27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Among older adults at risk of cognitive decline and dementia, a structured, higher-intensity intervention had a statistically significant greater benefit on global cognition compared with an unstructured, self-guided intervention. 5 key findings →
Participants: 1,056 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Addition of CAT to the PACC provides unique information about early cognitive decline not currently captured by the episodic memory, executive function, and global cognition components and may therefore improve detection of early Aβ-related cognitive decline. 1 key finding →
Design: longitudinal study Participants: 70 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Tai Chi shows potential to enhance cognitive function in older adults, particularly in the realm of executive functioning and in individuals without significant impairment. 5 key findings →
Design: systematic review Participants: 2,553 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
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
In clinically normal older adults, lower functional connectivity predicted more rapid decline in PACC scores over time, particularly when coupled with increased Aβ burden. 2 key findings →
Design: longitudinal study Participants: 237 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
This study found that a high-intensity multidomain lifestyle intervention did not affect brain biomarker trajectories and was not associated with Aβ pathology, but older adults with specific at-risk brain characteristics, including lower baseline HC volume, showed a greater cognitive benefit of the structured intervention. 4 key findings →
Design: RCT Participants: 983 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In this study, clinically normal adults with SNAP did not exhibit evidence of elevated tau levels, which suggests that this biomarker construct does not represent amyloid-independent tauopathy. 5 key findings →
Design: longitudinal study Participants: 247 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Sensitive detection of cognitive decline over the course of preclinical Alzheimer's disease is critical as the field moves toward secondary prevention trials. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Of 4413 individuals (mean [SD] age, 71.27 [4.66] years, 2617 women [59.3%]), mean Aβ-PET was elevated in individuals with history of memory impairment in both parents (n = 455; mean [SD] standardized uptake value ratio [SUVR] = 1.12 [0.19]; Wilcoxon P = 1.1 × 10-5) and in those with only maternal history (n = 1772; mean [SD] SUVR = 1.10 [0.19]; Wilcoxon P = 2.70 × 10-5) compared with those with only paternal history (n = 632; mean [SD] SUVR = 1.08 [0.18]; Wilcoxon P = 1.1 × 10-5) or no family history (n = 1554; mean [SD] SUVR = 1.08 [0.19]; Wilcoxon P = 1.1 × 10-5). 3 key findings →
Design: cross-sectional Participants: 455 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
These findings provide support for both the feasibility and validity of C3 and computerized cognitive outcomes more generally in AD secondary prevention trials. 3 key findings →
Design: cross-sectional Participants: 4,486 Evidence: low
Full summary, score breakdown and related studies → Original source
Animal models of Alzheimer's disease have suggested that tau pathology propagation, facilitated by amyloid pathology, may occur along connected pathways. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Characterizing subtle cognitive changes in preclinical Alzheimer's disease (AD) is difficult using traditional neuropsychological assessments. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
We sought to identify cognitive measures associated with the earliest detectable signs of emerging Aβ and tau pathology. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
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
Full summary, score breakdown and related studies → Original source Free full text
Although Aβ did not differ by sex, cognitive decline was greater in females with higher Aβ. 3 key findings →
Participants: 755 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
DCTclock discriminates between diagnostic groups and improves upon traditional cognitive tests for detecting biomarkers of amyloid and tau pathology in CN older adults. 3 key findings →
Participants: 300 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
BRANCH reliably captures meaningful cognitive information remotely, suggesting promise as a digital cognitive marker sensitive early in the AD trajectory. 2 key findings →
Participants: 234 Evidence: low
Full summary, score breakdown and related studies → Original source
The presubiculum captures unique AD-related biological variation that is not reflected in total hippocampal volume. 2 key findings →
Participants: 127 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Participants had a mean age of 71.3 (SD 4.6) years; 40.6% were male; and 34.6% were APOE ε4 positive. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Future longitudinal studies examining the association of more severe depressive symptoms and cerebral tau accumulation are needed to substantiate this finding and to guide prevention and treatment in AD. 4 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
There is a pressing need to capture and track subtle cognitive change at the preclinical stage of Alzheimer's disease (AD) rapidly, cost-effectively, and with high sensitivity. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Animal studies demonstrate that hyperactive neurons facilitate early accumulation and spread of tau and amyloid-β proteins in the pathological cascade of Alzheimer's disease (AD). 3 key findings →
Participants: 120 Evidence: low
Full summary, score breakdown and related studies → Original source
Preliminary findings suggest that the NIH Toolbox has the advantage of showing the strongest overall clustering and alignment with standardized paper-and-pencil tasks. 5 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
Excellent reliability was observed among the 6 C3-PAD alternate versions (Cronbach alpha coefficient=0.93). 5 key findings →
Participants: 49 Evidence: low
Full summary, score breakdown and related studies → Original source
Our results are consistent with the supposition that both Aβ and tau are necessary for memory decline in the preclinical stages of AD. 5 key findings →
Evidence: low
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 →