ApoE variant p.V236E is associated with markedly reduced risk of Alzheimer’s disease
Open accessAbstract
Recent genome-wide association studies (GWAS) of late-onset Alzheimer's disease (LOAD) have identified single nucleotide polymorphisms (SNPs) which show significant association at the well-known APOE locus and at nineteen additional loci. Among the functional, disease-associated variants at these loci, missense variants are particularly important because they can be readily investigated in model systems to search for novel therapeutic targets. It is now possible to perform a low-cost search for these "actionable" variants by genotyping the missense variants at known LOAD loci already cataloged on the Exome Variant Server (EVS). In this proof-of-principle study designed to explore the efficacy of this approach, we analyzed three rare EVS variants in APOE, p.L28P, p.R145C and p.V236E, in our case control series of 9114 subjects. p.R145C proved to be too rare to analyze effectively. The minor allele of p.L28P, which was in complete linkage disequilibrium (D' = 1) with the far more common APOE ϵ4 allele, showed no association with LOAD (P = 0.75) independent of the APOE ϵ4 allele. p.V236E was significantly associated with a marked reduction in risk of LOAD (P = 7.5 × 10⁻⁰⁵; OR = 0.10, 0.03 to 0.45). The minor allele of p.V236E, which was in complete linkage disequilibrium (D' = 1) with the common APOE ϵ3 allele, identifies a novel LOAD-associated haplotype (APOE ϵ3b) which is associated with decreased risk of LOAD independent of the more abundant APOE ϵ2, ϵ3 and ϵ4 haplotypes. Follow-up studies will be important to confirm the significance of this association and to better define its odds ratio. The ApoE p.V236E substitution is the first disease-associated change located in the lipid-binding, C-terminal domain of the protein. Thus our study (i) identifies a novel APOE missense variant which may profitably be studied to better understand how ApoE function may be modified to reduce risk of LOAD and (ii) indicates that analysis of protein-altering variants cataloged on the EVS can be a cost-effective way to identify actionable functional variants at recently discovered LOAD loci.
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The APOE3-V236E variant is protective against Alzheimer's disease dementia with a population carrier frequency of 0.3%.
“We previously identified the APOE3-V236E variant to be protective against AD dementia with a population carrier frequency of 0.3% (10).”
From <i>APOE3</i> -Jacksonville (V236E) variant reduces self-aggregation and risk of dementia (2021) · cites this paper as [10]
The Results and Discussion report that APOE3-V236E is associated with markedly reduced risk of late-onset Alzheimer’s disease. They do not report a 0.3% population carrier frequency: the Discussion gives a 0.12% minor allele frequency in European Americans, while the Results report carriers in a case-control sample. Those figures do not establish the stated population carrier frequency. (LLM, conf=0.85)
Experimental — accuracy not yet measuredThe rare APOE3-Jac variant occurs on the APOE3 backbone and confers a reduced risk of Alzheimer's disease (OR = 0.10, 0.03 to 0.45) equal to or superior to the APOE2 allele (OR = 0.46, 0.38 to 0.54).
“To date, this rare APOE3-Jac variant (0.12%) occurs on the APOE3 backbone and confers a reduced risk of AD (OR = 0.10, 0.03 to 0.45) equal to or superior to the APOE2 allele (OR = 0.46, 0.38 to 0.54).”
From <i>APOE3</i> -Jacksonville (V236E) variant reduces self-aggregation and risk of dementia (2021) · cites this paper as [10]
The Introduction reports a 0.12% frequency for p.V236E in European Americans, and the Results place it on the APOE ε3 backbone and report reduced late-onset AD risk (OR 0.10, 0.03–0.45). The Discussion says the resulting ε3b allele reduced risk as much as or more than ε2 in this series. The claim omits those population and study qualifiers, and it pairs the p.V236E estimate from Fisher’s exact test with the ε2 estimate from multivariate regression; the latter analysis gives ε3b a different confidence interval (0.02–0.35). (LLM, conf=0.85)
Experimental — accuracy not yet measuredExome sequencing in 46 autopsy-confirmed exceptional aging individuals identified the APOE3-Jac variant in one exceptional aging brain.
“By examining the genes known to play a role in neurodegenerative disorders we again identified APOE3-Jac variant in one of the exceptional aging brains (Fig. 1A) (10).”
From <i>APOE3</i> -Jacksonville (V236E) variant reduces self-aggregation and risk of dementia (2021) · cites this paper as [10]
The Results and Discussion (no page available) identify APOE p.V236E as a variant on the APOE ε3 backbone, supporting the citation’s use as background for an APOE3 variant. Our copy does not call it “APOE3-Jac” or report exome sequencing of 46 exceptional-aging individuals or its identification in one such brain; the paper instead describes an EVS-based search and genotyping in a larger case-control series. (LLM, conf=0.76)
Experimental — accuracy not yet measuredThe Jacksonville (V236E) and R251G mutations are protective against sporadic AD.
“The discovery of the protective roles of Christchurch (R136S) in autosomal dominant PSEN1 familial AD and the Jacksonville (V236E), & R251G mutations that are protective against sporadic AD [17–20].”
From Discovery of a Missense Mutation (Q222K) of the <i>APOE</i> Gene from the Australian Imaging, Biomarker and Lifestyle Study (2023) · cites this paper as [18]
The Results report that p.V236E was associated with markedly reduced risk of late-onset Alzheimer’s disease in the case-control series. The Results and Genotyping sections identify the variants studied, but our copy does not report a protective association for R251G. (LLM, conf=0.88)
Experimental — accuracy not yet measuredRare APOE missense variants impact protein function and modify disease risk.
“This includes the important discoveries about rare APOE missense variants that impact protein function and modify disease risk.”
From Discovery of a Missense Mutation (Q222K) of the <i>APOE</i> Gene from the Australian Imaging, Biomarker and Lifestyle Study (2023) · cites this paper as [18]
The Discussion reports that the rare APOE missense variant p.V236E was associated with markedly decreased risk of late-onset Alzheimer’s disease. It describes effects on ApoE lipid binding, aggregation, and receptor binding as possibilities still under investigation, not demonstrated changes in protein function. The other rare variants studied were not shown to independently modify risk. (LLM, conf=0.88)
Experimental — accuracy not yet measured
Leu46Pro is in linkage disequilibrium with ε4, and Leu46Pro did not increase risk of Alzheimer's disease beyond ε4.
“In accordance with previous studies, we found Leu46Pro in linkage disequilibrium with ε4, and whereas some studies reported Leu46Pro to add risk beyond ε4 33 , 34 through a destabilized apoE structure, 35 others found that Leu46Pro did not increase risk of AD beyond ε4. 36 , 37 Our study confirmed the latter.”
From <i>APOE</i> and dementia – resequencing and genotyping in 105,597 individuals (2020) · cites this paper as [36]
We did not find risk associations for Val254Glu and Arg269Gly, although Val254Glu was previously reported to be protective.
“We did not find risk associations, although Val254Glu was previously reported to be protective. 36”
From <i>APOE</i> and dementia – resequencing and genotyping in 105,597 individuals (2020) · cites this paper as [36]
The APOE3-V236E substitution is the first Alzheimer's disease-associated variant within the C-terminal domain, a region critical for apoE oligomerization and lipidation.
“Notably, the apoE3-V236E substitution is the first AD-associated variant within the C-terminal domain, a region critical for apoE oligomerization and lipidation (10, 36).”
From <i>APOE3</i> -Jacksonville (V236E) variant reduces self-aggregation and risk of dementia (2021) · cites this paper as [10]
The V236E (Jacksonville) mutation has been described only in the APOEε3 allele and reduces the risk of Alzheimer disease down to that of APOEε2 carriers or even further.
“The V236E (Jacksonville) mutation has been described only in the APOEε3 allele and reduces the risk of AD down to that of APOEε2 carriers or even further42,43.”
From Multifaceted roles of APOE in Alzheimer disease (2024) · cites this paper as [42]
The APOE Christchurch variant rs121918393 and the APOE Jacksonville variant rs199768005 are protective against Alzheimer's disease in Caucasians.
“The Christchurch variant rs121918393 (APOEChc: CGC > aGC, p.Arg[R]136Ser[S]) [19–21] and the Jacksonville variant rs199768005 (APOEJax: GTG > GaG, p.Val[V]236Glu[E]) [22, 23] have been identified as protective variants against AD in Caucasians”
From Genetics of Alzheimer’s disease: An East Asian perspective (2023) · cites this paper as [22]
APOEJax is equally or more protective against Alzheimer's disease than the ε2 allele.
“Genetic analysis demonstrated that APOEJax was equally or more protective against AD than the ε2 allele [22].”
From Genetics of Alzheimer’s disease: An East Asian perspective (2023) · cites this paper as [22]
V236E and R251G have been associated with reduced AD risk.
“V236E and R251G have been associated with reduced AD risk.4,5”
From Association of African Ancestry–Specific <i>APOE</i> Missense Variant R145C With Risk of Alzheimer Disease (2023) · cites this paper as [4]
An individual carrying two copies of the APOE3-Christchurch (R136S) mutation did not develop Alzheimer's disease three decades after the expected disease onset.
“A recent case report found that an individual carrying two copies of the APOE3-Christchurch (R136S) mutation did not develop AD three decades after the expected disease onset (10).”
From <i>APOE3</i> -Jacksonville (V236E) variant reduces self-aggregation and risk of dementia (2021) · cites this paper as [10]
The Results discuss a different APOE variant, p.V236E, and report no homozygotes for it in the study sample. Searches for APOE3-Christchurch, R136S, and the claimed three-decade delay found no passage addressing that case report in our copy. (LLM, conf=0.78)
Experimental — accuracy not yet measured
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- Authors
- Medway, C. W., Abdul-Hay, S., Mims, T., Ma, L., Bisceglio, G., Zou, F., Pankratz, S., Sando, S. B., Aasly, J. O., Barcikowska, M., Siuda, J., Wszolek, Z. K., Ross, O. A., Carrasquillo, M., Dickson, D. W., Graff-Radford, N., Petersen, R. C., Ertekin-Taner, N., Morgan, K., Bu, G., & Younkin, S. G.
- Affiliations
- Mayo Clinic (US)
- Norwegian University of Science and Technology (NO)
- Mossakowski Medical Research Institute, Polish Academy of Sciences (PL)
- University of Nottingham (GB)
- Corresponding author
- Bu, Guojun
- Younkin, Steven G
- ORCID
- Venue
- Molecular Neurodegeneration
- Published
- 2014-03-10
- Volume
- 9
- Issue
- 1
- Pages
- 11-11
- ISSN
- 1750-1326 (ISSN-L)
- PMC
- PMC3995879
- OpenAlex
- W2139824081
- Cited by
- 82
- References
- 3
- Citations by year
- 2026: 3 · 2025: 13 · 2024: 12 · 2023: 10 · 2022: 14 · 2021: 6 · 2020: 5 · 2018: 5 · 2017: 4 · 2016: 4 · 2015: 3 · 2014: 3
- FWCI
- 3.11
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Molecular Neurodegeneration (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Rare & Special e-Zone (The Hong Kong University of Science and Technology) (submittedVersion)
- Funders
- Michael J. Fox Foundation for Parkinson's Research
- National Institutes of Health (AG016574, AG046139, AG027924, NINDS P50 NS072187, NS072187)
- National Institute on Aging (P01AG030128, R01AG027924, R01AG018023, R01-AG18023, R01AG032990, R01AG031784, RF1AG046205, U01AG046139, R01AG035355, P50AG016574)
- National Institute of Neurological Disorders and Stroke (R01NS080820, NS080820, NS072187, P50NS072187, P01NS074969)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Keywords
- late-onset Alzheimer's disease, linkage disequilibrium, risk mitigation, actionable mutations
- MeSH terms
- Aged, Alzheimer Disease, Apolipoproteins E, Female, Genotype, Humans, Male, Middle Aged, Case-Control Studies, Age of Onset, Genetic Predisposition to Disease, Polymorphism, Single Nucleotide, Genome-Wide Association Study
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