ABeta2M amyloidosis

Summary

ABeta2M amyloidosis (MONDO:0018590) is a disease. A subtype of amyloidosis — 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	ABeta2M amyloidosis
Mondo ID	MONDO:0018590
Orphanet	439246
DOID	DOID:0080928
ICD-11	448754119
UMLS	C5680053
MedGen	1842860
GARD	0021829
Is cancer (heuristic)	no

Also known as: Beta2-microglobulinic amyloidosis

Disease family

This is a subtype of amyloidosis. 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 › metabolic disease › proteostasis deficiencies › amyloidosis › ABeta2M amyloidosis

Related subtypes (11): primary cutaneous amyloidosis, wild type ATTR amyloidosis, ALECT2 amyloidosis, AApoAIV amyloidosis, AH amyloidosis, hereditary amyloidosis, AL amyloidosis, AA amyloidosis, amyloidosis bronchopulmonary, soft tissue amyloid neoplasm, immunoglobulin heavy-and-light chain

Subtypes (2): variant ABeta2M amyloidosis, wild type ABeta2M amyloidosis

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.