Disease-modifying drug use necessitates better Alzheimer disease (AD) detection. 4 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Research
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Accumulation of β-amyloid protein (Aβ) and tau protein is the main feature of Alzheimer disease neuropathogenesis. 4 key findings →
Participants: 35 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Heterozygosity of the KL-VS haplotype has been associated with reduced amyloid and tau burden. 4 key findings →
Design: case-control study Participants: 243 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
However, a recent systematic review and meta-analysis did not support differences in orexin-A between AD and controls. 4 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
58/100
Previous studies reported substantial contributions of neurofibrillary tangles (NFT), amyloid deposits, and neuronal loss to the development of dementia. 4 key findings →
Evidence: low
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Six thousand thirty community-dwelling persons aged 65 to 95. 4 key findings →
Design: longitudinal study Evidence: moderate
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Cerebral microbleeds are frequently found in the general elderly population and may reflect underlying vascular disease, but their role in cognitive function is unknown. 4 key findings →
Participants: 3,979 Evidence: low
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Donanemab (Kisunla®), an IgG1 monoclonal antibody targeting N-terminal pyroglutamate-modified forms of amyloid-β, is approved in the United States for treatment of early symptomatic Alzheimer's disease (AD). 4 key findings →
Evidence: low
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Alzheimer's disease (AD) is the cause of more than two-thirds of all dementia cases. 4 key findings →
Design: meta-analysis Evidence: high
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58/100
Knight Alzheimer's Disease Research Center (ADRC) at Washington University (WU). 4 key findings →
Design: longitudinal study Participants: 118 Evidence: moderate
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This study evaluated efficacy and safety of donepezil hydrochloride (donepezil) at 5 mg/day in patients with mild to moderately severe Alzheimer's disease for 24 weeks in a double-blind, placebo-controlled comparative trial. 4 key findings →
Participants: 228 Evidence: low
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Although many studies have found a cross-sectional relation between depression and dementia or depressive symptomatology and cognitive functioning, the direction of the association is still unknown. 4 key findings →
Design: cohort study Participants: 1,600 Evidence: moderate
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The sensitivity of MRI volumetric measures to detect cognitive dysfunction is examined in 39 participants of an epidemiological field study (age 75-85, MMSE 19-30). 4 key findings →
Participants: 39 Evidence: low
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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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58/100
The authors used mixed-effects growth models to examine longitudinal change in neuropsychological performance over a 4-year period among 197 individuals who were either normal or had mild cognitive impairment (MCI) at baseline. 4 key findings →
Design: longitudinal study Participants: 33 Evidence: moderate
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Cerebral blood flow (CBF) velocity is decreased in patients with Alzheimer's disease. 4 key findings →
Participants: 1,716 Evidence: low
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The gap between predicted brain age using magnetic resonance imaging (MRI) and chronological age may serve as a biomarker for early-stage neurodegeneration. 4 key findings →
Design: longitudinal study Evidence: moderate
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Sleep is essential for life, including daily cognitive processes, yet the amount of sleep required for optimal brain health as we grow older is unclear. 4 key findings →
Participants: 479,420 Evidence: low
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Orthostatic hypotension (OH) is a common cause of transient cerebral hypoperfusion in the population. 4 key findings →
Participants: 6,204 Evidence: low
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58/100
Total hippocampal volume has been consistently linked to cognitive function and dementia. 4 key findings →
Participants: 5,035 Evidence: moderate
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Apolipoprotein (APOE) e4 genotype is an accepted risk factor for accelerated cognitive aging and dementia, though its neurostructural substrates are unclear. 4 key findings →
Design: cross-sectional Participants: 8,395 Evidence: moderate
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This study aimed to investigate the associations of grip strength with incidence and mortality from dementia and whether these associations differ by sociodemographic and lifestyle factors. 4 key findings →
Participants: 788 Evidence: low
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Total tau protein (T-Tau) and neurofilament light chain (NfL) have emerged as candidate plasma biomarkers of neurodegeneration, but studies have not compared how these biomarkers cross-sectionally or longitudinally associate with cognitive and neuroimaging measures. 4 key findings →
Design: cross-sectional Participants: 995 Evidence: moderate
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Medical imaging provides numerous insights into the subclinical changes that precede serious diseases such as heart disease and dementia. 4 key findings →
Design: cross-sectional Evidence: low
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Sedentary behavior (SB) is associated with cardiometabolic disease and mortality, but its association with dementia is currently unclear. 4 key findings →
Participants: 146,651 Evidence: low
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Where “Free full text” comes from
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
How the 0–100 score works — and why some entries are capped
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.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
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 28,180 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.
What this library is — and isn't
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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.
1,034 records (3.7% 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 →