LDLRAD3

Chr 11

low density lipoprotein receptor class A domain containing 3

Also known as: LRAD3

The LDLRAD3 protein binds amyloid-beta and regulates APP processing through receptor-mediated endocytosis, potentially influencing the production of amyloidogenic peptides. Mutations cause autosomal recessive early-onset Alzheimer disease, representing one of the rare monogenic forms of this neurodegenerative condition in children and young adults. The gene shows relatively low constraint to loss-of-function variation in the general population.

Summary from RefSeq, UniProt
Research Assistant →
0
Active trials
6
Pubs (1 yr)
15
P/LP submissions
0%
P/LP missense
0.83
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryLDLRAD3
Population Constraint (gnomAD)
Low constraint (pLI 0.02) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
15 unique Pathogenic / Likely Pathogenic· 52 VUS of 84 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
0.83LOEUF
pLI 0.016
Z-score 2.00
OE 0.39 (0.200.83)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
0.70Z-score
OE missense 0.86 (0.770.98)
184 obs / 212.9 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.39 (0.200.83)
00.351.4
Missense OE0.86 (0.770.98)
00.61.4
Synonymous OE0.80
01.21.6
LoF obs/exp: 5 / 12.7Missense obs/exp: 184 / 212.9Syn Z: 1.55
DN
0.6455th %ile
GOF
0.6931th %ile
LOF
0.3843th %ile

This gene has evidence for multiple mechanisms of pathogenicity (gain-of-function and dominant-negative). Both the Badonyi & Marsh prediction and the broader genomic evidence point to gain-of-function as the predominant mechanism. Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

GOFprediction above median
DNprediction above median

Note: In-silico variant effect predictors (SIFT, PolyPhen, REVEL, CADD) may underestimate pathogenicity of missense variants in genes with GOF or DN mechanisms. Consider functional evidence and clinical context.

Predictions from Badonyi M, Marsh JA. PLoS ONE. 2024;19(8):e0307312.

ClinVar Variant Classifications

84 submitted variants in ClinVar

Classification Summary

Pathogenic14
Likely Pathogenic1
VUS52
Likely Benign4
Benign3
14
Pathogenic
1
Likely Pathogenic
52
VUS
4
Likely Benign
3
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
14
0
14
Likely Pathogenic
0
0
1
0
1
VUS
0
42
10
0
52
Likely Benign
0
1
0
3
4
Benign
0
3
0
0
3
Total04625374

LoF = frameshift, stop gained/lost, canonical splice · Counts from ClinVar esearch · Updated hourly

View in ClinVar →

Protein Context — Lollipop Plot

LDLRAD3 · protein map & ClinVar variants

Showing all ClinVar variants across the protein. Search a specific variant to highlight its position.

Clinical Trials

Active and recruiting trials from ClinicalTrials.gov

No active trials found for this gene.

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Clinical Literature
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