27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Among persons without dementia, the prevalence of cerebral amyloid pathology as determined by positron emission tomography or cerebrospinal fluid findings was associated with age, APOE genotype, and presence of cognitive impairment. 4 key findings →
Design: meta-analysis Participants: 2,914 Evidence: high
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The likelihood of amyloid positivity was associated with age and APOE ε4 status. 3 key findings →
Design: meta-analysis Participants: 377 Evidence: high
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There were 813 participants in CREAD (mean [SD] age, 70.7 [8.2] years; 483 female and 330 male) and 806 in CREAD2 (mean [SD] age, 70.9 [7.7] years; 456 female and 350 male). 2 key findings →
Design: clinical trial Participants: 3,664 Evidence: high
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Among persons with early Alzheimer's disease, the use of gantenerumab led to a lower amyloid plaque burden than placebo at 116 weeks but was not associated with slower clinical decline. 2 key findings →
Design: clinical trial Participants: 980 Evidence: low
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We found a sequence to pathological changes, with rates of Aβ deposition in mutation carriers being significantly different from those in non-carriers first (across regions that showed a significant difference, at a mean of 18·9 years [SD 3·3] before expected onset), followed by hypometabolism (14·1 years [5·1] before expected onset), and lastly structural decline (4·7 years [4·2] before expected onset). 2 key findings →
Design: longitudinal study Participants: 346 Evidence: moderate
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Amyloid-beta 42 (Aβ42) and phosphorylated tau (pTau) levels in cerebrospinal fluid (CSF) reflect core features of the pathogenesis of Alzheimer's disease (AD) more directly than clinical diagnosis. 2 key findings →
Participants: 8,074 Evidence: low
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Coding variants in the triggering receptor expressed on myeloid cells 2 (TREM2) are associated with late-onset Alzheimer's disease (AD). 4 key findings →
Design: longitudinal study Evidence: moderate
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This study found that CSF-based estimates using adjusted data-driven cutoffs were up to 10% higher than PET-based estimates in people without dementia, whereas the results were similar among people with dementia. 3 key findings →
Design: cross-sectional Participants: 97 Evidence: moderate
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This study investigated a subtype of reactive astrocytes called A1 and discovered that they are induced by classically activated neuroinflammatory microglia. 4 key findings →
Evidence: low
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In this genetic association study, a novel variant associated with AD was identified: R251G always coinherited with ε4 on the APOE gene, which mitigates the ε4-associated AD risk. 5 key findings →
Design: case-control study Participants: 37 Evidence: moderate
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The ε4 allele of apolipoprotein E (APOE) gene and increasing age are two of the most important known risk factors for developing Alzheimer disease (AD). 4 key findings →
Design: cohort study Participants: 1,593 Evidence: moderate
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The maximal tolerated dose of PQ912 has been identified and the results support future studies at still lower doses reaching > 50% target occupancy, a longer up-titration phase to potentially induce adaptation and longer treatment periods to confirm the early signals of efficacy as seen in this study. 4 key findings →
Design: randomized controlled trial Evidence: high
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A high percentage of patients with mild cognitive impairment (MCI) develop clinical dementia of the Alzheimer type (AD) within 1 year. 3 key findings →
Design: longitudinal study Evidence: moderate
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Debate surrounds the role of chronic pain as a risk factor for cognitive decline and dementia. 4 key findings →
Design: longitudinal study Participants: 995 Evidence: moderate
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Cognitive rehabilitation (CR) is a promising treatment approach for older adults with dementia because it aims at supporting the management of day-to-day problems. 2 key findings →
Participants: 201 Evidence: high
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Cerebral amyloid-β aggregation is an early event in Alzheimer disease (AD). 4 key findings →
Design: cross-sectional Participants: 2,908 Evidence: low
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The genetic variant rs72824905-G (minor allele) in the PLCG2 gene was previously associated with a reduced Alzheimer's disease risk (AD). 4 key findings →
Participants: 53,627 Evidence: low
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An estimated 40% of dementia is potentially preventable by modifying 12 risk factors throughout the life course. 4 key findings →
Participants: 39 Evidence: moderate
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In vivo imaging and quantification of amyloid-β plaque (Aβ) burden in small-animal models of Alzheimer's disease (AD) is a valuable tool for translational research such as developing specific imaging markers and monitoring new therapy approaches. 4 key findings →
Design: longitudinal study Evidence: moderate
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Reliable blood biomarkers for Alzheimer's disease (AD) are missing. 1 key finding →
Participants: 28 Evidence: low
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It is assumed that atherosclerotic arteries contain several macrophage subsets endowed with specific functions. 4 key findings →
Evidence: low
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Atherosclerotic plaques are complex tissues composed of a heterogeneous mixture of cells. 4 key findings →
Participants: 21 Evidence: low
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Greater intracranial volume (ICV) has been associated with less severe Alzheimer's disease (AD) symptoms at a given level of cerebral pathology. 4 key findings →
Design: longitudinal study Participants: 204 Evidence: moderate
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As serum NfL correlates with functional impairment and brain atrophy in bvFTD at different disease stages, we propose it as marker of disease severity, paving the way for its future use as outcome measure for clinical trials. 1 key finding →
Participants: 74 Evidence: low
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Microglial activation distributes preferentially along highly connected brain regions, similar to tau pathology. 5 key findings →
Participants: 32 Evidence: low
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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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% of the library) are not peer-reviewed — 962 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 →