27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Hereditary frontotemporal dementia associated with mutations in the microtubule-associated protein tau gene (MAPT) is a protean disorder. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Much of the genetic basis for Alzheimer disease (AD) is unexplained. 4 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
This text discusses the characterisation of subjective cognitive decline (SCD), a term conceived in 2014 to describe cognitively unimpaired individuals who are concerned about reduced cognitive function and seek medical help. 3 key findings →
Full summary, score breakdown and related studies → Original source Free full text
Each additional copy of the apolipoprotein E4 (APOE4) allele is associated with a higher risk of Alzheimer's dementia, while the APOE2 allele is associated with a lower risk of Alzheimer's dementia, it is not yet known whether APOE2 homozygotes have a particularly low risk. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In the new AA diagnostic criteria, AD can be defined clinically as encompassing cognitively normal people having a core 1 AD biomarker. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Exposure to medications with severe AC cognitive burden may be a risk factor for developing MCI. 2 key findings →
Design: cohort study Participants: 3,690 Evidence: moderate
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Longitudinal analysis identified significant associations between the change in ether lipid species (including alkylphosphatidylcholine, alkenylphosphatidylcholine, lysoalkylphosphatidylcholine, and lysoalkenylphosphatidylcholine) and AD dementia conversion. 5 key findings →
Design: cross-sectional Participants: 1,393 Evidence: moderate
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This randomized clinical trial found that ADRD screening in PC was not associated with improvement in family member health-related quality of life, caregiver preparedness, or caregiving self-efficacy. 5 key findings →
Design: RCT Participants: 1,808 Evidence: null result
Full summary, score breakdown and related studies → Original source Free full text
Clinicopathological evidence suggests that the pathology of Alzheimer's disease (AD) begins many years before the appearance of cognitive symptoms. 3 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Limiting the clinical use of definite anticholinergics may reduce the incidence of cognitive impairment among African Americans. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
A total of 844 eligible individuals were consecutively approached, 294 consented to participate, and 204 completed the study (mean [SD] age, 70.0 [5.1] years; 127 women [62.3%]). 5 key findings →
Design: cross-sectional Participants: 127 Evidence: low
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In addition to known candidate genes, APOE, TOMM40, and one hypothetical gene LOC100129500 partially overlapping APOE; one novel gene, EPC2, and several other interesting genes were associated with CSF biomarkers that are related to AD. 3 key findings →
Participants: 374 Evidence: moderate
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Symptomatic mutation carriers also demonstrated elevated tau PET binding in the basal ganglia, consistent with prior work with amyloid-β. 2 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Pathogenic mutations in APP, PSEN1, PSEN2, MAPT and GRN have previously been linked to familial early onset forms of dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Increasing evidence points to a pivotal role of immune processes in the pathogenesis of Alzheimer disease, which is the most prevalent neurodegenerative and dementia-causing disease of our time. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In DIAD, clinical disease stage and BDNF Met66 were associated with cognitive impairment and levels of site-specific tau phosphorylation. 5 key findings →
Design: cohort study Participants: 527 Evidence: moderate
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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
Full summary, score breakdown and related studies → Original source Free full text
Dementia is an increasing focus for policymakers, civil organizations and multidisciplinary researchers. 5 key findings →
Design: narrative review Evidence: low
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Declines in heart disease and stroke mortality rates are conventionally attributed to reductions in cigarette smoking, recognition and treatment of hypertension and diabetes, effective medications to improve serum lipid levels and to reduce clot formation, and general lifestyle improvements. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Cognitive functions and self-reported drinking habits were assessed at 2-year intervals over an average of 7 years of follow-up. 4 key findings →
Design: longitudinal study Evidence: moderate
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The extent to which the pathophysiology of autosomal dominant Alzheimer's disease corresponds to the pathophysiology of 'sporadic' late onset Alzheimer's disease is unknown, thus limiting the extrapolation of study findings and clinical trial results in autosomal dominant Alzheimer's disease to late onset Alzheimer's disease. 3 key findings →
Participants: 559 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The six-item screener is a brief and reliable instrument for identifying subjects with cognitive impairment and its diagnostic properties are comparable to the full MMSE. 1 key finding →
Evidence: moderate
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Metabolomics identified key disease-related metabolic changes and disease-progression-related changes. 1 key finding →
Evidence: low
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Alzheimer's disease (AD) pathology is defined by β-amyloid (Aβ) plaques and neurofibrillary tau, but Lewy bodies (LBs; 𝛼-synuclein aggregates) are a common co-pathology for which effective biomarkers are needed. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The precise mechanism through which many of these genes are associated with AD remains unknown. 3 key findings →
Participants: 977 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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.
1,034 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 →