GAA

Chr 17AR

alpha glucosidase

Also known as: IOPD, LOPD, LYAG

This gene encodes lysosomal alpha-glucosidase, which is essential for the degradation of glycogen to glucose in lysosomes. The encoded preproprotein is proteolytically processed to generate multiple intermediate forms and the mature form of the enzyme. Defects in this gene are the cause of glycogen storage disease II, also known as Pompe's disease, which is an autosomal recessive disorder with a broad clinical spectrum. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Jan 2016]

Primary Disease Associations & Inheritance

Pompe disease, infantile-onsetMIM #232300
AR
Pompe disease, late-onsetMIM #621314
AR
587
ClinVar variants
144
Pathogenic / LP
0.00
pLI score
12
Active trials
Clinical SummaryGAA
🧬
Gene-Disease Validity (ClinGen)
glycogen storage disease II · ARDefinitive

Definitive — sufficient evidence for diagnostic panels

Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
144 Pathogenic / Likely Pathogenic· 184 VUS of 587 total submissions
💊
Clinical Trials
12 active or recruiting trials — potential therapeutic options may be available

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint?LOEUF (Loss-of-function Observed/Expected Upper bound Fraction) is the upper bound of the 90% CI for LoF OE — the preferred gnomAD v4 metric. Lower = more intolerant to LoF. LOEUF < 0.35 = highly constrained.
0.98LOEUF
pLI 0.000
Z-score 1.66
OE 0.74 (0.560.98)
Tolerant

Typical tolerance to LoF variation

Missense Constraint?Missense Z-score: standard deviations fewer missense variants observed vs. expected. Z > 3.09 (p < 0.001) = gene does not tolerate missense variation. OE missense < 0.6 is also considered constrained.
-0.63Z-score
OE missense 1.07 (1.001.15)
646 obs / 602.3 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios?Shaded band = 90% confidence interval. Vertical tick = point estimate. Grey threshold line = gnomAD constraint cutoff for that variant class.
LoF OE?Ratio of observed to expected LoF variants. Upper CI bound (LOEUF) ≤ 0.35 = strong LoF constraint signal.0.74 (0.560.98)
00.351.4
Missense OE?Ratio of observed to expected missense variants. OE ≤ 0.6 = fewer missense variants than expected by chance.1.07 (1.001.15)
00.61.4
Synonymous OE?Control metric — synonymous variants are largely neutral and expected near OE = 1.0. Significant deviation may indicate annotation issues.1.07
01.21.6
LoF obs/exp: 34 / 46.1Missense obs/exp: 646 / 602.3Syn Z: -0.90

ClinVar Variant Classifications

587 submitted variants in ClinVar

Classification Summary

Pathogenic61
Likely Pathogenic83
VUS184
Likely Benign253
Benign2
Conflicting4
61
Pathogenic
83
Likely Pathogenic
184
VUS
253
Likely Benign
2
Benign
4
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
35
6
19
1
61
Likely Pathogenic
29
43
11
0
83
VUS
0
150
24
10
184
Likely Benign
0
1
140
112
253
Benign
0
0
2
0
2
Conflicting
4
Total64200196123587

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

View in ClinVar →

Protein Context — Lollipop Plot

GAA · protein map & ClinVar variants

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

Gene2Phenotype Curations

GAA-related Pompe disease

definitive
ARLoss Of FunctionAltered Gene Product Structure, Decreased Gene Product Level
Cardiac
G2P ↗
splice region variantsplice acceptor variantsplice donor variantstart lostframeshift variantstop gainedmissense variantinframe deletion5 prime UTR variantframeshift variant NMD escaping

GAA-related glycogen storage disease

definitive
ARLoss Of FunctionAbsent Gene Product
Dev. Disorders
G2P ↗

Gene2Phenotype curations · DECIPHER consortium patient cohort (public variants) · deciphergenomics.org

OMIM — Genotype-Phenotype Relationships

1 OMIM entry

Pompe disease, infantile-onset

MIM #232300

Molecular basis of disorder known

Autosomal recessive

Pompe disease, late-onset

MIM #621314

Molecular basis of disorder known

Autosomal recessive
📖
GeneReview available — GAA
Authoritative clinical overview · NCBI Bookshelf · Recommended first read
Open GeneReview ↗
Clinical Literature
Landmark / reviewRecent case evidence

Clinical Trials

Active and recruiting trials from ClinicalTrials.gov

Rare Genetic Muscle DiseasesMuscular Dystrophy, DuchenneMuscular Dystrophy, Becker

Transcriptomic Analysis to Put an End to Misdiagnosis in Patients With Rare Muscle Diseases

RECRUITING
NCT06833489Phase NAAssistance Publique Hopitaux De MarseilleStarted 2025-03-01
ARN extraction from muscle biopsies
Inherited Non-Duchenne Myopathies

Clinical and Functional Assessment of Patients With Inherited Non-Duchenne Myopathies in Sohag University Hospital

RECRUITING
NCT06574919Sohag UniversityStarted 2024-08-01
Pompe DiseasePompe Disease (Late-onset)Glycogen Storage Disease Type 2

A Gene Transfer Study for Late-Onset Pompe Disease (RESOLUTE)

ACTIVE NOT RECRUITING
NCT04093349Phase PHASE1, PHASE2Spark Therapeutics, Inc.Started 2020-10-01
SPK-3006
Friedreich Ataxia

Characterisation of the Cognitive Profile of Patients Suffering From Friedreich's Ataxia

RECRUITING
NCT05874388Institut National de la Santé Et de la Recherche Médicale, FranceStarted 2023-06-19
Glycogen Storage Disease Type II, Adult

Natural History of Pompe Disease

RECRUITING
NCT03564561Assistance Publique - Hôpitaux de ParisStarted 2019-06-07
Pompe Disease (Late-onset)Pompe Disease Late-OnsetLOPD

A Study to Evaluate Safety, Tolerability, and Efficacy of AB-1009 Gene Therapy (GAA Gene) in Adult Participants With Late Onset Pompe Disease (PROGRESS-GT LOPD)

RECRUITING
NCT07282847Phase PHASE1, PHASE2AskBio IncStarted 2026-02-10
AB-1009 (GAA Gene)
Spinocerebellar Ataxia 27B (SCA27B)

A Randomized, Parallel-arm, Double Blind, Placebo-controlled Study to Assess the Efficacy of Fampridine for Patients With Spinocerebellar Ataxia SCA27B Caused by a GAA Expansion in the FGF14 Gene

RECRUITING
NCT07185347Phase PHASE3Assistance Publique - Hôpitaux de ParisStarted 2025-10-21
Fampridine 10 mg prolonged-release tablet (per os)Placebo (tablets per os)
Pompe Disease (Late-onset)

A Study About Antibody Levels and Biomarkers in the Blood in People With Late-onset Pompe Disease

ACTIVE NOT RECRUITING
NCT06150820Phase NAAstellas Gene TherapiesStarted 2024-02-01
No Intervention
Pompe Disease (Late-onset)

Evaluation of the Safety, Tolerability and Efficacy of Gene Therapy Drug for Late Onset Pompe Disease (LOPD)

NOT YET RECRUITING
NCT06178432Phase EARLY_PHASE1Huashan HospitalStarted 2023-12
CRG003 injection
Friedreich Ataxia

A Natural History Study to TRACK Brain and Spinal Cord Changes in Individuals with Friedreich Ataxia (TRACK-FA)

ACTIVE NOT RECRUITING
NCT04349514Monash UniversityStarted 2021-02-10
Natural history
Ataxia, Gait

Ataxia GAA-FGF14 - Descriptive Genetic and Clinical Study

ACTIVE NOT RECRUITING
NCT05884086Central Hospital, Nancy, FranceStarted 2023-05-01
Pompe Disease (Late-onset)

Evaluation of the Safety and Efficacy of Late-onset Pompe Disease Gene Therapy Drug

RECRUITING
NCT06391736Phase PHASE1, PHASE2GeneCradle IncStarted 2024-04-19
GC301