

COP9 signalosome and PRMT5 methylosome complexes are essential regulators of Lis1-dynein-based transport.

Cell reports
2025

Compound Heterozygous PNKP Variants Causing Developmental and Epileptic Encephalopathy with Severe Microcephaly: Natural History of Two New Cases and Literature Review.

NeuroSci
2026

Expanding genetic and clinical spectra of β-tubulinopathies: A Korean study.

Journal of human genetics
2025

Subcortical band heterotopia: electroclinical, radiological, and prognostic features in adults.

Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
2025

Diagnosis of Lissencephaly in a Neonate After Antenatal Polyhydramnios and Suspicion of Fetal Esophageal Atresia: A Case Report.

Cureus
2025

Capturing disease severity in LIS1-lissencephaly reveals proteostasis dysregulation in patient-derived forebrain organoids.

Nature communications
2025

Pearls & Oy-sters: Acute Obstructive Hydrocephalus Co-Occurrence With Vigabatrin-Associated MRI Changes in an Infant With LIS1-Related Classical Lissencephaly.

Neurology
2025

Neuropathological findings of very low-density lipoprotein receptor-related cerebellar hypoplasia in a full-term fetus.

Journal of neuropathology and experimental neurology
2025

A clinical and genotype-phenotype analysis of MACF1 variants.

American journal of human genetics
2025

A case of Baraitser-Winter cerebrofrontofacial syndrome diagnosed by whole-exome sequencing.

Human genome variation
2025

Overview and expansion of CEP85L-associated lissencephaly.

European journal of medical genetics
2025

Understanding the Molecular Basis of Miller-Dieker Syndrome.

International journal of molecular sciences
2025

Paediatric cranial ultrasound: abnormalities of the brain in term neonates and young infants.

Insights into imaging
2025

Spatial Proteomics Reveals Distinct Protein Patterns in Cortical Migration Disorders Caused by LIN28A Overexpression and WNT Activation.

Molecular & cellular proteomics : MCP
2025

Domain specific phenotypic expansion associated with variants in MACF1.

medRxiv : the preprint server for health sciences
2025

Tracheal Complications Following Prolonged Invasive Ventilation in Tracheostomized Pediatric Patients with Complex Chronic Conditions.

Children (Basel, Switzerland)
2025

Multiple steps of dynein activation by Lis1 visualized by cryo-EM.

Nature structural & molecular biology
2025

Deep clinical and genetic analysis of 17p13.3 region: 38 pediatric patients diagnosed using next-generation sequencing and literature review.

BMC medical genomics
2025

Identification of MACF1 as a causative gene of generalised epilepsy.

Journal of medical genetics
2025

WDR62 controls cortical radial migration and callosal projection of neurons in the developing cerebral cortex.

Neurobiology of disease
2025

Altered extracellular matrix structure and elevated stiffness in a brain organoid model for disease.

Nature communications
2025

Two New Cases Expand the Phenotypic Spectrum of TUBG1 Missense Variants.

American journal of medical genetics. Part A
2025

Manatee cognition and behavior: a neurobiological perspective on an unusual constellation of senses and a unique brain.

Frontiers in behavioral neuroscience
2025

Corpus Callosotomy for Atonic Drop Seizures in Bilateral Malformations of Cortical Development: A Systematic Review of Literature.

Cureus
2026

A Bioinformatic Investigation into a Unique Human FOXM1 Exon Variant and Its Relevance to Gyrencephaly.

Developmental neuroscience
2025

Multidisciplinary approach to reach a foetal diagnosis of Walker-Warburg syndrome: From autopsy to genetics and back.

Revista espanola de patologia : publicacion oficial de la Sociedad Espanola de Anatomia Patologica y de la Sociedad Espanola de Citologia
2025

"Hair-on-end" appearance in thickened cortex in a case of classic lissencephaly due to DCX gene mutation.

Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
2025

P253 Next-generation phenotyping facilitates the identification of structural brain malformations in rare disorders through computational brain MRI analysis.

Genetics in medicine open
2025

The response to anti-seizure medications and the development of pharmacoresistant epilepsy in malformations of cortical development.

BMC medicine
2025

A Novel Variant c.149G>A in CDK5 Gene Causing Lissencephaly Type 7.

Clinical genetics
2025

Unilateral schizencephaly open lip with septo optic dysplasia in adult woman with glaucoma: A rare case.

Radiology case reports
2025

The fetal neurologist: Strategies to improve training, practice, and clinical care.

Developmental medicine and child neurology
2025

Fetal malformations of cortical development: review and clinical guidance.

Brain : a journal of neurology
2025

Catatonia in a Patient With Lissencephaly Treated With ECT: A Case Report and Literature Review.

The journal of ECT
2025

TUBGCP2 variants cause lissencephaly spectrum disorders: a case report and literature review.

Frontiers in pediatrics
2025

Neonatal Microcephaly and Central Nervous System Abnormalities During the Zika Outbreak in Rio de Janeiro.

Viruses
2025

Immediate Therapeutic Response to Vigabatrin in Lissencephaly-Related Epileptic Spasms due to TUBA1A R402H Variant.

American journal of medical genetics. Part A
2025

Pt-LIS1 participates nuclear deformation and acrosome formation via regulating Dynein-1 during spermatogenesis in Portunus trituberculatus.

Scientific reports
2025

Doublecortin restricts neuronal branching by regulating tubulin polyglutamylation.

Nature communications
2025

DNA ligase IV deficiency identified in a patient with hypergonadotropic hypogonadism: a case report.

Journal of pediatric endocrinology & metabolism : JPEM
2025

NuMA is a mitotic adaptor protein that activates dynein and connects it to microtubule minus ends.

The Journal of cell biology
2025

Dab1 expression level controls Reelin-induced PI3K-Akt activation in early GABAergic neurons.

Biochemical and biophysical research communications
2025

A Novel MACF1 Gene Mutation: Expanding the Fetal and Neonatal Phenotype.

Pediatric neurology
2025

Coexisting Congenital Mesoblastic Nephroma and Lissencephaly: Unique Case Report with Pathological Analysis and Its Clinical Significance.

Biomedicines
2025

Dysregulation of mTOR signalling is a converging mechanism in lissencephaly.

Nature
2024

Brain malformation, neurodevelopmental disorder and epilepsy in a case of two rare genetic diseases: overlapping phenotype.

Neurogenetics
2025

Heterozygous inversion on chromosome 17 involving PAFAH1B1 detected by whole genome sequencing in a patient suffering from pachygyria.

European journal of medical genetics
2025

CASP2 biallelic truncating variants: a new case supports the link with lissencephaly/pachygyria and expands the clinical spectrum.

European journal of human genetics : EJHG
2025

Anatomo-Electro-Clinical Phenotypes in Children With Epilepsy and DYNC1H1 Mutations.

Pediatric neurology
2024

Doublecortin reinforces microtubules to promote growth cone advance in soft environments.

Current biology : CB
2025

Lissencephaly with subcortical band heterotopia in an East African child: A case report.

Radiology case reports
2025

Ring Chromosome 17 Syndrome-A Case Report and Discussion of Diagnostic Methods.

American journal of medical genetics. Part A
2024

Morphometric Development of Medial Surface of Cerebrum in Fetal Cadavers.

Turkish neurosurgery
2024

Cryo-EM visualizes multiple steps of dynein's activation pathway.

bioRxiv : the preprint server for biology
2024

The Aggravation of Neuropsychiatric Symptoms in the Offspring of a Korean Family with Intellectual Disability and Developmental Delay Caused by a Novel ARX p.Lys385Ter Variant.

International journal of molecular sciences
2025

A novel missense variant in the RELN gene in sheep with lissencephaly and cerebellar hypoplasia.

Veterinary pathology
2024

[Malformations of cortical development: what's new?].

Medicina
2024

Walker-Warburg syndrome: A case report of congenital muscular dystrophy with hydrocephalus.

Radiology case reports
2024

Cobblestone lissencephaly (Type II), clinical, and neuroimaging: A case report and literature review.

Radiology case reports
2024

[Genetic analysis of a child with pachygyria due to variant of ADGRG1 gen].

Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics
2025

tubg1 Somatic Mutants Show Tubulinopathy-Associated Neurodevelopmental Phenotypes in a Zebrafish Model.

Molecular neurobiology
2024

Characterization of the Epileptogenic Phenotype and Response to Antiseizure Medications in Lissencephaly Patients.

Neuropediatrics
2024

A Novel Pathogenic TUBA1A Variant in a Croatian Infant Is Linked to a Severe Tubulinopathy with Walker-Warburg-like Features.

Genes
2024

Exploring unsolved cases of lissencephaly spectrum: integrating exome and genome sequencing for higher diagnostic yield.

Journal of human genetics
2024

Sonographic Cortical Development and Anomalies in the Fetus: A Systematic Review and Meta-Analysis.

Biomedicines
2024

Multiplex Consanguineous Family Highlights CLASP1 as a Candidate Gene for Lissencephaly.

Neurology. Genetics
2024

Role of Physiotherapy in Pediatric Lissencephaly: A Case Report and Therapeutic Insights.

Cureus
2024

DCX knockout ferret reveals a neurogenic mechanism in cortical development.

Cell reports
2024

De novo monoallelic Reelin missense variants cause dominant neuronal migration disorders via a dominant-negative mechanism.

The Journal of clinical investigation
2024

Lissencephaly and Advanced-Stage Congenital Cytomegalovirus Infection in a Neonate.

Cureus
2024

Clinical features and genotype-phenotype correlations in epilepsy patients with de novo DYNC1H1 variants.

Epilepsia
2024

Altered thalamocortical tract trajectory growth with undisrupted thalamic parcellation pattern in human lissencephaly brain at mid-gestational stage.

Neurobiology of disease
2024

Gamma-Tubulin 1 (TUBG1) Mutation-Associated Lissencephaly and Microcephaly in an Indian Child: A Rare Case.

Cureus
2024

Lissencephaly caused by a de novo mutation in tubulin TUBA1A: a case report and literature review.

Frontiers in pediatrics
2024

Phenotypic Variability in Novel Doublecortin Gene Variants Associated with Subcortical Band Heterotopia.

International journal of molecular sciences
2024

Total callosotomy ameliorates epileptic activity and improves cognitive function in a patient with Miller-Dieker syndrome.

Epilepsy & behavior reports
2023

Lissencephaly: presentation of a clinical case of LIS 1 with a diagnosis confirmed by MLPA method and indications for rehabilitation treatment in childhood.

Neurocase
2024

Infantile epileptic spasms syndrome in a child with lissencephaly associated with de novo PAFAH1B1 variant and coincidental CMV infection.

Epilepsy & behavior reports
2024

PRDM16 co-operates with LHX2 to shape the human brain.

Oxford open neuroscience
2024

Molecular mechanism of dynein-dynactin complex assembly by LIS1.

Science (New York, N.Y.)
2024

PAEDIATRIC SYMPTOMATIC SEIZURES IN INDIA: UNRAVELLING VARIED ETIOLOGIES AND NEUROIMAGING PATTERNS - A MULTICENTRIC STUDY.

Georgian medical news
2024

Diagnostic utility of exome sequencing followed by research reanalysis in human brain malformations.

Brain communications
2024

NUDC is critical for rod photoreceptor function, maintenance, and survival.

FASEB journal : official publication of the Federation of American Societies for Experimental Biology
2024

Diagnostic work-up in malformations of cortical development.

Developmental medicine and child neurology
2024

Clinical analysis of PAFAH1B1 gene variants in pediatric patients with epilepsy.

Seizure
2024

Extensive Phenotypic Variability in Syndrome Dysmorphic Facies, Renal Agenesis, Ambiguous Genitalia, Microcephaly, Polydactyly, and Lissencephaly (DREAM-PL): A Case Report Highlighting Diagnostic and Management Challenges.

Cureus
2024

Genetic blueprint of congenital muscular dystrophies with brain malformations in Egypt: A report of 11 families.

Neurogenetics
2024

A genetic variant in the MAST1 gene is associated with mega-corpus-callosum syndrome with hypoplastic cerebellar vermis, in a fetus.

Molecular genetics & genomic medicine
2024

The people behind the papers - Meng-Han Tsai, Wan-Cian Lin and Jin-Wu Tsai.

Development (Cambridge, England)
2024

Novel lissencephaly-associated NDEL1 variant reveals distinct roles of NDE1 and NDEL1 in nucleokinesis and human cortical malformations.

Acta neuropathologica
2024

A lissencephaly-associated BAIAP2 variant causes defects in neuronal migration during brain development.

Development (Cambridge, England)
2023

Brain Pathways in LIS1-Associated Lissencephaly Revealed by Diffusion MRI Tractography.

Brain sciences
2024

Leveraging multiple approaches for the detection of pathogenic deep intronic variants in developmental and epileptic encephalopathies: A case report.

Epilepsia open
2024

Expanding association between BICD2 variants and brain malformations and associated lissencephaly.

Clinical and experimental pediatrics
2023

Bálint syndrome in a patient with drug-resistant epilepsy having underlying X-linked lissencephaly with subcortical band heterotopia/"double cortex" syndrome.

Neurology perspectives
2025

OPTIC NERVE HYPOPLASIA AND BILATERAL PERSISTENT FETAL VASCULATURE DUE TO TUBA1A TUBULINOPATHY.

Retinal cases & brief reports
2024

Monogenic conditions and central nervous system anomalies: A prospective study, systematic review and meta-analysis.

Prenatal diagnosis
2023

Automatic Quantification of Normal Brain Gyrification Patterns and Changes in Fetuses with Polymicrogyria and Lissencephaly Based on MRI.

AJNR. American journal of neuroradiology
2023

DCX variants in two unrelated Chinese families with subcortical band heterotopia: Two case reports and review of literature.

Heliyon
2024

Bi-allelic truncating variants in CASP2 underlie a neurodevelopmental disorder with lissencephaly.

European journal of human genetics : EJHG
2024

Further characterisation of ARX-related disorders in females due to inherited or de novo variants.

Journal of medical genetics
2023

Lissencephaly With Cerebellar Hypoplasia Due To a New RELN Mutation.

Pediatric neurology
2023

Exacerbated Zika virus-induced neuropathology and microcephaly in fetuses of dengue-immune nonhuman primates.

Science translational medicine
2024

Homozygous MFN2 variants causing severe antenatal encephalopathy with clumped mitochondria.

Brain : a journal of neurology
2023

Brain pathology of lissencephaly type 2 with an ISPD pathogenic variant.

Neuropathology and applied neurobiology
2023

The people behind the papers - Matt Matrongolo and Max Tischfield.

Development (Cambridge, England)
2023

[Analysis of ARX gene variant in a child with X-linked lissencephaly with abnormal genitalia].

Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics
2023

Further characterization of CEP85L-associated lissencephaly type 10: Report of a three-generation family and review of the literature.

American journal of medical genetics. Part A
2024

The Control of Cortical Folding: Multiple Mechanisms, Multiple Models.

The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry
2023

Lis1 relieves cytoplasmic dynein-1 autoinhibition by acting as a molecular wedge.

Nature structural & molecular biology
2023

Loss of Twist1 and balanced retinoic acid signaling from the meninges causes cortical folding in mice.

Development (Cambridge, England)
2023

X-linked neuronal migration disorders: Gender differences and insights for genetic screening.

International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience
2023

Acute Bowel Ischemia in a Premature Neonate with Miller-Dieker Syndrome and Anomalous Right Coronary Artery From the Pulmonary Artery.

Pediatric annals
2024

Prenatal diagnosis of microcephaly with simplified gyral pattern: series of eight cases.

Ultrasound in obstetrics & gynecology : the official journal of the International Society of Ultrasound in Obstetrics and Gynecology
2023

Long-term follow-up and novel variant in Suleiman-El-Hattab syndrome: Expanding the genotypic and clinical spectrum of a rare neurodevelopmental disorder.

European journal of medical genetics
2023

Novel homozygous LAMB1 in-frame deletion in a pediatric patient with brain anomalies and cerebrovascular event.

American journal of medical genetics. Part A
2023

Novel loss of function mutation in TUBA1A gene compromises tubulin stability and proteostasis causing spastic paraplegia and ataxia.

Frontiers in cellular neuroscience
2023

Bilateral cryptophthalmos with overlapping features of Manitoba oculo-tricho-anal (MOTA) syndrome and Fraser syndrome 2.

BMJ case reports
2023

Microtubule-binding-induced allostery triggers LIS1 dissociation from dynein prior to cargo transport.

Nature structural & molecular biology
2023

LIS1 RNA-binding orchestrates the mechanosensitive properties of embryonic stem cells in AGO2-dependent and independent ways.

Nature communications
2023

Anesthetic Management and Bispectral Index in a Child with Miller-Dieker Syndrome: A Case Report.

Children (Basel, Switzerland)
2023

Brain MRI Abnormalities, Epilepsy and Intellectual Disability in LAMA2 Related Dystrophy - a Genotype/Phenotype Correlation.

Journal of neuromuscular diseases
2023

Schizencephaly diagnosed after an episode of seizure during labor: A case report.

Clinical case reports
2023

PAFAH1B1 Gene Deletion-Associated Classic Lissencephaly and Infantile Spasms.

Neurology India
2023

Diagnosis of fetal cortical abnormalities by new reference charts for assessment of sylvian fissure biometry.

Prenatal diagnosis
2023

YWHAE loss of function causes a rare neurodevelopmental disease with brain abnormalities in human and mouse.

Genetics in medicine : official journal of the American College of Medical Genetics
2023

Insights on the Role of α- and β-Tubulin Isotypes in Early Brain Development.

Molecular neurobiology
2023

MAPping tubulin mutations.

Frontiers in cell and developmental biology
2023

A likely pathogenic ACTG1 variant in a child showing partial phenotypic overlap with Baraitser-Winter syndrome.

American journal of medical genetics. Part A
2023

Missed diagnosis of lissencephaly after prenatal diagnosis: A case report.

Medicine
2023

Modeling congenital brain malformations with brain organoids: a narrative review.

Translational pediatrics
2022

Lissencephaly with Congenital Hypothyroidism: A Case Report.

JNMA; journal of the Nepal Medical Association
2023

Prenatal diagnosis of SMPD4 loss - A neurodevelopmental disorder with microcephaly, arthrogryposis and structural brain anomalies.

Prenatal diagnosis
2023

Structures of human dynein in complex with the lissencephaly 1 protein, LIS1.

eLife
2023

Lissencephaly-1 mutations enhance traumatic brain injury outcomes in Drosophila.

Genetics
2022

Malformation of the Cortical Development Associated with Severe Clusters of Epileptic Seizures.

Veterinary sciences
2023

RanBP9 controls the oligomeric state of CTLH complex assemblies.

The Journal of biological chemistry
2022

Autosomal Recessive Primary Microcephaly (MCPH) and Novel Pathogenic Variants in ASPM and WDR62 Genes.

Molecular syndromology
2023

Role of intracortical neuropil growth in the gyrification of the primate cerebral cortex.

Proceedings of the National Academy of Sciences of the United States of America
2022

Dual Molecular Diagnoses of Recessive Disorders in a Child from Consanguineous Parents: Case Report and Literature Review.

Genes
2023

Spectrum of brain malformations in fetuses with mild tubulinopathy.

Ultrasound in obstetrics & gynecology : the official journal of the International Society of Ultrasound in Obstetrics and Gynecology
2022

Doublecortin and JIP3 are neural-specific counteracting regulators of dynein-mediated retrograde trafficking.

eLife
2023

Further expansion and confirmation of phenotype in rare loss of YWHAE gene distinct from Miller-Dieker syndrome.

American journal of medical genetics. Part A
2022

Human SERPINA3 induces neocortical folding and improves cognitive ability in mice.

Cell discovery
2022

Histopathologic Findings Associated with Miller-Dieker Syndrome: An Autopsy Report.

Diseases (Basel, Switzerland)
2022

Familial posterior predominant subcortical band heterotopia caused by a CEP85L missense mutation.

Seizure
2022

Bi-allelic CAMSAP1 variants cause a clinically recognizable neuronal migration disorder.

American journal of human genetics
2023

Lis1-dynein drives corona compaction and limits erroneous microtubule attachment at kinetochores.

Journal of cell science
2022

Obsessive-compulsive symptoms in ACTG1-associated Baraitser-Winter cerebrofrontofacial syndrome.

Journal of neural transmission (Vienna, Austria : 1996)
2022

MiR-582 Down-Regulates Lissencephaly-1 (LIS1) via P-Akt and MMP-2 to Inhibit Cholangiocarcinoma Cell Proliferation and Invasion.

Iranian journal of biotechnology
2023

Prenatal Diagnosis of Lissencephaly Associated with Biallelic Pathologic Variants in the COQ2 Gene.

Acta medica portuguesa
2022

Abnormal course of the corticospinal tracts in KIF5C-related encephalopathy.

European journal of medical genetics
2022

Imaging of Congenital Malformations of the Brain.

Clinics in perinatology
2022

LIS1 interacts with CLIP170 to promote tumor growth and metastasis via the Cdc42 signaling pathway in salivary gland adenoid cystic carcinoma.

International journal of oncology
2022

Novel frameshift mutation in LIS1 gene is a probable cause of lissencephaly: a case report.

BMC pediatrics
2023

Fetal Presentation of Walker-Warburg Syndrome with Compound Heterozygous POMT2 Missense Mutations.

Fetal and pediatric pathology
2023

Tubulin mutations in human neurodevelopmental disorders.

Seminars in cell & developmental biology
2022

A homozygous loss-of-function variant in BICD2 is associated with lissencephaly and cerebellar hypoplasia.

Journal of human genetics
2022

Tubulinopathy Presenting as Developmental and Epileptic Encephalopathy.

Children (Basel, Switzerland)
2022

Seizures and EEG characteristics in a cohort of pediatric patients with dystroglycanopathies.

Seizure
2022

Catatonic syndrome and Baraitser Winter syndrome: Case report and review of the literature.

European journal of medical genetics
2022

Monoallelic and biallelic mutations in RELN underlie a graded series of neurodevelopmental disorders.

Brain : a journal of neurology
2022

Fetal Brain Development: Regulating Processes and Related Malformations.

Life (Basel, Switzerland)
2022

Broadening the phenotypic spectrum of TUBA1A tubulinopathy to syndromic arthrogryposis multiplex congenita.

American journal of medical genetics. Part A
2022

Loss of BAF (mSWI/SNF) chromatin-remodeling ATPase Brg1 causes multiple malformations of cortical development in mice.

Human molecular genetics
2022

Generation of FLAG-tagged Arx knock-in mouse model.

Genesis (New York, N.Y. : 2000)
2022

Brain Organization and Human Diseases.

Cells
2022

Prenatal diagnosis of Miller-Dieker syndrome/PAFAH1B1-related lissencephaly: Ultrasonography and genetically investigative results.

European journal of obstetrics, gynecology, and reproductive biology
2022

Lissencephaly causing refractory neonatal seizures in a term neonate.

BMJ case reports
2022

Lack of association of TP73 with amyotrophic lateral sclerosis in a large cohort of cases.

Neurobiology of aging
2022

TUBA1A tubulinopathy mutants disrupt neuron morphogenesis and override XMAP215/Stu2 regulation of microtubule dynamics.

eLife
2022

LIS1 and NDEL1 Regulate Axonal Trafficking of Mitochondria in Mature Neurons.

Frontiers in molecular neuroscience
2022

Quantitative Structural Brain Magnetic Resonance Imaging Analyses: Methodological Overview and Application to Rett Syndrome.

Frontiers in neuroscience
2022

A de novo Non-sense Nuclear Factor I B Mutation (p.Tyr290*) Is Responsible for Brain Malformation and Lung Lobulation Defects.

Frontiers in pediatrics
2022

Perioperative total intravenous anesthesia in a child with Walker-Warburg syndrome: A case report.

Saudi journal of anaesthesia
2022

Long-term Outcome of Epilepsy and Cortical Malformations Due to Abnormal Migration and Postmigrational Development: A Cohort Study.

Neurology
2021

Ambiguous Genitalia and Lissencephaly in A 46,XY Neonate with a Novel Variant of Aristaless Gene.

Acta endocrinologica (Bucharest, Romania : 2005)
2022

Stem cell-based region-specific brain organoids: Novel models to understand neurodevelopmental defects.

Birth defects research
2022

Structural Consequence of Non-Synonymous Single-Nucleotide Variants in the N-Terminal Domain of LIS1.

International journal of molecular sciences
2022

Novel finding of lissencephaly and severe osteopenia in a Chinese patient with SATB2-associated syndrome and a brief review of literature.

American journal of medical genetics. Part A
2022

[Genetic and clinical analysis of KIF2A gene variant in a Chinese patient with complex cortical dysplasia and other brain malformations].

Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics
2022

Frameshift mutation S368fs in the gene encoding cytoskeletal β-actin leads to ACTB-associated syndromic thrombocytopenia by impairing actin dynamics.

European journal of cell biology
2022

Abnormalities in Cortical GABAergic Interneurons of the Primary Motor Cortex Caused by Lis1 (Pafah1b1) Mutation Produce a Non-drastic Functional Phenotype.

Frontiers in cell and developmental biology
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Referências e fontes

Bases de dados externas citadas neste artigo

Publicações científicas

Artigos indexados no PubMed ligados a esta doença no grafo RarasNet — título, periódico e PMID direto da fonte, sem intermediação de IA.

  1. Genetic landscape and phenotypic correlations of lissencephaly: prenatal and postnatal insights.
    Brain communications· 2026· PMID 41853045mais citado
  2. Bi-allelic variants in NRDC cause a neurodevelopmental disorder characterized by neonatal lethality, microcephaly, and brain abnormalities.
    American journal of human genetics· 2026· PMID 41734767mais citado
  3. Roles of microtubules and LIS1 in dynein transport machinery assembly.
    Nature· 2026· PMID 41708859mais citado
  4. Bi-allelic variants in neuronal adhesion molecule astrotactin 1 gene ASTN1 cause diverse neurodevelopmental disorders.
    American journal of human genetics· 2026· PMID 41544630mais citado
  5. A rare complication of vagus nerve stimulation surgery: the Horner Syndrome. Case report and systematic review.
    Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology· 2026· PMID 41486386mais citado
  6. Miller-Dieker Syndrome: Genetic Etiology, Neurocognitive Impact, and Clinical Implications in a Neuronal Migration Disorder.
    Dev Neuropsychol· 2026· PMID 41979906recente
  7. Malformations of Cortical Development.
    Neuroimaging Clin N Am· 2026· PMID 41932774recente
  8. Architects of the Developing Brain: Cytoskeleton-Organizing Molecules in Neurodevelopmental Disorders.
    Cells· 2026· PMID 41892327recente
  9. CEP170 as a novel molecular link between centrosomal function and cerebral cortical development.
    J Biomed Sci· 2026· PMID 41888776recente

Bases de dados e fontes oficiais

Identificadores e referências canônicas usadas para montar este verbete.

  1. ORPHA:48471(Orphanet)
  2. MONDO:0018838(MONDO)
  3. GARD:12291(GARD (NIH))
  4. Variantes catalogadas(ClinVar)
  5. Busca completa no PubMed(PubMed)
  6. Artigo Wikipedia(Wikipedia)
  7. Q1544416(Wikidata)

Dados compilados pelo RarasNet a partir de fontes abertas (Orphanet, OMIM, MONDO, PubMed/EuropePMC, ClinicalTrials.gov, DATASUS, PCDT/MS). Este conteúdo é informativo e não substitui avaliação médica.

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