30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
This study provides corroborating evidence that solanezumab does not slow cognitive decline in preclinical AD as exhibited with a computerized cognitive assessment with some evidence that solanezumab may exacerbate cognition on select digital outcomes. 4 key findings →
Design: longitudinal study Participants: 1,117 Evidence: moderate
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
Overall, 1795 participants from Core and 1612 participants with at least one dose of lecanemab (Core + OLE) were included. 1 key finding →
Design: open-label trial Participants: 1,795 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
Among the 445 participants (243 with normal amyloid, 202 with elevated amyloid), mean (SD) age was 74.0 (5.9) years, mean education was 16.4 (2.7) years, and 52% were women. 2 key findings →
Design: longitudinal study Participants: 243 Evidence: moderate
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
The pathophysiological process of Alzheimer's disease (AD) is thought to begin many years before the diagnosis of AD dementia. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Levels of plasma p-tau217 increased significantly in Aβ+ participants before showing significant deceleration (χ2 = 21.7; P Conclusions and relevance This study found that tau PET is valuable for both prognostic and real-time tracking of disease progression. 2 key findings →
Design: cohort Participants: 1,707 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The large number of participants screened with amyloid positron emission tomography (PET) and standardized assessments provides an unprecedented opportunity to evaluate factors associated with elevated brain amyloid. 5 key findings →
Design: cross-sectional Participants: 4,486 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Higher tau levels are associated with the fastest decline in everyday functioning in the presence of elevated amyloid, and those accumulating more tau show a faster decline in everyday functioning. 3 key findings →
Design: randomized controlled trial Participants: 434 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Florbetapir F 18 PET can image amyloid-β (Aβ) aggregates in the brains of living subjects. 4 key findings →
Design: longitudinal study Participants: 51 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
In ADNI, Aβ-positive participants showed more decline than did Aβ-negative participants with regard to the ADCS-PACC score at 24 months (mean [SE] difference, -1.239 [0.522] [95% CI, -2.263 to -0.215]; P = .02). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
There were no statistical differences between the placebo or solanezumab groups in CDR-G, CDR-SB, specific CDR boxes or CDR composite scores over the course of the trial. 3 key findings →
Participants: 583 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Both participant and study partner CFI increased over the duration of the study indicating worsening cognitive functioning. 3 key findings →
Design: longitudinal study Participants: 1,147 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Genetic risk factors of AD dementia demonstrate effects related to Aβ, as well as synergistic interactions with Aβ. 2 key findings →
Design: longitudinal study Participants: 702 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
AD-signature cortical thinning in CN-AD converters in both samples was remarkably similar, about 0.2 mm (p 1). 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
APOE ε4 count was associated with higher TDP-43 proteinopathy stage (odds ratio [OR] 2·0, 95% CI 1·6-2·6; p=1·9 × 10 -9 ) and TDP-43 burden (0·40, 0·28-0·52; p=1·2 × 10 -10 ). 3 key findings →
Design: cohort study Participants: 15 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
This study suggests that early tau deposition may follow multiple trajectories during preclinical AD and may involve several cortical regions. 3 key findings →
Design: cross-sectional Participants: 447 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Longitudinal fMRI provides a reliable indicator of brain activation over time, and may prove useful in identifying functional brain changes associated with cognitive decline on the trajectory toward clinical Alzheimer disease. 3 key findings →
Design: cross-sectional Participants: 21 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The data are consistent with expected rates of amyloid positivity among individuals with clinical diagnoses of AD and MCI, and indicate the potential value of florbetapir F18 PET as an adjunct to clinical diagnosis. 2 key findings →
Design: clinical trial Participants: 184 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
From a longitudinal study of normal (Clinical Dementia Rating [CDR] = 0; n = 77) and mildly impaired (CDR = 0.5; n = 167) participants with 5 or more annual clinical assessments, baseline level of cognitive impairment in daily life was graded using CDR sum of boxes (CDR-SB) and level of cognitive performance impairment was graded using neuropsychological test scores. 4 key findings →
Design: longitudinal study Participants: 77 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Higher amyloid beta burden was associated with increasing anxious-depressive symptoms over time in cognitively normal older individuals. 4 key findings →
Design: longitudinal study Participants: 270 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Predictive algorithms in a web-based registry can improve the efficiency of screening in future secondary prevention trials. 1 key finding →
Design: cross-sectional Participants: 4,486 Evidence: moderate
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 30,980 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 30,980 records, built mostly from automated pulls of Europe PMC (65.2% of the library) and OpenAlex (16.4%), 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.
1,042 records (3.4% of the library) are not peer-reviewed — 967 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