Genomics implicates adaptive and innate immunity in Alzheimer’s and Parkinson’s diseases
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Abstract
OBJECTIVES: We assessed the current genetic evidence for the involvement of various cell types and tissue types in the etiology of neurodegenerative diseases, especially in relation to the neuroinflammatory hypothesis of neurodegenerative diseases. METHODS: We obtained large-scale genome-wide association study (GWAS) summary statistics from Parkinson's disease (PD), Alzheimer's disease (AD), and amyotrophic lateral sclerosis (ALS). We used multiple sclerosis (MS), an autoimmune disease of the central nervous system, as a positive control. We applied stratified LD score regression to determine if functional marks for cell type and tissue activity, and gene-set lists were enriched for genetic heritability. We compared our results to those from two gene-set enrichment methods (Ingenuity Pathway Analysis and enrichr). RESULTS: There were no significant heritability enrichments for annotations marking genes active within brain regions, but there were significant heritability enrichments for annotations marking genes active within cell types that form part of both the innate and adaptive immune systems. We found this for MS (as expected) and also for AD and PD. The strongest signals were from the adaptive immune system (e.g., T cells) for PD, and from both the adaptive (e.g., T cells) and innate (e.g., CD14: a marker for monocytes, and CD15: a marker for neutrophils) immune systems for AD. Annotations from the liver were also significant for AD. Pathway analysis provided complementary results. INTERPRETATION: For AD and PD, we found significant enrichment of heritability in annotations marking gene activity in immune cells.
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These associations were observed whether APOE was included or not, confirming the enrichment was not driven by a single moderate-effect variant.
“These associations were observed whether APOE was included or not, confirming the enrichment was not driven by a single moderate-effect variant [183].”
From Genetic architecture of Alzheimer's disease (2020) · cites this paper as [183]
Gagliano et al. identified a significant enrichment for AD-associated variants in functional annotations active in the "immune/hematopoietic cell" and "liver" categories, but not in other categories such as brain, cardiovascular, kidney, etc.
“In combination with additional annotation information including chromatin accessibility as measured by DNase hypersensitivity, Gagliano et al. [183] identified a significant enrichment for AD-associated variants in functional annotations active in the “immune/hematopoietic cell” and “liver” categories, but not in other categories such as brain, cardiovascular, kidney, etc.”
From Genetic architecture of Alzheimer's disease (2020) · cites this paper as [183]
Since the discovery that genetic variants are enriched within regulatory regions active in myeloid cells, a large emphasis has been placed on improving resources to better model the impact of these variants in a disease-relevant context.
“Since the discovery that genetic variants are enriched within regulatory regions active in myeloid cells [173, 183, 184], a large emphasis in the field has been placed on improving resources to better model the impact of these variants in a disease-relevant context.”
From Genetic architecture of Alzheimer's disease (2020) · cites this paper as [183]
Common genetic variants impacting AD are not randomly distributed across the genome; instead, they are enriched for localization to regulatory elements active largely in human monocytes, macrophages, and microglia.
“we now understand that common genetic variants impacting AD are not randomly distributed across the genome. Instead, these variants seem to be enriched for localization to regulatory elements active largely in human monocytes, macrophages, and microglia.”
From Genetic architecture of Alzheimer's disease (2020) · cites this paper as [183]
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- Authors
- Gagliano, S. A., Pouget, J. G., Hardy, J., Knight, J., Barnes, M. R., Ryten, M., & Weale, M. E.
- Affiliations
- Department of Medical & Molecular Genetics Guy's Hospital King's College London 8th Floor Tower Wing London SE1 9RT United Kingdom
- Centre for Addiction and Mental Health (CA)
- National Hospital for Neurology and Neurosurgery (GB)
- Queen Mary University of London (GB)
- Guy's Hospital (GB)
- ORCID
- Venue
- Annals of Clinical and Translational Neurology
- Publisher
- Wiley
- Published
- 2016-11-04
- Volume
- 3
- Issue
- 12
- Pages
- 924-933
- ISSN
- 2328-9503 (ISSN-L)
- PMC
- PMC5224821
- OpenAlex
- W2531792466
- Cited by
- 85
- References
- 56
- Citations by year
- 2026: 6 · 2025: 4 · 2024: 5 · 2023: 8 · 2022: 6 · 2021: 13 · 2020: 11 · 2019: 13 · 2018: 12 · 2017: 7
- FWCI
- 5.84
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Annals of Clinical and Translational Neurology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Lancaster EPrints (Lancaster University) (acceptedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Queen Mary Research Online (Queen Mary University of London) (submittedVersion, cc-by)
- Funders
- Fulbright Canada
- Fondation Brain Canada
- National Institute for Health Research
- Medical Research Council (G0901254/1)
- Labex
- Alzheimer’s Research UK (503176)
- Wellcome Trust (082604/2/07/Z)
- Bundesministerium für Bildung und Forschung
- Alzheimer's Association (ADGC–10–196728)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
- Keywords
- Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, neuroinflammation, innate immunity, adaptive immunity, immune cell gene expression, heritability, cell type enrichment, T cells, monocytes, neutrophils, hepatic gene expression, multiple sclerosis, neurodegenerative disease genetics
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