Late onset Alzheimer’s disease genetics implicates microglial pathways in disease risk
Open accessAbstract
Alzheimer's disease (AD) is a highly heritable complex disease with no current effective prevention or treatment. The majority of drugs developed for AD focus on the amyloid cascade hypothesis, which implicates Aß plaques as a causal factor in the disease. However, it is possible that other underexplored disease-associated pathways may be more fruitful targets for drug development. Findings from gene network analyses implicate immune networks as being enriched in AD; many of the genes in these networks fall within genomic regions that contain common and rare variants that are associated with increased risk of developing AD. Of these genes, several (including CR1, SPI1, the MS4As, TREM2, ABCA7, CD33, and INPP5D) are expressed by microglia, the resident immune cells of the brain. We summarize the gene network and genetics findings that implicate that these microglial genes are involved in AD, as well as several studies that have looked at the expression and function of these genes in microglia and in the context of AD. We propose that these genes are contributing to AD in a non-Aß-dependent fashion.
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Many immune molecules either express specifically in microglia or are enriched in microglial cells, suggesting that microglia plays a crucial role in the immune regulation of AD.
“Interestingly, many of these immune molecules either express specifically in microglia (e.g., the MS4As, CD33, SPI1, and INPP5D) or are enriched in microglial cells (e.g., CR1, ABCA7, and CLU), suggesting that microglia plays crucial role in the immune regulation of AD.247”
From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [247]
The Background and Conclusion implicate microglial immune pathways in Alzheimer’s disease, and the AD GWAS sections describe several named genes as expressed in microglia. But the paper also says MS4As, SPI1, CD33 and INPP5D are expressed in other immune cells, so it does not support calling them microglia-specific; the searched passages do not establish the claimed microglial enrichment of CR1, ABCA7 or CLU. The Conclusion also leaves open whether peripheral immune cells contribute to the immune effect. (LLM, conf=0.88)
Experimental — accuracy not yet measuredLarge-scale GWAS identified many additional genetic risk factors linked with immune response (odds ratio 0.9-1.15).
“Except APOE and TREM2, large-scale genome-wide association study (GWAS) has identified many additional genetic risk factors linked with immune response (odds ratio 0.9–1.15).”
From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [247]
The AD GWAS studies sections report 25 AD-risk loci from GWAS meta-analyses and discuss several loci associated with microglial or immune-related genes, including CR1 and the MS4A cluster. The passages do not give the claimed odds-ratio range of 0.9–1.15; they also caution that GWAS identifies loci, not necessarily the specific causal genes. (LLM, conf=0.87)
Experimental — accuracy not yet measuredHuman genome-wide association studies have implicated mutations in microglial receptors in the development of several neurodegenerative diseases.
“Indeed, human genome-wide association studies (GWAS) have implicated mutations in microglial receptors in the development of several neurodegenerative diseases (Cooper-Knock et al., 2017; Efthymiou and Goate, 2017; IMSG, 2019).”
From SYK coordinates neuroprotective microglial responses in neurodegenerative disease (2022) · cites this paper as Efthymiou and Goate, 2017
In ‘AD GWAS studies > Additional plausible microglial genes’ (page unavailable), the paper reports GWAS-associated variants at CD33, a microglial receptor, in Alzheimer’s disease. Its TREM2 discussion mentions possible links to other neurodegenerative diseases but says those links are far less compelling than the Alzheimer’s evidence; it does not establish that GWAS implicated receptor mutations across several such diseases. (LLM, conf=0.84)
Experimental — accuracy not yet measuredSome Alzheimer's disease risk loci are highly enriched within or near genes encoding microglia-specific transcription factors.
“Interestingly, some Alzheimer's disease risk loci are highly enriched within or near genes encoding microglia‐specific transcription factors, highlighting their crucial roles in the pathogenesis of Alzheimer's disease (Table 1) [5, 7, 20, 21].”
From Targeting Microglial Transcriptional Reprogramming as a Therapy Strategy for Alzheimer's Disease (2026) · cites this paper as [20]
The AD GWAS studies section identifies SPI1, which encodes the transcription factor PU.1, as the likely gene affected at one AD-risk locus. The epigenetic-signals section also reports enrichment of AD-associated loci in enhancer regions and enrichment of a PU.1 binding motif. Neither passage establishes that multiple AD-risk loci are highly enriched within or near genes encoding microglia-specific transcription factors; the paper describes PU.1 as associated with microglial activation, not as microglia-specific. (LLM, conf=0.84)
Experimental — accuracy not yet measuredRecent AD genetic studies have demonstrated that immune and microglia networks are critical players in AD.
“In support of this, recent AD genetic studies have demonstrated that immune and microglia networks are critical players in AD (3, 4).”
From Deletion of <i>Abi3</i> gene locus exacerbates neuropathological features of Alzheimer’s disease in a mouse model of Aβ amyloidosis (2021) · cites this paper as [4]
The Background says GWAS findings and gene-expression network analyses implicate immune and microglial networks as important players in AD. It also says their exact contribution is not well understood, so “demonstrated” and “critical” express more certainty than the source does. (LLM, conf=0.83)
Experimental — accuracy not yet measured
Over 70 loci are associated with conferring risk for late-onset Alzheimer's disease.
“In recent years, genome wide association studies (GWASs) and analyses of rare-coding variants have identified over 70 loci associated with conferring risk for late-onset AD (LOAD).”
From Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease (2023) · cites this paper as [5]
The AD GWAS studies section reports 25 AD-risk loci detected through GWAS meta-analyses and discusses rare variants associated with AD. It does not support the claim that GWAS and rare-coding-variant analyses had identified over 70 LOAD-risk loci. (LLM, conf=0.87)
Experimental — accuracy not yet measuredGWAS have strongly implicated microglial genes involved in ligand recognition and phagocytosis, such as APOE, TREM2, CD33 and the MS4A cluster, in the biology of AD.
“GWAS have strongly implicated microglial genes involved in ligand recognition and phagocytosis, such as APOE, TREM2, CD33 and the MS4A cluster, in the biology of AD36.”
From Clonal hematopoiesis is associated with protection from Alzheimer’s disease (2023) · cites this paper as [36]
The AD GWAS studies section links the MS4A cluster to AD risk, and the sequencing and rare-variants section describes TREM2’s role in ligand binding and microglial phagocytosis. The Conclusion also implicates CD33 and TREM2 in phagocytosis. But the common-variants section says the MS4A proteins’ exact function and ligand-binding partners remain unknown, so the claim overstates the evidence that all the listed genes have the stated functions. (LLM, conf=0.86)
Experimental — accuracy not yet measuredMany AD risk genes are primarily expressed in microglia.
“Most notably, these genetic studies implicate central roles for the innate immune system, with many AD risk genes being primarily expressed in microglia (Efthymiou and Goate, 2017; Karch and Goate, 2015; Lopes et al., 2022).”
From Alzheimer’s genetic risk factor CASS4 controls microglial focal adhesion biology and amyloidosis (2026) · cites this paper as Efthymiou and Goate, 2017
The Abstract (page unavailable) names several AD-associated genes expressed by microglia, and “AD-risk genes in microglia” describes several genes in AD-risk loci that are expressed there. Neither passage establishes that these genes are primarily expressed in microglia rather than other cell types. (LLM, conf=0.85)
Experimental — accuracy not yet measuredMicroglia play a defining role in the progression of Alzheimer's disease.
“Microglia, the innate immune cells of the brain, play a defining role in the progression of Alzheimer’s disease (AD)1.”
From Lymphoid gene expression supports neuroprotective microglia function (2025) · cites this paper as [1]
GWASs of AD have identified many risk genes that are highly or selectively expressed in microglia.
“Genome-wide association studies (GWASs) of AD have identified many risk genes that are highly or selectively expressed in microglia, the predominant immune cells of the brain (4).”
From Deletion of <i>Abi3</i> gene locus exacerbates neuropathological features of Alzheimer’s disease in a mouse model of Aβ amyloidosis (2021) · cites this paper as [4]
Loci associated with Alzheimer's disease risk are enriched in genes expressed in microglia.
“Recent genetic studies on Alzheimer’s disease (AD) have brought microglia under the spotlight, as loci associated with AD risk are enriched in genes expressed in microglia.”
From Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease (2023) · cites this paper as [5]
Several LOAD-associated variants in genes expressed within microglia have been identified, which have direct effects on microglial phenotype, and can alter the course of the disease.
“Several LOAD-associated variants in genes expressed within microglia have been identified [92], which have direct effects on microglial phenotype [93], and can alter the course of the disease.”
From TREM2/PLCγ2 signalling in immune cells: function, structural insight, and potential therapeutic modulation (2021) · cites this paper as [92]
Genetic association data implicate microglial expressed genes, and hence microglia, with altered risk for developing the disease, but the underlying mechanisms are not yet fully understood.
“Genetic association data implicate microglial expressed genes, and hence microglia, with altered risk for developing the disease, but the underlying mechanisms are not yet fully understood [93–95].”
From APOE Christchurch enhances a disease-associated microglial response to plaque but suppresses response to tau pathology (2025) · cites this paper as [95]
About 75% of mutations in PLCG2 previously implicated in various inflammatory diseases map to the autoinhibitory interface on the PLCγ2 model structure and can be considered pathogenic.
“A number of mutations in PLCG2 (about 75%), that have been previously implicated in various inflammatory diseases [92–102], actually map to the autoinhibitory interface on the PLCγ2 model structure and can be considered as pathogenic (Fig. 2c)”
From TREM2/PLCγ2 signalling in immune cells: function, structural insight, and potential therapeutic modulation (2021) · cites this paper as [92]
The AD GWAS studies section discusses other risk genes and variants, but no passage in our copy addresses PLCG2 mutations or a PLCγ2 structural model. Searches for PLCG2, phospholipase C gamma 2, the autoinhibitory interface, and the claimed 75% figure found no support for the mapping or pathogenicity claim. (LLM, conf=0.74)
Experimental — accuracy not yet measuredGenome-wide association studies have revealed that various polymorphic variants of genes implicated in inflammation serve as risk factors for AD.
“Genome‐wide association studies have revealed that various polymorphic variants of genes implicated in inflammation serve as risk factor for AD, suggesting an important role of inflammation in AD. 121”
From Senescence, brain inflammation, and oligomeric tau drive cognitive decline in Alzheimer's disease: Evidence from clinical and preclinical studies (2024) · cites this paper as [121]
Genome-wide association studies have identified several single nucleotide polymorphisms in immune-related genes that are linked to increased risk of AD.
“Genome-wide association studies have identified several single nucleotide polymorphisms in immune-related genes that are linked to increased risk of AD.8”
From CSF biomarkers of neuroinflammation and cerebrovascular dysfunction in early Alzheimer disease (2018) · cites this paper as [8]
GWAS have demonstrated that most AD risk genes are highly or exclusively expressed in microglia.
“Recently, genome-wide association studies (GWAS) have demonstrated that most AD risk genes are highly or exclusively in microglia”
From Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets (2023) · cites this paper as [124]
Microglia play an essential role in AD development.
“suggesting that microglia play an essential role in AD development.”
From Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets (2023) · cites this paper as [124]
GWAS showed that most AD risk genes were highly or exclusively expressed in microglia in the brain, such as TREM2 and MS4A4A.
“Recently, GWAS showed that most AD risk genes were highly or exclusively expressed in microglia in the brain such as TREM2 and MS4A4A.124”
From Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets (2023) · cites this paper as [124]
The network includes genes linked to late-onset AD implicated in microglia activation (Abi3, Sall1, Spi1, Trem2), immune response (Bcl3, Gal3st4, Hla-Dqa1, Inpp5d, Lrrc25, Pycard, Sbno2), and complement pathway (Clu, Ms4a6a).
“Significantly, the network includes a group of genes linked to late-onset AD implicated in microglia activation: (Abi3, Sall1, Spi1, Trem2), immune response (Bcl3, Gal3st4, Hla-Dqa1, Inpp5d, Lrrc25, Pycard, Sbno2), and the complement pathway (Clu, Ms4a6a) (Efthymiou and Goate, 2017; Sims et al., 2017; Zhang et al., 2013).”
From Complement C3aR Inactivation Attenuates Tau Pathology and Reverses an Immune Network Deregulated in Tauopathy Models and Alzheimer’s Disease (2018) · cites this paper as Efthymiou and Goate, 2017
Little is known about the origins of Aβ deposition and neurodegeneration in sporadic Alzheimer's disease, which represents the greatest proportion of all AD cases.
“By contrast, still little is known about the origins of the Aβ deposition and neurodegeneration occurring in the sporadic AD, which represents the greatest proportion of all AD cases (Efthymiou and Goate, 2017).”
From Exploring the Therapeutic Potential of Phytochemicals in Alzheimer’s Disease: Focus on Polyphenols and Monoterpenes (2022) · cites this paper as Efthymiou and Goate, 2017
Genetic analyses have revealed the central role of microglial cells and of their crosstalk with neurons in Alzheimer's disease.
“Genetic analyses have revealed the central role of microglial cells and of their crosstalk with neurons in the disease (Efthymiou and Goate, 2017).”
From Selective Neuronal Vulnerability in Alzheimer’s Disease: A Network-Based Analysis (2020) · cites this paper as Efthymiou and Goate, 2017
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Alzheimer’s disease phospholipase C-gamma-2 (PLCG2) protective variant is a functional hypermorph
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β-amyloid redirects norepinephrine signaling to activate the pathogenic GSK3β/tau cascade
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Cellular Receptors of Amyloid β Oligomers (AβOs) in Alzheimer’s Disease
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“SHIP1 negatively regulates targets such as immune cell surface receptors by catalyzing the conversion of phosphatidylinositol (3,4,5)-trisphosphate (PI[3,4,5]P3) to phosphatidylinositol (3,4)-bisphosphate (PI[3,4]P2).”
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“2), which are consistent with prior studies [56, 57].”
ResultSelf-citationAlzheimer’s disease-related transcriptional sex differences in myeloid cells
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Identification of distinct and age‐dependent p16<sup>High</sup> microglia subtypes
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Lymphoid gene expression supports neuroprotective microglia function
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The effect of Abi3 locus deletion on the progression of Alzheimer’s disease-related pathologies
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“Importantly, pathway analyses of common and rare AD risk variants converge on immune response, phagocytosis, and lipid metabolism (4, 5).”
BackgroundDeletion of Abi3/Gngt2 influences age-progressive amyloid β and tau pathologies in distinctive ways
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Loss of <i>Inpp5d</i> has disease‐relevant and sex‐specific effects on glial transcriptomes
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“Given the increasing evidence that microglia play a critical role in AD pathogenesis 30 and that Inpp5d is exclusively expressed in microglia, we believe that our data will be invaluable resources for the research community for designing future experiments.”
PLCG2 as a Risk Factor for Alzheimer's Disease.
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Network analysis identifies strain-dependent response to tau and tau seeding-associated genes
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Targeting Microglial Transcriptional Reprogramming as a Therapy Strategy for Alzheimer's Disease
Kim, B., Wang, S. S., Kim, J. R., & Kim, J. (2026) · BioEssays · doi:10.1002/bies.70186
Alzheimer’s genetic risk factor CASS4 controls microglial focal adhesion biology and amyloidosis
Walsh, A. E., Davis, B. A., Samuels, J. D., Mills, W. A., Thanos, J. M., Johnson, A. M., Moore, K. A., Puchalski, M. A., Steacy, E. J., Wendell, B. W., et al. (2026) · Journal of Experimental Medicine · doi:10.1084/jem.20260104
- Authors
- Efthymiou, A. G., & Goate, A. M.
- Affiliations
- Icahn School of Medicine at Mount Sinai (US)
- Corresponding author
- Goate, Alison M.
- Venue
- Molecular Neurodegeneration
- Published
- 2017-05-26
- Volume
- 12
- Issue
- 1
- Pages
- 43-43
- ISSN
- 1750-1326 (ISSN-L)
- PMC
- PMC5446752
- OpenAlex
- W2617693460
- Cited by
- 562
- References
- 102
- Citations by year
- 2026: 40 · 2025: 59 · 2024: 78 · 2023: 68 · 2022: 84 · 2021: 80 · 2020: 56 · 2019: 41 · 2018: 45 · 2017: 10 · 2012: 1
- FWCI
- 5.10
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Molecular Neurodegeneration (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- National Institutes of Health (U01AG049508, U01AG052411)
- JPB Foundation
- Foundation for the National Institutes of Health (RF1AG054011)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- late-onset Alzheimer's disease, microglia, genetic risk, gene networks, immune pathways, TREM2, CD33, ABCA7, complement receptor 1, PU.1, INPP5D, amyloid plaques, therapeutic target
- MeSH terms
- Alzheimer Disease, Animals, Humans, Risk Factors, Microglia, Age of Onset, Genetic Predisposition to Disease, Gene Regulatory Networks
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