Seizures, benign familial neonatal, autosomal recessive

Summary

Seizures, benign familial neonatal, autosomal recessive (MONDO:0010021) is a disease. A subtype of benign neonatal seizures — broader associated-gene and molecular evidence is on the parent page (see Disease family below).

Clinical features

No curated clinical features (Orphanet) for this disease.

Identifiers

Disease identifiers

Field	Value
Canonical name	seizures, benign familial neonatal, autosomal recessive
Mondo ID	MONDO:0010021
MeSH	C564823
OMIM	269720
UMLS	C1849250
MedGen	338640
GARD	0015234
Is cancer (heuristic)	no

Also known as: autosomal dominant form of benign neonatal seizures · convulsions benign familial neonatal dominant form · seizures, benign familial neonatal, autosomal recessive

Disease family

This is a subtype of benign neonatal seizures. Genetic, therapeutic, and trial evidence is largely curated at the broader-term level — see the parent page for the associated-gene cohort and molecular evidence.

Classification path: disease › human disease › disease by body system or component › nervous system disorder › central nervous system disorder › brain disorder › epilepsy › epilepsy syndrome › neonatal epilepsy syndrome › benign neonatal seizures › seizures, benign familial neonatal, autosomal recessive

Related subtypes (3): seizures, benign familial neonatal, 1, seizures, benign familial neonatal, 2, seizures, benign familial neonatal, 3

Genetics & variants

GWAS landscape

No GWAS associations recorded — common-variant (GWAS) studies don’t cover this disease (typical for Mendelian / rare diseases). See the curated gene cohort and Mendelian overlap below.

Variant details and genetic-evidence tiers

No tiered GWAS variants or ClinVar records for this disease.

Genes & proteins

No associated-gene cohort resolved for this disease. Atlas builds the molecular and therapeutic sections — associated genes, protein families, druggability, pathways, interactions, and drug associations — by aggregating over a disease’s associated genes (resolved via GWAS / GenCC / ClinVar / CIViC), and none resolved here. This is expected for antibody-mediated, autoimmune, or otherwise non-gene-defined conditions; the curated evidence for this disease is its clinical features, GWAS susceptibility, and clinical trials (above).

Function

No pathway enrichment — requires an associated-gene cohort.

Therapeutics

No druggable-target or therapeutic data for this disease’s cohort.

Clinical trials & evidence

Clinical trials

Clinical trials: 0.