27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Our results demonstrate the feasibility and potential of immunoassay-based multiplexing to provide a comprehensive view of AD-associated proteomic changes, consistent with the recently revised biological and diagnostic framework. 5 key findings →
Design: cross-sectional Participants: 113 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Racial/ethnic groups differed in sources of recruitment, reasons for screen failure, and overall probability of eligibility in a preclinical AD trial. 5 key findings →
Design: cross-sectional Participants: 5,945 Evidence: low
Full summary, score breakdown and related studies → Original source
Early tau deposition was elevated in women compared with men in individuals on the Alzheimer disease trajectory. 5 key findings →
Design: cross-sectional Participants: 89 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The agreement between Aβ classification with CSF Aβ42 and 18F-flutemetamol positron emission tomography was very high (κ = 0.85). 3 key findings →
Design: cross-sectional Participants: 118 Evidence: moderate
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Neurodegeneration rather than cerebrovascular lesions may play a key role in T2DM-related cognitive impairment. 2 key findings →
Design: cross-sectional Participants: 350 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is a progressive neurodegenerative condition marked by a decline in cognitive functions with no validated disease modifying treatment. 1 key finding →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
An algorithm-derived diagnosis of aMCI showed few sociodemographic associations but was consistently associated with higher disability and neuropsychiatric symptoms in addition to showing substantial variation in prevalence across LAMIC populations. 4 key findings →
Design: cross-sectional Participants: 15,376 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Plasma phosphorylated tau at threonine 181 (p-tau181), a well-validated marker of Alzheimer disease (AD) pathologic change, could be a more efficient way to diagnose AD than invasive or expensive biomarkers requiring CSF or PET. 4 key findings →
Design: cross-sectional Participants: 571 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Patients with preserved cognition and mild-verbal memory/semantic fluency were younger (mean [SD] age, 36.5 [9.8] years and 38.2 [11.1] years) and had shorter disease duration (mean [SD] 8.0 [7.3] years and 8.3 [7.6] years) compared with patients with mild-multidomain (mean [SD] age, 42.6 [11.2] years; mean [SD] disease duration, 12.8 [9.6] years; P < .001), severe-executive/attention (mean [SD] age, 42.9 [11.7] years; mean [SD] disease duration, 12.2 [9.5] years; P < .001), and severe-multidomain (mean [SD] age, 44.0 [11.0] years; mean [SD] disease duration, 13.3 [10.2] years; P < .001) phenotypes. 3 key findings →
Design: cross-sectional Participants: 235 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma phosphorylated-tau181 (p-tau181) showed the potential for Alzheimer's diagnosis and prognosis, but its role in detecting cerebral pathologies is unclear. 3 key findings →
Design: cross-sectional Participants: 1,189 Evidence: low
Full summary, score breakdown and related studies → Original source
Our study highlights factors associated with the development of CMHs in individuals with DIAD. 5 key findings →
Design: cross-sectional Participants: 310 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The current literature includes several studies investigating the association between physical activity and risk of Alzheimer's disease (AD). 2 key findings →
Design: cross-sectional Participants: 18 Evidence: low
Full summary, score breakdown and related studies → Original source
Long-term exposure to PM 2.5 contributed to the development of cognitive decline, which may be partly explained by brain amyloid accumulation indicative of increased AD risk. 1 key finding →
Design: cross-sectional Participants: 31,573 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma p-tau biomarkers had a greater diagnostic performance and larger effect sizes compared to t-tau and Aβ42/40 assays in detecting Aβ pathology. 5 key findings →
Design: cross-sectional Participants: 197 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We analysed 461 participants from the DABNI and SPIN cohorts. 5 key findings →
Design: cross-sectional Participants: 461 Evidence: low
Full summary, score breakdown and related studies → Original source
We found that plasma p-tau217 was more associated with cognitive performance than p-tau181 and p-tau231 and that this relationship was particularly strong for memory scores (TRIAD: βp-tau217 = -0.53, βp-tau181 = -0.35 and βp-tau231 = -0.24; BioFINDER-2: βp-tau217 = -0.52, βp-tau181 = -0.24 and βp-tau231 = -0.29). 4 key findings →
Design: cross-sectional Participants: 103 Evidence: moderate
Full summary, score breakdown and related studies → Original source
(N = 558, mean age = 69.2 ± 8.8, 56.5% women) were diagnosed with AD (n = 274, considering dementia and MCI stages), frontotemporal dementia (FTD, n = 55), Lewy body disease (LBD, n = 40, considering MCI and dementia stages), other neurodegenerative diseases, n = 57 (e.g Supranuclear Palsy, Corticobasal syndrome), non-neurodegenerative cognitive impairment (NND, n = 79, e.g. vascular lesions, epilepsy or psychiatric disorders) or subjective cognitive impairment (SCI, n = 53). 4 key findings →
Design: cross-sectional Participants: 558 Evidence: moderate
Full summary, score breakdown and related studies → Original source
In the multivariable linear regression models, a doubling of serum molybdenum level was associated with 9.4% higher Aβ42/40 ratio (95% CI: 0.8, 18.6%; p = 0.03), and a doubling of serum cobalt level with 17.5% higher p-tau181 level (95% CI: 3.1, 33.8%; p = 0.02). 5 key findings →
Design: cross-sectional Participants: 194 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Social participation may theoretically decrease risk for mild cognitive impairment (MCI). 2 key findings →
Design: cross-sectional Participants: 32,715 Evidence: low
Full summary, score breakdown and related studies → Original source
Emerging evidence suggests a potential role of gut dysbiosis in neurodegenerative disorders and, in particular, Alzheimer's disease (AD) pathology and cognitive decline. 4 key findings →
Design: cross-sectional Participants: 49 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Included in the analysis were 48,330 participants across 46 ADRCs (mean [SD] age, 71.3 [10.5] years; 20,767 female [57%]; 4,138 Hispanic [8.6%]; 1,392 non-Hispanic Asian [2.9%]; 6,766 non-Hispanic Black [14%] individuals; and 676 individuals [1.4%] of other races. 4 key findings →
Design: cross-sectional Participants: 48,330 Evidence: low
Full summary, score breakdown and related studies → Original source
The final sample comprised 2478 individuals, of which 59 (2.4%) were Asian, 63 (2.5%) were Black, and 2356 (95.1%) were White. 5 key findings →
Design: cross-sectional Participants: 2,478 Evidence: low
Full summary, score breakdown and related studies → Original source
This study validated PrecivityAD2, a mass-spectrometry blood test made by C2N Diagnostics that combines two markers (%p-tau217 and the amyloid-beta 42/40 ratio) into a single 'Amyloid Probability Score 2.' 4 key findings →
Design: cross-sectional Participants: 583 Evidence: high
Full summary, score breakdown and related studies → Original source
Comparing two nationally representative surveys of older Americans 12 years apart, researchers found the share of seniors with dementia fell substantially, from 11.6% in 2000 to 8.8% in 2012. 4 key findings →
Design: cross-sectional Participants: 21,057 Evidence: high
Full summary, score breakdown and related studies → Original source
Researchers re-ran the same detailed dementia survey in the same three parts of England twenty years apart. 4 key findings →
Design: cross-sectional Participants: 15,431 Evidence: high
Full summary, score breakdown and related studies → Original source
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 →