Genetic and genome-wide association studies suggest a central role for microglia in Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
28,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
Genetic and genome-wide association studies suggest a central role for microglia in Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The mechanism of sphingosine-1-phosphate (S1P)-mediated phagocytosis remains unknown. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
A non-coding variant (rs35349669) in INPP5D increases the risk for Alzheimer's disease (AD), and elevated INPP5D expression is associated with increased plaque deposition. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Triggering receptor expressed on myeloid cells 2 (TREM2), a receptor exclusively expressed by microglia in the brain, modulates microglial immune homeostasis. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The Trem2 variant R47H, confers substantially elevated risk of developing late onset Alzheimer's disease, while NHD-linked Trem2 variants like Y38C, are associated with development of early onset dementia with white matter pathology. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The antemortem diagnosis of Alzheimer disease (AD) requires time-consuming and costly procedures. 4 key findings →
Evidence: low
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Cerebrospinal fluid values of total tau (T-tau) and β-amyloid 1-42 (Aβ 1-42) obtained using the Innotest enzyme-linked immunosorbent assay were transformed using a linear regression model to equivalent values obtained using the INNO-BIA AlzBio3 (xMAP; Luminex) assay. 4 key findings →
Evidence: low
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Physical exercise may have some effect on cognition in patients with Alzheimer disease (AD). 4 key findings →
Participants: 53 Evidence: low
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Alzheimer disease (AD) is characterized by amyloid-β plaques (A), tau tangles (T), and neurodegeneration (N), collectively defining the ATN framework. 4 key findings →
Design: longitudinal study Evidence: moderate
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Recent evidence has suggested a role for soluble oligomeric Abeta species in the pathology of Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The hippocampus is one of the most well studied structures in the human brain. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Postmortem demonstration of increased expression of biologically active S100B in Alzheimer's disease (AD) and its relation to progression of neuropathological changes across the cortical regions suggests involvement of this astrocytic cytokine in the pathophysiology of AD. 4 key findings →
Evidence: low
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Alzheimer's disease (AD) is the most common neurodegenerative disorder that affects the elderly. 4 key findings →
Evidence: low
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Huntington's disease (HD) is a fatal inherited neurodegenerative disorder characterized by personality changes, motor impairment, and subcortical dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Sporadic, late-onset Alzheimer disease (AD) constitutes the most frequent cause of dementia in the elderly population. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is a late-onset dementia that is characterized by the loss of memory and an impairment of multiple cognitive functions. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cerebrovascular dysfunction contributes to the cognitive decline and dementia in Alzheimer's disease (AD), and may precede cerebral amyloid angiopathy and brain accumulation of the Alzheimer's neurotoxin, amyloid beta-peptide (Abeta). 4 key findings →
Evidence: low
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Neuropathologic examination of 3 patients with Alzheimer disease in the Elan Pharmaceuticals trial using antibodies specific for different Abeta species showed in one case, 4 months after the immunization, evidence of a stage of active plaque clearance with "moth-eaten" plaques and abundant Abeta phagocytosis by microglia. 4 key findings →
Evidence: low
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Stress granules (SGs) are RNA-containing cytoplasmic foci formed in response to stress exposure. 4 key findings →
Evidence: low
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Gangliosides are the main glycolipids of neuronal plasma membranes. 4 key findings →
Evidence: low
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TDP-43 is an RNA/DNA-binding protein implicated in transcriptional repression and mRNA processing. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Microglia are a major ghal component of the central nervous system (CNS) and are extremely sessile. 4 key findings →
Evidence: low
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Alzheimer Disease (AD) is a neurodegenerative disorder and the most common form of dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The colony-stimulating factor-1 receptor (CSF-1R) kinase regulates tissue macrophage homeostasis, osteoclastogenesis, and Paneth cell development. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Recent findings suggest that hypercholesterolemia may contribute to the onset of Alzheimer's disease-like dementia but the underlying mechanisms remain unknown. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
10 of the 7,799 studies in this tag that have a study page, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
Free full text links and the Full text may need a subscription label come from Unpaywall, Europe PMC and OpenAlex records of free copies, checked 10 Oct 2026. A study with neither is unknown, not paywalled. Show only studies that are free to read
This is alzhub's own score. It is not an official metric, not an impact factor, and no journal, publisher or ranking body endorses it. We built it so that a reader who is not a scientist can tell a landmark trial from a conference abstract without having to already know the difference. Every point comes from one of 20 components, all of them printed on the study itself, so you can disagree with our arithmetic rather than having to trust the total.
Journals are placed in ordered tiers, never given a numeric impact factor — we could not verify current impact factors from a source we control, and an invented one would be worse than none. Tier 1 is the top-tier general journals (NEJM, The Lancet, JAMA, Nature, Science, Nature Medicine); tier 2 is the leading specialty journals; tier 3 is every other peer-reviewed journal. A separate part scores how much the journal's own papers are cited, which tells the tier-3 journals apart.
Two rules we don't bend. First, we never fill in a missing value: if a record does not state a sample size or a design, that component scores zero, and if we simply have no data for a part, such as a citation count, that part is left out and the study is scored on the parts we could check. The study card says which. Second, anything that is not a peer-reviewed article is capped at 16/100 and carries a warning chip — so a conference abstract or a company press release can never outrank a peer-reviewed paper, no matter how good it looks.
We rank a rigorous null result — a good trial showing that something does not work — above an early positive finding. Someone deciding whether to buy a supplement is served by that, and the rigour is already counted by the design and journal components.
The score is computed from the published data alone and is reproducible: the same file always yields the same numbers.
See the whole rubric drawn out → — four charts covering all 28,980 studies: how the scores are spread and where the cap bites, which of the 20 components the library is strong and weak on, which subjects rest on stronger evidence, and what kinds of study each subject is actually built from.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 28,980 records, built mostly from automated pulls of Europe PMC (62.8% of the library) and OpenAlex (17.6%), plus smaller pulls from PubMed, Crossref and medRxiv. If a study, a drug, or a finding isn't here, that is not evidence it doesn't exist in the literature — it may simply not have been pulled in yet.
1,038 records (3.6% of the library) are not peer-reviewed — 966 of those are preprints posted before any journal review, and the rest are conference abstracts, regulatory notices and reports. Every study card on this page states its status plainly, and the score above is capped for anything that isn't a peer-reviewed article.
See the full, machine-readable breakdown of this library's coverage →