Familial temporal lobe epilepsy 4

Summary

Familial temporal lobe epilepsy 4 (MONDO:0012706) is a disease. A subtype of temporal lobe epilepsy — 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	familial temporal lobe epilepsy 4
Mondo ID	MONDO:0012706
MeSH	C566902
OMIM	611631
DOID	DOID:0060753
UMLS	C1968847
MedGen	368897
GARD	0015523
Is cancer (heuristic)	no

Also known as: epilepsy, familial temporal lobe, 4 · EPOLM · ETL4 · familial temporal lobe epilepsy type 4

Disease family

This is a subtype of temporal lobe epilepsy. 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 › focal epilepsy › familial partial epilepsy › temporal lobe epilepsy › familial temporal lobe epilepsy 4

Related subtypes (5): familial temporal lobe epilepsy 2, familial temporal lobe epilepsy 7, familial temporal lobe epilepsy 8, epilepsy, familial temporal lobe, 1, familial mesial temporal lobe epilepsy

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.