31,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
A key driver of patients' well-being and clinical trials for Parkinson's disease (PD) is the course that the disease takes over time (progression and prognosis). 5 key findings →
Design: longitudinal study Participants: 3,821 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Rates of cognitive decline in Alzheimer's disease (AD) are extremely heterogeneous. 1 key finding →
Design: case-control study Participants: 3,397 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Compelling experimental evidence suggests that microglial activation is involved in the spread of tau tangles over the neocortex in Alzheimer's disease (AD). 4 key findings →
Design: longitudinal study Participants: 130 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
A total of 17 articles were identified. Plasma Aβ42/40 ratio was inversely correlated with aPET positivity r = -0.48 (95% confidence interval (CI): -0.65--0.31). 5 key findings →
Design: systematic review Participants: 17 Evidence: high
Full summary, score breakdown and related studies → Original source
Of 65 participants with biomarker-confirmed AD, 21 (32.3%) were αS-SAA positive. 4 key findings →
Design: longitudinal study Participants: 108 Evidence: moderate
Full summary, score breakdown and related studies → Original source
VE seems to be rare at baseline in patients with AD in clinical trials, 2 of 2,762 associated with AD. 5 key findings →
Design: clinical trial Participants: 621 Evidence: high
Full summary, score breakdown and related studies → Original source
Synthesis methods We meta-analysed results for each outcome within each comparison using the inverse variance method and the random-effects model. 5 key findings →
Design: meta-analysis Participants: 20,342 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
In BioFINDER-2, the mean (SD) age was 65.7 (14.4) with 261 females (52.7%). 3 key findings →
Design: cohort Participants: 983 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The neuropathological confirmation of amyloid-β (Aβ) plaques and tau neurofibrillary tangles (NFT) remains the gold standard for a definitive diagnosis of Alzheimer's disease (AD). 4 key findings →
Design: longitudinal study Participants: 115 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
A major unanswered question in the dementia field is whether cognitively unimpaired individuals who harbor both Alzheimer's disease neuropathological hallmarks (that is, amyloid-β plaques and tau neurofibrillary tangles) can preserve their cognition over time or are destined to decline. 3 key findings →
Participants: 1,325 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Daily oral DHA supplementation (2 g/day) for 24 months may improve cognitive function and change blood biomarker-related Aβ-mediated autophagy in people with MCI. 2 key findings →
Participants: 120 Evidence: high
Full summary, score breakdown and related studies → Original source
According to studies, lecanemab lessens clinical deterioration and reduces brain amyloid-beta plaques (difference,.45; 95% confidence interval,.67 to.23; p < .001). 1 key finding →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Patients with Alzheimer disease treated with gantenerumab showed significant improvement in the ADAS score, FAQ score, hippocampal volume, and CSF biomarkers compared with those treated with placebo. 5 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
The strong associations between baseline tau-PET and longitudinal cognition, with marginal contributions of longitudinal tau-PET and MRI, emphasize the importance of baseline tau aggregates for prognostics and treatments in Alzheimer's disease (AD). 2 key findings →
Design: longitudinal study Participants: 761 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Phosphorylated-tau (p-tau217) is a promising blood-based biomarker for Alzheimer's dementia (AD) in clinical settings. 3 key findings →
Design: cohort study Participants: 779 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Baseline sleep disturbance was associated with a faster rate of longitudinal CSF Aβ42 decline. 4 key findings →
Design: longitudinal study Participants: 1,205 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The use of quantitative endophenotypes in genetic studies may provide greater power, allowing for the use of powerful statistical methods and a biological model for the effects of the disease-associated genetic variation. 1 key finding →
Design: meta-analysis Participants: 313 Evidence: high
Full summary, score breakdown and related studies → Original source
Lewy body dementia (LBD) is the second most prevalent dementia, however most genetic risk remains uncharacterized. 5 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Despite significant progress, applications of astrocyte biomarkers in AD remain in their early days. 4 key findings →
Design: systematic review Participants: 3,204 Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Among 1736 randomized participants (mean age, 73.0 years; 996 [57.4%] women; 1182 [68.1%] with low/medium tau pathology and 552 [31.8%] with high tau pathology), 1320 (76%) completed the trial. 3 key findings →
Design: clinical trial Participants: 860 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
At baseline, significantly higher Aβ burdens were noted in patients with AD (2·27, SD 0·43) and those with MCI (1·94, 0·64) than in healthy controls (1·38, 0·39). 1 key finding →
Design: cohort study Participants: 200 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The APOE ε4 allele remains the strongest genetic risk factor for sporadic Alzheimer's disease and the APOE ε2 allele the strongest genetic protective factor after multiple large scale genome-wide association studies and genome-wide association meta-analyses. 5 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Alzheimer's disease neuropathology positivity was present in 86 (6%) participants based on p-tau217/Aβ42, 196 (15%) based on Aβ42/40, and 48 (4%) based on p-tau217, and was associated with worse performance on processing speed (standardised cognitive difference comparing Alzheimer's disease neuropathology positive to negative for Aβ42/40, p-tau217, and p-tau217/Aβ42 -0·54 to -0·25; p values 0·0001 to 0·0048) and executive function (-0·42 to -0·19; p values 0·0070 to 0·049). 3 key findings →
Design: cohort study Participants: 1,500 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Significantly altered levels of inflammatory markers were verified in comparison between AD, MCI and control, supporting the notion that AD and MCI are accompanied by inflammatory responses in both the periphery and CSF. 5 key findings →
Design: systematic review Participants: 170 Evidence: high
Full summary, score breakdown and related studies → Original source
Numerous clinical trials of anti-amyloid beta (Aβ) immunotherapy in Alzheimer's disease have been performed. 2 key findings →
Design: meta-analysis 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 31,780 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 31,780 records, built mostly from automated pulls of Europe PMC (66% of the library) and OpenAlex (16%), 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.
1,052 records (3.3% of the library) are not peer-reviewed — 973 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events