In TRAILBLAZER-ALZ, 272 participants (mean [SD] age, 75.2 [5.5] years; 145 [53.3%] female) were randomized. 5 key findings →
Participants: 1,955 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Research
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Plasma p-tau217 and tau positron emission tomography (PET) are strong prognostic biomarkers in Alzheimer's disease (AD), but their relative performance in predicting future cognitive decline among cognitively unimpaired (CU) individuals is unclear. 2 key findings →
Design: cohort Participants: 1,474 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Reduction of amyloid via amyloid-targeting therapies may result in clinical benefit. 2 key findings →
Design: clinical trial Participants: 1,582 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
In a large cohort of cognitively unimpaired individuals enrolled in a Phase 3 clinical trial and companion observational study, these findings confirm that higher baseline levels of amyloid and tau markers are associated with increased rates of cognitive decline and progression to functional impairment. 5 key findings →
Design: longitudinal study Participants: 583 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Of 236 eligible participants screened, 43 were excluded. 2 key findings →
Design: longitudinal study Participants: 142 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Baseline and 3-month visit data were available for 272 participants in arm 1 and 260 in arm 2 (median [IQR] age: 71 [65-77] and 71 [65-77] years; 150/272 male [55%] and 135/260 male [52%]; 122/272 female [45%] and 125/260 female [48%]; median [IQR] education: 12 [10-15] and 13 [10-16] years, respectively). 3 key findings →
Participants: 844 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
In participants with early symptomatic AD, zagotenemab failed to achieve significant slowing of clinical disease progression compared with placebo. 5 key findings →
Design: clinical trial Participants: 360 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Sixty consecutive patients with prodromal or mild AD were screened; 50 were randomized to gamma or sham tACS (mean [SD] age, 67.3 [7.8] years; 25 [50.0%] female and 25 [50.0%] male). 5 key findings →
Design: open-label trial Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
68/100
Baseline biomarkers largely do not predict risk for developing ARIA-E. ARIA-E was associated with significant longitudinal changes in several biomarkers, with larger reductions in amyloid PET and CSF p-tau and t-tau concentrations, and paradoxically greater hippocampal volume reduction and ventricular enlargement, suggesting that ARIA-E in bapineuzumab-treated cases may be related to increased Aβ efflux from the brain and affecting downstream pathogenic processes. 4 key findings →
Design: longitudinal study Participants: 1,512 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
A total of 716 individuals were included in the analysis: 413 cognitively unimpaired (CU) participants (58.6% female; mean age = 70.6 years, SD = 7.9) and 303 cognitively impaired (CI) participants (54.7% female; mean age = 73.2 years, SD = 7.4). 5 key findings →
Design: longitudinal study Participants: 716 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In DIAD, solanezumab was not associated with ARIA. 5 key findings →
Design: cross-sectional Participants: 52 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Future research should examine whether minimizing drawbacks at the pre-imaging stage has adverse consequences on results disclosure. 5 key findings →
Design: randomized controlled trial Participants: 59 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Obicetrapib significantly slowed AD biomarker progression over 12 months in participants with ASCVD, with the greatest effects in ApoE4 carriers. 5 key findings →
Design: clinical trial Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
These findings suggest a benefit of MI plus omega 3 in positive blood amyloid subjects. 4 key findings →
Participants: 483 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Amyloid beta (Aβ) plaque is a defining pathologic feature of Alzheimer disease (AD). 5 key findings →
Design: case report Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
56/100
Individuals with early AD show heterogeneity in disease progression, which increases when stratifying on risk factors associated with progression. 3 key findings →
Participants: 302 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
55/100
The findings do not support an effect of the exercise intervention on a single measure of neurodegeneration in AD. 2 key findings →
Participants: 136 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
< 0.001). Stage-specific tau-PET region-of-interest selection reduced required sample sizes by 30%-93% for detecting hypothetical disease-modifying drug effects. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Despite reductions in plasma p-tau217 with donanemab treatment, this biomarker cannot currently be used to accurately detect TRAC by PET (< 24.1 CL) in individuals with early symptomatic AD. 1 key finding →
Design: phase-3-trial Participants: 830 Evidence: null result
Full summary, score breakdown and related studies → Original source Free full text
These findings emphasize the necessity of tailoring mAb trials for DS, considering age-related AD characteristics. 5 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Our trial showed that olfactory-stimulated oxygenation differences in the orbitofrontal cortex detected by fNIRS were associated with cognitive impairment and cognitive-related objectives. 5 key findings →
Design: open-label trial Participants: 97 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Lecanemab reduced amyloid PET in symptomatic participants with DIAD at Week 24. 3 key findings →
Participants: 97 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Clinical trials of anti-amyloid-β (Aβ) monoclonal antibodies in Alzheimer disease (AD) infer target engagement from Aβ positron emission tomography (PET) and/or fluid biomarkers such as cerebrospinal fluid (CSF) Aβ42/40. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Incorporating AD blood tests into screening for AD clinical trials may reduce the time and financial cost of enrollment. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The concentration of 124 I-RmAb158-scFv8D3, as measured in vivo with PET, increased with age and corresponded well with the ex vivo autoradiography and Aβ immunohistochemistry results. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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.
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 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.
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 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 →