Association between genetic traits for immune-mediated diseases and Alzheimer disease
Open accessAbstract
IMPORTANCE: Late-onset Alzheimer disease (AD), the most common form of dementia, places a large burden on families and society. Although epidemiological and clinical evidence suggests a relationship between inflammation and AD, their relationship is not well understood and could have implications for treatment and prevention strategies. OBJECTIVE: To determine whether a subset of genes involved with increased risk of inflammation are also associated with increased risk for AD. DESIGN, SETTING, AND PARTICIPANTS: In a genetic epidemiology study conducted in July 2015, we systematically investigated genetic overlap between AD (International Genomics of Alzheimer's Project stage 1) and Crohn disease, ulcerative colitis, rheumatoid arthritis, type 1 diabetes, celiac disease, and psoriasis using summary data from genome-wide association studies at multiple academic clinical research centers. P values and odds ratios from genome-wide association studies of more than 100 000 individuals were from previous comparisons of patients vs respective control cohorts. Diagnosis for each disorder was previously established for the parent study using consensus criteria. MAIN OUTCOMES AND MEASURES: The primary outcome was the pleiotropic (conjunction) false discovery rate P value. Follow-up for candidate variants included neuritic plaque and neurofibrillary tangle pathology; longitudinal Alzheimer's Disease Assessment Scale cognitive subscale scores as a measure of cognitive dysfunction (Alzheimer's Disease Neuroimaging Initiative); and gene expression in AD vs control brains (Gene Expression Omnibus data). RESULTS: Eight single-nucleotide polymorphisms (false discovery rate P < .05) were associated with both AD and immune-mediated diseases. Of these, rs2516049 (closest gene HLA-DRB5; conjunction false discovery rate P = .04 for AD and psoriasis, 5.37 × 10-5 for AD, and 6.03 × 10-15 for psoriasis) and rs12570088 (closest gene IPMK; conjunction false discovery rate P = .009 for AD and Crohn disease, P = 5.73 × 10-6 for AD, and 6.57 × 10-5 for Crohn disease) demonstrated the same direction of allelic effect between AD and the immune-mediated diseases. Both rs2516049 and rs12570088 were significantly associated with neurofibrillary tangle pathology (P = .01352 and .03151, respectively); rs2516049 additionally correlated with longitudinal decline on Alzheimer's Disease Assessment Scale cognitive subscale scores (β [SE], 0.405 [0.190]; P = .03). Regarding gene expression, HLA-DRA and IPMK transcript expression was significantly altered in AD brains compared with control brains (HLA-DRA: β [SE], 0.155 [0.024]; P = 1.97 × 10-10; IPMK: β [SE], -0.096 [0.013]; P = 7.57 × 10-13). CONCLUSIONS AND RELEVANCE: Our findings demonstrate genetic overlap between AD and immune-mediated diseases and suggest that immune system processes influence AD pathogenesis and progression.
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IPMK is implicated in neurodegeneration, cancer, and inflammation.
“Over two decades, multidisciplinary research has unveiled its far-reaching biological roles and implications in diverse diseases, including neurodegeneration, cancer, and inflammation.”
From From Obscurity to Prominence: IPMK’s Expanding Role in Cellular Signaling, Physiology, and Disease (2025) · cites this paper as [32]
The Discussion (page not provided) links IPMK to Alzheimer’s and Huntington’s disease and suggests a role in neurodegeneration. It also describes IPMK as an inflammation-associated gene, but the paper does not state that IPMK is implicated in cancer; its discussion of p53-mediated transcription and cell death does not establish that disease claim. (LLM, conf=0.88)
Experimental — accuracy not yet measuredIPMK is involved in inflammatory disorders, obesity, Alzheimer's disease, inflammatory bowel disease, and intestinal neuroendocrine tumors.
“Over the past two decades, research utilizing animal models and human mutation analyses has revealed IPMK’s involvement in a wide array of human diseases, including inflammatory disorders [28,29], obesity [30,31], Alzheimer’s disease [32], inflammatory bowel disease [33,34], and intestinal neuroendocrine tumors [35].”
From From Obscurity to Prominence: IPMK’s Expanding Role in Cellular Signaling, Physiology, and Disease (2025) · cites this paper as [32]
The enrichment of prioritized proteins in microglia and immune pathways supports a strong immunological role in AD, including TREM2, CD33, and IL34.
“supporting a strong immunological role in AD93–95 including TREM27,96, CD33, and IL34.”
From Proteogenomic analysis of human cerebrospinal fluid identifies neurologically relevant regulation and implicates causal proteins for Alzheimer’s disease (2024) · cites this paper as [94]
Overlap in the genetic architecture between AD and other diseases has been reported, including type 2 diabetes and immune-mediated diseases such as Crohn's disease.
“Overlap in the genetic architecture between AD and other diseases has also been reported, including type 2 diabetes [124] and immune-mediated diseases such as Crohn’s disease [125, 126], although the precise mechanisms underlying this overlap remain to be elucidated.”
From Genetic architecture of Alzheimer's disease (2020) · cites this paper as [125]
Genetic pleiotropy studies have found striking genetic overlap between AD and several autoimmune disorders, including psoriasis and Crohn disease.
“Although AD is not considered a classical autoimmune disease, genetic pleiotropy studies have found striking genetic overlap between AD and several autoimmune disorders, including psoriasis and Crohn disease (6).”
From The Transcriptional Landscape of Microglial Genes in Aging and Neurodegenerative Disease (2019) · cites this paper as [6]
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- Authors
- Yokoyama, J. S., Wang, Y., Schork, A. J., Thompson, W. K., Karch, C. M., Cruchaga, C., McEvoy, L. K., Witoelar, A., Chen, C.-H., Holland, D., Brewer, J. B., Franke, A., Dillon, W. P., Wilson, D. M., Mukherjee, P., Hess, C. P., Miller, Z., Bonham, L. W., Shen, J., Rabinovici, G. D., Rosen, H. J., Miller, B. L., Hyman, B. T., Schellenberg, G. D., Karlsen, T. H., Andreassen, O. A., Dale, A. M., Desikan, R. S., & Initiative, F. T. A. D. N.
- Affiliations
- University of California, San Francisco (US)
- Washington University in St. Louis (US)
- University of California San Diego (US)
- Oslo University Hospital (NO)
- Institute of Clinical Molecular Biology, Christian-Albrechts-University of Kiel, Kiel, Germany
- Massachusetts General Hospital (US)
- University of Pennsylvania (US)
- Corresponding author
- Yokoyama, Jennifer S.
- ORCID
- Yokoyama, Jennifer S.
- Wang, Yunpeng
- Schork, Andrew J.
- Thompson, Wesley K.
- Karch, Celeste M.
- Cruchaga, Carlos
- McEvoy, Linda K.
- Witoelar, Aree
- Chen, Chi-Hua
- Holland, Dominic
- Dillon, William P.
- Wilson, David M.
- Mukherjee, Pratik
- Hess, Christopher P.
- Miller, Zachary
- Bonham, Luke W.
- Rabinovici, Gil D.
- Miller, Bruce L.
- Hyman, Bradley T.
- Schellenberg, Gerard D.
- Karlsen, Tom H.
- Andreassen, Ole A.
- Dale, Anders M.
- Desikan, Rahul S.
- Venue
- JAMA Neurology
- Publisher
- American Medical Association (AMA)
- Published
- 2016-06-01
- Volume
- 73
- Issue
- 6
- Pages
- 691
- ISSN
- 2168-6149 (ISSN-L)
- PMC
- PMC4905783
- OpenAlex
- W2339196082
- Cited by
- 176
- References
- 33
- Citations by year
- 2026: 9 · 2025: 14 · 2024: 15 · 2023: 14 · 2022: 14 · 2021: 25 · 2020: 22 · 2019: 10 · 2018: 23 · 2017: 16 · 2016: 12 · 2015: 1
- FWCI
- 16.37
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- JAMA Neurology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- National Institute on Aging (R01AG045611, U24-AG041689-01, K01AG046374, U01AG016976, P50AG005131, P30AG010124, K01AG049152, U01AG032984, P50AG005681, RC2AG036528, K24AG045333, P01AG019724, U24AG041689, U24AG021886, P50AG023501)
- National Institute on Drug Abuse (RC2DA029475)
- National Institute of General Medical Sciences (R01GM104400)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (R01HD061414)
- 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, immune-mediated diseases, genetic overlap, pleiotropy, inflammation, HLA-DRB5, inositol polyphosphate multikinase, neurofibrillary tangles, neuritic plaques, cognitive decline, psoriasis, Crohn's disease, ulcerative colitis, rheumatoid arthritis, type 1 diabetes, celiac disease, single nucleotide polymorphisms, gene expression
- MeSH terms
- Alzheimer Disease, Cognition Disorders, Female, Humans, Inflammation, Male, Phosphotransferases (Alcohol Group Acceptor), Polymorphism, Single Nucleotide, Genome-Wide Association Study, HLA-DRB5 Chains
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