30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
General baseline characteristics of the study population were mean (standard deviation) age, 58.1 (8.8) years; 47% women. 5 key findings →
Design: meta-analysis Participants: 1,087 Evidence: high
Full summary, score breakdown and related studies → Original source
Solanezumab, which targets monomeric amyloid in persons with elevated brain amyloid levels, did not slow cognitive decline as compared with placebo over a period of 240 weeks in persons with preclinical Alzheimer's disease. 3 key findings →
Design: clinical trial Participants: 1,169 Evidence: low
Full summary, score breakdown and related studies → Original source
A total of 15 eligible studies were included in the meta-analysis. 5 key findings →
Design: systematic review Participants: 109 Evidence: high
Full summary, score breakdown and related studies → Original source
The study team reported a significant change in diagnoses and patient medication when tau PET was added to an already extensive diagnostic workup that included cerebrospinal fluid AD biomarkers. 5 key findings →
Design: cohort study Participants: 878 Evidence: moderate
Full summary, score breakdown and related studies → Original source
One hundred twenty-eight participants (21.9%) developed dementia over a median of 7.1 years. 5 key findings →
Design: longitudinal study Participants: 584 Evidence: moderate
Full summary, score breakdown and related studies → Original source
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
This study suggests that OA was associated with faster Aβ accumulation and higher Aβ-dependent future tau deposition in primary motor and somatosensory regions, providing novel insights into how OA increases the risk of AD. 4 key findings →
Design: longitudinal study Participants: 374 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Neuroinflammation is believed to be a key process in Alzheimer's disease (AD) pathogenesis. 5 key findings →
Design: longitudinal study Participants: 1,544 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Data from 3960 MRI sessions among 1141 participants were included: 252 pathogenic variant carriers from DIAN (mean [SD] age, 38.4 [11.2] years; 137 [54%] female), 571 older adults from ADNI (mean [SD] age, 72.8 [7.3] years; 274 [48%] female), and 318 older adults from HABS (mean [SD] age, 72.4 [7.6] years; 194 [61%] female). 3 key findings →
Design: cohort study Participants: 1,141 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
However, these abnormal levels do not appear to be the result of a high rate of accumulation in the short term, but possibly a more moderate rate occurring early with respect to age. 1 key finding →
Design: longitudinal study Participants: 447 Evidence: moderate
Full summary, score breakdown and related studies → Original source
These findings offer novel perspectives to the design of AD clinical trials and aid in understanding the tau accumulation inside and outside MTL in AD. 5 key findings →
Design: longitudinal study Participants: 143 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Deposition of amyloid and tau pathology can be quantified in vivo using positron emission tomography (PET). 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
In older adults, longitudinal hippocampal atrophy is associated with cognitive decline, independently of Aβ or tau, suggesting that non-AD pathologies (e.g., TDP-43, vascular) may contribute to hippocampal-mediated cognitive decline. 4 key findings →
Design: cohort study Participants: 283 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The site and rate of atrophy are different across the tau-PET patterns. 1 key finding →
Design: longitudinal study Participants: 366 Evidence: moderate
Full summary, score breakdown and related studies → Original source
In the Asan cohort, after adjusting for age and sex, p-tau181 (AUC = 0.854) or APOE ε4 status (AUC = 0.769) distinguished Aβ status with high accuracy. 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
LEADS data emphasizes the importance of biomarkers to enhance diagnostic accuracy in EOAD. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
We found that the association between higher baseline tau-PET levels (quantified in a temporal meta-region of interest) and rate of cognitive decline (measured with repeated Mini-Mental State Examination) was adversely modified by older age (Stβinteraction = -0.062, P = 0.032), higher education level (Stβinteraction = -0.072, P = 0.011) and higher intracranial volume (Stβinteraction = -0.07, P = 0.016). 5 key findings →
Design: cross-sectional Participants: 200 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Offspring participants (497 [33.9%]) had a mean (SD) age of 55 (10.7) years, had a mean (SD) of 13 (3.5) years of education, and included 117 Black individuals (23.5%), 348 Latinx individuals (70%), 32 White individuals (6.4%), and 324 women (65.2%). 1 key finding →
Design: cohort study Participants: 1,467 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
As cerebral regions correlating with symptomatology differ depending on the clinical phenotype, a precise knowledge of clinical signs and symptoms is necessary when interpreting [18F]PI-2620 PET results. 1 key finding →
Design: longitudinal study Participants: 72 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Cortical tau accumulation is a key pathological event that partly defines Alzheimer's disease (AD) onset and is associated with cognitive decline and future disease progression. 5 key findings →
Design: cohort study Participants: 59 Evidence: moderate
Full summary, score breakdown and related studies → Original source
This retrospective case-control study aimed to investigate associations between disease severity of Alzheimer's dementia (AD) and macular thickness. 3 key findings →
Design: case-control study Participants: 192 Evidence: moderate
Full summary, score breakdown and related studies → Original source
APOE influences early regional tau PET burden, above and beyond effects related to cross-sectional amyloid PET burden. 5 key findings →
Design: cross-sectional Participants: 4,486 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease and cerebral small vessel disease are the two leading causes of cognitive decline and dementia and coexist in most memory clinic patients. 3 key findings →
Design: cross-sectional Participants: 387 Evidence: low
Full summary, score breakdown and related studies → Original source
In this study, females exhibited higher tau compared with age-matched males, particularly in the setting of elevated Aβ. 5 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Recent studies on Alzheimer's disease (AD) suggest that tau proteins spread through the brain following neuronal connections. 4 key findings →
Design: cross-sectional Participants: 16 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 30,580 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 30,580 records, built mostly from automated pulls of Europe PMC (64.7% of the library) and OpenAlex (16.6%), 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.
1,037 records (3.4% of the library) are not peer-reviewed — 964 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