Combining plasma p-tau with Aβ42 or the Aβ42/40 ratio reduced the intermediate zone. 5 key findings →
Design: cross-sectional Participants: 326 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Research
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Neuropathology cases included 46 Parkinson's disease and 10 dementia with Lewy bodies, and clinical cases included 173 Parkinson's disease, and 64 controls. 5 key findings →
Design: cohort study Participants: 46 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Hallucinations, delusions, and depression were more common in DLB than in AD and, in a subgroup with longitudinal follow-up, persistent hallucinations and NPSs were associated with lower p-tau181 and p-tau231 in DLB. 5 key findings →
Design: longitudinal study Participants: 222 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The Core 1 biomarker PGSs predicted AD pathology and associated cognitive performance better than the AD PGSs in both populations. 5 key findings →
Design: longitudinal study Participants: 515 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Higher concentrations of plasma p-tau217, p-tau181, and NfL were correlated to higher decline speed of Mini-Mental State Examination score, and higher risk of incident dementia and AD. 3 key findings →
Design: longitudinal study Participants: 1,857 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Higher baseline pTau217 levels were associated with faster functional (QDRS) and cognitive (PACC3) decline. 4 key findings →
Design: longitudinal study Participants: 639 Evidence: moderate
Full summary, score breakdown and related studies → Original source
None of the three plasma biomarker was associated with NPS at baseline. 5 key findings →
Design: longitudinal study Participants: 76 Evidence: moderate
Full summary, score breakdown and related studies → Original source
In general linear models lower plasma Aβ42/40 was related to lower visuospatial ability, higher total tau was related to lower episodic memory, and higher NfL was related to lower visuospatial ability and lower episodic memory. 3 key findings →
Design: cohort study Participants: 260 Evidence: moderate
Full summary, score breakdown and related studies → Original source
SORL1 is associated with AD in the Hong Kong Chinese population. 5 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
A blood biomarker-based staging system for Alzheimer's disease (AD) could improve the diagnosis, prognosis and identification of individuals most likely to benefit from specific therapies. 3 key findings →
Design: longitudinal study Participants: 689 Evidence: moderate
Full summary, score breakdown and related studies → Original source
A smartphone application collected 2 modalities of cognitive data, digital voice and screen-based behaviors, from the FHS (Framingham Heart Study) multigenerational Generation 2 (Gen 2) and Generation 3 (Gen 3) cohorts. 5 key findings →
Design: longitudinal study Participants: 455 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Our TSMR analysis showed a significant positive association between genetic predisposition to methotrexate use and dementia risk. 5 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
To date, DNA methylation is the best characterized epigenetic modification in Alzheimer's disease. 1 key finding →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
The best-performing MRI-free approaches had high continuous and dichotomous agreement with MRI-dependent SUVRs for Aβ PET and temporal flortaucipir (R2 ≥0.95; ± agreement ≥92%) and for Alzheimer's disease-related effect sizes; agreement was slightly lower for entorhinal flortaucipir and longitudinal slopes. 2 key findings →
Design: longitudinal study Participants: 1,290 Evidence: moderate
Full summary, score breakdown and related studies → Original source
71/100
There were 571 participants in the normal cognition group, 625 participants in the subjective cognitive decline group, 155 participants in the objectively defined subtle cognitive decline group, 501 participants in the mild cognitive impairment group, 471 participants in Alzheimer's disease group, and 128 participants with cognitive impairment from other known causes. 5 key findings →
Design: longitudinal study Participants: 4,386 Evidence: moderate
Full summary, score breakdown and related studies → Original source
71/100
Alzheimer's disease is a common brain disorder affecting many people worldwide. 1 key finding →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
Ten studies assessing retinal properties in dementia were included. 5 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
A narrative synthesis approach will be used to analyse the results, with meta-analysis performed if there is sufficient data. 1 key finding →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
According to CDR-SB measurements, lecanemab showed effectiveness in reducing brain amyloid and cognitive decline, with a change from baseline of 1.21. 5 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source
Fifty-nine RCTs were included. Donanemab and lecanemab ranked among the most effective treatments for improving cognitive function (Clinical Dementia Rating Scale - Sum of Boxes P-scores: 0.88 and 0.77) and daily activities (Alzheimer's Disease Cooperative Study - Activities of Daily Living P-scores: 0.85 and 0.90), based on network meta-analysis findings. 3 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Donanemab (Kisunla) is a humanized IgG1 monoclonal antibody specifically targeting a modified form of β-amyloid found predominantly within plaques (characterized as N-terminal pyroglutamate Aβ). 1 key finding →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
All drugs improved the cognitive function, with the effect value ranging from -1.23 (95% CI -2.17 to -0.30) for 20 mg memantine to -3.29 (95% CI -4.14 to -2.45) for 32 mg galantamine. 5 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) affects millions of people worldwide. 2 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
Compared with low-dose donepezil, galantamine use was associated with a lower risk of mortality (adjusted hazard ratio: 0.84, 95% confidence interval: 0.60-1.18), cardiovascular serious adverse events (adjusted hazard ratio: 0.78, 95% confidence interval: 0.62-0.98), and entry into a residential care facility (adjusted hazard ratio: 0.72, 95% confidence interval: 0.59-0.89). 2 key findings →
Design: randomized controlled trial Evidence: high
Full summary, score breakdown and related studies → Original source
By addressing gaps in prior NMAs, this study aims to provide an in-depth evaluation of safety outcomes associated with different ChEI and memantine doses and formulations across various dementia types. 3 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
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 →