29,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Increased BPSD was reported in 59.6% of patients as worsening of preexisting symptoms (51.9%) or as new onset (26%), and requested drug modifications in 27.6% of these cases. 4 key findings →
Participants: 4,913 Evidence: low
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Midlife CVRFs, especially hypertension, diabetes mellitus, and smoking, are common and associated with accelerated cognitive decline at midlife. 5 key findings →
Participants: 143 Evidence: low
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Human DNA methylation data have been used to develop biomarkers of ageing, referred to as 'epigenetic clocks', which have been widely used to identify differences between chronological age and biological age in health and disease including neurodegeneration, dementia and other brain phenotypes. 2 key findings →
Participants: 1,397 Evidence: low
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Nationwide population-based cohort provides a new opportunity to build an automated risk prediction model based on individuals' history of health and healthcare beyond existing risk prediction models. 1 key finding →
Participants: 40,736 Evidence: moderate
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From molecular mechanisms to global brain networks, atypical fluctuations are the hallmark of neurodegeneration. 4 key findings →
Participants: 300 Evidence: low
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Sleep is evolutionarily conserved across all species, and impaired sleep is a common trait of the diseased brain. 5 key findings →
Evidence: low
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Our work shows that peripheral differential methylation between age-matched subjects with AD relative to healthy controls will provide opportunities to further investigate and validate differential methylation as a surrogate of disease. 2 key findings →
Design: longitudinal study Participants: 653 Evidence: moderate
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Immune-regulatory mechanisms of drug-free remission in rheumatoid arthritis (RA) are unknown. 4 key findings →
Evidence: low
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Parkinson's disease is the second most common neurodegenerative disease after Alzheimer's disease and affects 1% of the population above 60 years old. 4 key findings →
Design: cross-sectional Participants: 165 Evidence: low
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The innate immune system is implicated in Parkinson's disease (PD), but peripheral in-vivo clinical evidence of the components and driving mechanisms involved and their relationship with clinical heterogeneity and progression to dementia remain poorly explored. 4 key findings →
Design: longitudinal study Participants: 41 Evidence: moderate
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We identified individuals with an incident diagnosis of PD (n=1276) and controls (n=500 406) in UK Biobank. 4 key findings →
Participants: 1,276 Evidence: moderate
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During follow-up, 60 individuals developed dementia, of which 49 had Alzheimer's disease (AD). 4 key findings →
Participants: 1,322 Evidence: moderate
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Models of Alzheimer's disease (AD) pathophysiology posit that amyloidosis [A] precedes and accelerates tau pathology [T] that leads to neurodegeneration [N]. 4 key findings →
Design: longitudinal study Participants: 262 Evidence: moderate
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Between Feb 1, 2013, and June 28, 2019 (Barcelona), and between June 1, 2009, and Dec 31, 2014 (Cambridge), we included 388 participants with Down syndrome (257 [66%] asymptomatic, 48 [12%] with prodromal Alzheimer's disease, and 83 [21%] with Alzheimer's disease dementia) and 242 euploid controls.
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Accounting for educationalfactors, vascular factors, and Aβ burden diminished, but did not eliminate, racial differences in PACC5 performance longitudinally. 4 key findings →
Design: longitudinal study Participants: 296 Evidence: moderate
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A faster termination of the stress response (higher coping ability) may limit the negative effects of stress on tau deposition. 5 key findings →
Design: cross-sectional Participants: 225 Evidence: moderate
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Within APOE ε4 carriers, sex differences in CSF p-Tau are more evident in early disease stages, whereas for APOE ε4 noncarriers, sex differences are more evident in advanced disease stages. 3 key findings →
Participants: 1,801 Evidence: low
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Benefit-finding is an efficacious intervention for depressive symptoms in Alzheimer caregivers, with strong effects in the medium-term post-intervention and possible moderate effects in the longer-term post-intervention. 2 key findings →
Evidence: low
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In mild cognitive impairment (MCI) due to Alzheimer disease (AD), also known as prodromal AD, there is evidence for a pathologic shortage of uridine, choline, and docosahexaenoic acid [DHA]), which are key nutrients needed by the brain. 3 key findings →
Design: randomized controlled trial Evidence: high
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Of 502 535 participants in UK Biobank, 143 215 met the inclusion criteria and were included in our analyses. 68 500 (47·8%) of the participants were pre-frail and 5565 (3·9%) were frail. 4 key findings →
Participants: 535 Evidence: moderate
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There were detectable WMH, enlarged PVS, infarcts, and microbleeds as early as the 5th decade of life. 2 key findings →
Design: cross-sectional Participants: 138 Evidence: low
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This association may be partially mediated by air pollution, whereas noise exposure did not affect associations. 1 key finding →
Design: case-control study Evidence: moderate
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Four subphenotypes were computationally derived that correlated with cardiovascular diseases and mental health illnesses. 3 key findings →
Design: longitudinal study Participants: 273 Evidence: moderate
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APOE4 is the strongest genetic risk factor associated with late-onset Alzheimer's disease (AD). 3 key findings →
Evidence: low
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Checkpoint immunotherapy unleashes T cell control of tumors, but is undermined by immunosuppressive myeloid cells. 4 key findings →
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.
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 29,380 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 29,380 records, built mostly from automated pulls of Europe PMC (63.3% of the library) and OpenAlex (17.3%), 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.
1,037 records (3.5% of the library) are not peer-reviewed — 964 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 →