The DOI matches its Crossref record; 202 of the 202 references it cites were found in a registry or an index.
Emerging roles of innate and adaptive immunity in Alzheimer’s disease
Open accessAbstract
Alzheimer's disease (AD) is the most common neurodegenerative disease, with characteristic extracellular amyloid-β (Aβ) deposition and intracellular accumulation of hyperphosphorylated, aggregated tau. Several key regulators of innate immune pathways are genetic risk factors for AD. While these genetic risk factors as well as in vivo data point to key roles for microglia, emerging evidence also points to a role of the adaptive immune response in disease pathogenesis. We review the roles of innate and adaptive immunity, their niches, their communication, and their contributions to AD development and progression. We also summarize the cellular compositions and physiological functions of immune cells in the parenchyma, together with those in the brain border structures that form a dynamic disease-related immune niche. We propose that both innate and adaptive immune responses in brain parenchyma and border structures could serve as important therapeutic targets for treating both the pre-symptomatic and the symptomatic stages of AD.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“The connection between AD and T-cell function was reported for neuronal signaling and AD pathology (4,47).”
From Alzheimer's Disease–Associated Amyloid-β Precursor Protein Prevents Aging Stress–Induced Mitophagy and Fumarate Depletion to Improve Antitumor Immunity (2025) · cites this paper as [4]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“The possible contribution of the adaptive immune system in AD patients to reducing cancer incidence has not been studied (4,5).”
From Alzheimer's Disease–Associated Amyloid-β Precursor Protein Prevents Aging Stress–Induced Mitophagy and Fumarate Depletion to Improve Antitumor Immunity (2025) · cites this paper as [4]
Experimental — accuracy not yet measured
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Items 201–202 of 202
Henningfield, C. M., Arreola, M. A., Soni, N., Spangenberg, E. E., & Green, K. N. (2022) · Glia · doi:10.1002/glia.24105 · Cited by 40
Diagnostic criteria for primary progressive mutiple sclerosis: a position paper.
(2000) · Pure Amsterdam UMC · doi:10.1002/1531-8249(200006)47:6 · Cited by 2
Self-citation
Flagged first, then by citations
Research works printed but not linked: 2
- Alzheimer, 1907, Über eine eigenartige Erkrankung der Hirnrinde. Allg, Z. Psychiatr., 64, 146
- Merlini, 2019, Fibrinogen Induces Microglia-Mediated Spine Elimination and Cognitive Impairment in an Alzheimer’s, Disease Model, 101, 1099
Cited by
Sorted by citations
Microglia-mediated T cell infiltration drives neurodegeneration in tauopathy
Chen, X., Firulyova, M., Manis, M., Herz, J., Smirnov, I., Aladyeva, E., Wang, C., Bao, X., Finn, M. B., Hu, H., et al. (2023) · Nature · doi:10.1038/s41586-023-05788-0 · Cited by 609
Self-citationEmerging diagnostics and therapeutics for Alzheimer disease
Self, W. K., & Holtzman, D. M. (2023) · Nature Medicine · doi:10.1038/s41591-023-02505-2 · Cited by 381
Self-citationCellular and pathological functions of tau
Bravo, C. P., Naguib, S. A., & Gan, L. (2024) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-024-00753-9 · Cited by 271
Tripathi, P. N., Lodhi, A., Rai, S., Nandi, N., Dumoga, S., Yadav, P., Tiwari, A., Singh, S. K., El‐Shorbagi, A., & Chaudhary, S. (2024) · Degenerative Neurological and Neuromuscular Disease · doi:10.2147/dnnd.s452009 · Cited by 152
Baligács, N., Albertini, G., Borrie, S. C., Serneels, L., Pridans, C., Balusu, S., & De Strooper, B. (2024) · Nature Communications · doi:10.1038/s41467-024-54779-w · Cited by 123
Metadata
- Authors
- Chen, X., & Holtzman, D. M.
- Affiliations
- Washington University in St. Louis (US)
- Corresponding author
- Holtzman, David M.
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2022-12
- Volume
- 55
- Issue
- 12
- Pages
- 2236-2254
- ISSN
- 1074-7613 (ISSN-L)
- PMC
- PMC9772134
- OpenAlex
- W4308510589
- Cited by
- 297
- References
- 202
- Citations by year
- 2026: 57 · 2025: 100 · 2024: 93 · 2023: 47
- FWCI
- 6.26
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 538 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Immunity (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (RF1AG047644)
- National Institute of Neurological Disorders and Stroke (RF1NS090934)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, innate immunity, adaptive immunity, microglia, amyloid-beta, tau hyperphosphorylation, genetic risk factors, neuroinflammation, immune niches, immune cell composition, therapeutic target
- MeSH terms
- Alzheimer Disease, Humans, Immunity, Innate, Amyloid beta-Peptides, Microglia, Neurodegenerative Diseases, Adaptive Immunity
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
