27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Elderly patients with diabetes develop more extensive vascular pathology, which alone or together with AD-type pathology (particularly in APOE ε4 carriers) results in increased dementia risk. 2 key findings →
Participants: 553 Evidence: low
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The risk of dementia and Alzheimer's disease (AD) probably results from an interaction between genetic and environmental factors. 3 key findings →
Participants: 1,449 Evidence: low
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Recent findings suggest that a rich social network may decrease the risk of developing dementia. 3 key findings →
Design: longitudinal study Evidence: moderate
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Although cross-sectional studies found an association between anaemia and dementia, longitudinal studies provided contradictory results. 4 key findings →
Design: cross-sectional Participants: 1,139 Evidence: moderate
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Obesity at midlife is associated with an increased risk of dementia and AD later in life. 3 key findings →
Participants: 1,449 Evidence: low
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Diabetes and pre-diabetes substantially accelerate the progression from MCI to dementia, and anticipate dementia occurrence by more than 3 years in people with MCI. 3 key findings →
Participants: 302 Evidence: moderate
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Cerebrospinal fluid tau and CSF-Abeta42 have so far been studied in research settings, under conditions providing data on the optimal performance. 1 key finding →
Participants: 105 Evidence: low
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Family history of dementia was associated with an increased risk of dementia and AD in this very old population, but only among APOE epsilon4 carriers. 5 key findings →
Design: cohort study Participants: 907 Evidence: moderate
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The association between low education and dementia is probably not explained by the unhealthy lifestyles of the less educated compared with higher educated persons. 4 key findings →
Participants: 1,449 Evidence: low
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During the 6534 person-years of follow-up (mean, 5.02 years per person), 440 subjects were diagnosed as having dementia, including 333 with Alzheimer disease. 3 key findings →
Participants: 1,301 Evidence: moderate
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Uncontrolled diabetes increases the risk of Alzheimer's disease and VaD. 4 key findings →
Participants: 1,248 Evidence: moderate
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Worldwide costs of dementia are enormous and distributed inequitably. 1 key finding →
Evidence: low
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Our results suggest that risperidone may affect the CSF profile of AD biomarkers indicating more amyloid pathology. 5 key findings →
Participants: 44 Evidence: high
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Moreover, there is limited knowledge regarding associations with domain-specific cognitive decline and modifying effects of key individual characteristics. 4 key findings →
Design: cohort study Participants: 2,008 Evidence: moderate
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The sensitivity of CSF-beta-amyloid(1-42) level as a diagnostic marker for AD is high. 2 key findings →
Evidence: low
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We studied CSF-tau and CSF-Abeta42 in 16 patients with mild cognitive impairment (MCI) who at follow-up investigations 6-27 months later had progressed to Alzheimer's disease (AD) with dementia. 1 key finding →
Participants: 15 Evidence: low
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More open debates of practical experiences from different trial centres and sponsors are essential for optimizing trial designs and improving conditions for participants. 2 key findings →
Participants: 20 Evidence: high
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Both low diastolic and high systolic pressure are associated with an increased risk of Alzheimer disease and dementia in this elderly population. 4 key findings →
Participants: 1,270 Evidence: moderate
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In order to observe changes owing to aging and Alzheimer's disease (AD) in the volumes of subdivisions of the hippocampus and the number of neurons of the hippocampal formation, 18 normal brains from subjects who died of nonneurological causes and had no history of long-term illness or dementia (ten of these brains comprised the aged control group) and 13 AD brains were analyzed. 3 key findings →
Design: cross-sectional Evidence: low
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Three-, 6-, and 9-year follow-up study. 4 key findings →
Evidence: low
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The future price of lecanemab in European countries is unknown. 2 key findings →
Design: modelling Evidence: moderate
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Although possession of the APOE epsilon4 allele is a risk factor for AD in old age, it does not modify the progression of the disease during the preclinical period. 1 key finding →
Evidence: low
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Brain zinc accumulation is a prominent feature of advanced Alzheimer disease (AD) and is biochemically linked to brain amyloid beta-peptide accumulation and dementia severity in AD. 3 key findings →
Evidence: low
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The 39- to 43-amino acid amyloid beta-protein (A beta), which is progressively deposited in cerebral plaques and blood vessels in Alzheimer disease (AD), is secreted by cultured human cells during normal metabolism. 4 key findings →
Evidence: low
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The aim of this study was to explore the relationship between cerebrospinal fluid Alzheimer's disease (AD) markers and depression in elderly people. 4 key findings →
Participants: 183 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 →