premature aging syndrome, Okamoto type

Summary

premature aging syndrome, Okamoto type (MONDO:0011149) is a disease. A subtype of premature aging syndrome — 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	premature aging syndrome, Okamoto type
Mondo ID	MONDO:0011149
MeSH	C566621
OMIM	601811
UMLS	C1866183
MedGen	356468
GARD	0004478
Is cancer (heuristic)	no

Also known as: premature ageing Okamoto type · premature ageing syndrome with osteosarcoma cataracts diabetes osteoporosis erythroid macrocytosis severe developmental delay · premature aging Okamoto type · premature aging syndrome with osteosarcoma cataracts diabetes osteoporosis erythroid macrocytosis severe developmental delay · premature aging syndrome, Okamoto type

Disease family

This is a subtype of premature aging syndrome. 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 developmental or physiological process › premature aging syndrome › premature aging syndrome, Okamoto type

Related subtypes (7): Flynn-Aird syndrome, acrogeria, acroosteolysis-keloid-like lesions-premature aging syndrome, progeroid syndrome, de Barsy syndrome, LMNA-related cardiocutaneous progeria syndrome, telomere syndrome

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.