27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
The results indicate that lithium treatment may have beneficial effects on cognitive performance in subjects with MCI and AD dementia. 4 key findings →
Design: meta-analysis Participants: 199 Evidence: high
Full summary, score breakdown and related studies → Original source
Recently, several genome-wide association studies (GWASs) have led to the discovery of nine new loci of genetic susceptibility in Alzheimer's disease (AD). 2 key findings →
Design: case-control study Participants: 2,025 Evidence: moderate
Full summary, score breakdown and related studies → Original source
This fully-automated and available blood-based biomarker assay therefore may be useful for early detection, diagnosis, prognosis, and treatment monitoring of AD. 5 key findings →
Design: longitudinal study Participants: 463 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
Across the cohorts, each 10-year increase in BAI was associated with a 39% higher risk of incident dementia (hazard ratio [HR], 1.39 [95% CI, 1.21-1.59]; P Conclusions and relevance In this IPD meta-analysis, a higher sleep EEG-based BAI was associated with a higher risk of incident dementia. 3 key findings →
Design: meta-analysis Participants: 7,105 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Plasma p-tau217/Aβ42 has high performance in detecting cerebral AD pathologies, thus offering a promising tool for clinical diagnosis and community screening of AD. 1 key finding →
Design: cross-sectional Participants: 512 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The main findings demonstrated an association between serum GFAP level and post-mortem tau pathology (β = 12.85; P < 0.001) that was independent of amyloid deposits (β = 13.23; P = 0.02). 5 key findings →
Design: cohort Participants: 139 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The mean (SD) age of the 842 participants in cohort 1 was 72 (5.6) years, with a range of 59 to 88 years, and 446 (52.5%) were female. 3 key findings →
Design: cross-sectional Participants: 842 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
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
Full summary, score breakdown and related studies → Original source Free full text
High and increasing blood pressure from early adulthood into midlife seems to be associated with increased WMHV and smaller brain volumes at 69-71 years of age. 5 key findings →
Design: longitudinal study Participants: 5,362 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
These two conclusions support a dynamic biomarker model in which Alzheimer's disease is characterized first by the appearance of amyloidosis and later by tauopathy, with tauopathy being the proteinopathy associated with clinical symptoms. 1 key finding →
Design: longitudinal study Participants: 1,343 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The largest cohort, the Anti-Amyloid Treatment in Asymptomatic Alzheimer Disease Study (n = 3154), was the PET screening cohort used for a secondary prevention trial designed to slow cognitive decline associated with brain amyloidosis. 3 key findings →
Design: meta-analysis Participants: 3,154 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
To define Alzheimer's disease with biomarkers rather than clinical assessment, we assessed prediction of research-diagnosed disease status using these biomarkers and tested genetic variants associated with the biomarkers that may reflect more accurately the risk of biochemically defined Alzheimer's disease instead of the risk of dementia. 5 key findings →
Design: case-control study Participants: 1,439 Evidence: moderate
Full summary, score breakdown and related studies → Original source
An accurate blood test for Alzheimer's disease that is sensitive to preclinical proteinopathy and cognitive decline has clear implications for early detection and secondary prevention. 2 key findings →
Design: cohort study Participants: 165 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Blood biomarkers have great potential to advance clinical care and accelerate trials in Alzheimer's disease (AD). 1 key finding →
Design: longitudinal study Participants: 70 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Blood biomarkers have been considered tools for the diagnosis, prognosis, and monitoring of Alzheimer's disease (AD). 2 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
It is currently unclear whether plasma biomarkers can be used as independent prognostic tools to predict changes associated with early Alzheimer's disease. 4 key findings →
Design: longitudinal study Participants: 123 Evidence: moderate
Full summary, score breakdown and related studies → Original source
In the precuneus, we observed an inverted U-shaped pattern of novelty-related activity across groups, with higher activity in SCD and MCI compared with HC, but not in patients with AD who showed relatively lower activity than MCI. 3 key findings →
Design: longitudinal study Participants: 499 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We demonstrated that higher amyloid burden as measured by both CSF amyloid beta 42/40 ratio and non-displaceable binding potential in the posterior cingulate cortex was associated with lower functional connectivity in the default mode network. 3 key findings →
Design: longitudinal study Participants: 173 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Blood exosomes, which are extracellular vesicles secreted by living cells into the circulating blood, are regarded as a relatively noninvasive novel tool for monitoring brain physiology and disease states. 2 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
Our systematic review shows evidence for disruptions in (night-time) melatonin levels in AD as compared to age-matched controls. 3 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
Emerging plasma biomarkers of Alzheimer's disease might be non-invasive tools to trace early Alzheimer's disease-related abnormalities such as the accumulation of amyloid-beta peptides, neurofibrillary tau tangles, glial activation and neurodegeneration. 4 key findings →
Design: longitudinal study Participants: 164 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma p-tau217 showed the strongest individual association with Aβ PET status (area under the curve [AUC], 0.85). 5 key findings →
Design: cohort study Participants: 1,407 Evidence: moderate
Full summary, score breakdown and related studies → Original source
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
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 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.
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 →