30,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
A mean value of 85.7% was achieved for overall diagnostic accuracy, 82.4% for positive predictive value, and 87.5% for negative predictive value. 2 key findings →
Participants: 94 Evidence: low
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There was a statistically significant increase in the global estimate of cortical tau burden as measured by standardized uptake value ratio (SUVr) from baseline to 18 months in amyloid-β+ but not amyloid-β- subjects (least squared mean change in flortaucipir SUVr : 0.0524 ± 0.0085, P < 0.0001 and 0.0007 ± 0.0024 P = 0.7850, respectively), and a significant association between magnitude of SUVr increase and baseline tau burden. 4 key findings →
Design: longitudinal study Participants: 202 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Our aim was to test the association of vascular risk factor exposure in midlife with progression of MRI markers of brain aging and measures of cognitive decline. 1 key finding →
Design: cohort study Participants: 1,352 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Older adults with CVD other than stroke had a higher risk of dementia and AD than did those without CVD. 5 key findings →
Design: cohort study Participants: 3,602 Evidence: moderate
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Cerebral accumulation of amyloid-β is thought to be the starting mechanism in Alzheimer's disease. 4 key findings →
Design: longitudinal study Participants: 437 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The Alzheimer's Disease Neuroimaging Initiative (ADNI) is a longitudinal multisite observational study of healthy elders, mild cognitive impairment (MCI), and Alzheimer's disease. 5 key findings →
Design: longitudinal study Evidence: moderate
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SNAP-25 and 14-3-3 zeta/delta also had the strongest associations with tau-PET, amyloid-β-PET and cortical thickness at baseline and were associated with longitudinal changes in these imaging biomarkers [β(standard error, SE) = -0.056(0.0006) to 0.058(0.005), P < 0.0001]. 3 key findings →
Design: longitudinal study Participants: 205 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Hippocampal volume is reduced in patients with unipolar depression, maybe as a consequence of repeated periods of major depressive disorder. 2 key findings →
Design: systematic review Participants: 351 Evidence: high
Full summary, score breakdown and related studies → Original source
These findings are consistent with smaller hippocampal volume in adult subjects with chronic PTSD. 5 key findings →
Design: meta-analysis Participants: 133 Evidence: high
Full summary, score breakdown and related studies → Original source
Posttraumatic stress disorder (PTSD) is a debilitating condition associated with mild to moderate cognitive impairment and with a prevalence rate of up to 22% in veterans. 5 key findings →
Design: systematic review Participants: 846 Evidence: high
Full summary, score breakdown and related studies → Original source
These preliminary results suggest that donepezil may have a potentially protective effect in Alzheimer's disease. 3 key findings →
Participants: 67 Evidence: high
Full summary, score breakdown and related studies → Original source
Relative to control subjects, patients had significantly smaller HCVs (standardized mean difference = -0.32 [95% confidence interval, -0.44 to -0.19]). 5 key findings →
Design: cohort study Participants: 2,702 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The prospective cohort data from the JPSC-AD will provide valuable insights regarding the risk factors and etiology of dementia as well as for the development of predictive models and diagnostic markers for the future onset of dementia. 2 key findings →
Design: cohort study Participants: 11,410 Evidence: moderate
Full summary, score breakdown and related studies → Original source
These findings suggest that the plasma Aβ42/Aβ40 may be useful in identifying individuals with very low levels of amyloid pathology, whereas p-tau, GFAP, and NfL may be useful in staging disease progression. 3 key findings →
Design: longitudinal study Participants: 784 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Retinal thickness is decreased in AD and MCI patients compared to HC. 2 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Lecanemab was generally well tolerated by most patients with early AD and treatment appeared to be more effective and safer in patients with low CSF-ptau181 levels. 5 key findings →
Design: longitudinal study Participants: 234 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Deep learning, a state-of-the-art machine learning approach, has shown outstanding performance over traditional machine learning in identifying intricate structures in complex high-dimensional data, especially in the domain of computer vision. 5 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
The systemic underrepresentation of Black participants in AD research impacts the ability to generalize research findings and determine the effectiveness and safety of disease-modifying treatments. 1 key finding →
Design: longitudinal study Participants: 629 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Both plasma p-tau181 and GFAP appear to reflect disease progression, as indicated by 7T MR-derived brain changes which are not limited to areas known to be affected by tau pathology and neuroinflammation measured by MRS myo-inositol, respectively. 1 key finding →
Design: longitudinal study Participants: 127 Evidence: moderate
Full summary, score breakdown and related studies → Original source
These findings revealed the dynamic changes of microstructural and macrostructural indicators and their associations with AD and SNAP, providing novel insights into understanding upstream and downstream events of cMD in neurodegenerative disease. 2 key findings →
Design: longitudinal study Participants: 617 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Glymphatic failure may precede amyloid pathology, and predicts amyloid deposition, neurodegeneration, and clinical progression in AD. 2 key findings →
Design: cohort Participants: 419 Evidence: moderate
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For all 4 phosphorylation sites assessed in CSF, p-tau was significantly more closely associated with amyloid-PET values than tau-PET values (p-tau181 difference, 13%; 95% CI, 3%-22%; P = .006; p-tau217 difference, 11%; 95% CI, 3%-20%; P = .003; p-tau231 difference, 15%; 95% CI, 5%-22%; P Conclusions and relevance Results of this cross-sectional study of 2 observational cohorts suggest that the p-tau abnormality as an early event in AD pathogenesis was associated with amyloid-β accumulation and highlights the need for careful interpretation of p-tau biomarkers in the context of the amyloid/tau/neurodegeneration, or A/T/(N), framework. 2 key findings →
Design: cross-sectional Participants: 609 Evidence: moderate
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There was no difference between groups in time to emergence of agitation or psychosis (Cox proportional hazard ratio, 0.96; P = .88). 3 key findings →
Participants: 122 Evidence: high
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Intensive treatment was associated with a small but statistically significant greater decrease in hippocampal volume compared with standard treatment, consistent with the observation that intensive treatment is associated with greater decreases in total brain volume. 5 key findings →
Design: meta-analysis Participants: 1,267 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Progressive dementia was detected by PET with a sensitivity of 93% (191/206) and a specificity of 76% (59/78). 4 key findings →
Design: longitudinal study Participants: 146 Evidence: moderate
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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 30,180 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.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 30,180 records, built mostly from automated pulls of Europe PMC (64.2% of the library) and OpenAlex (16.9%), 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 →