Neuronal intestinal dysplasia

Summary

Neuronal intestinal dysplasia (MONDO:0000858) is a disease. A subtype of colonic disorder — 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	neuronal intestinal dysplasia
Mondo ID	MONDO:0000858
DOID	DOID:0080072
SNOMED CT	253783001
UMLS	C0345244
MedGen	576840
Is cancer (heuristic)	no

Disease family

This is a subtype of colonic disorder. 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 › digestive system disorder › intestinal disorder › large intestine disorder › colonic disorder › neuronal intestinal dysplasia

Related subtypes (12): functional diarrhea, megacolon, diverticulitis of colon, cecal disorder, sigmoid disease, functional colonic disease, colitis, colonic neoplasm, colon dysplasia, polyp of colon, Chilaiditi syndrome, colonic duplication

Subtypes (2): neuronal intestinal dysplasia, type B, visceral neuropathy, familial, 1, autosomal recessive

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.