30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
Oligodendrocyte dysfunction has been implicated in the pathogenesis of neurodegenerative diseases, so understanding oligodendrocyte activation states would shed light on disease processes. 1 key finding →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Aβ plaques removal in the brain due to amyloid therapy is strongly correlated with a better clinical response in patients with early Alzheimer's disease and a higher ARIA-E rate for the treatment groups and clinical trials in this meta-analysis. 2 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Modifiable risk factors identified in this study, especially those with high-level evidence, should be considered in dementia prevention. 2 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Dual-eligible older persons are at greater risk for decline in function and cognition after an ICU hospitalization than their more advantaged counterparts. 2 key findings →
Design: cohort study Participants: 641 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease has a long asymptomatic phase that offers a substantial time window for intervention. 2 key findings →
Design: longitudinal study Participants: 410 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Baseline CSF Aβ42/Aβ40 ratio was decreased in MCI and AD compared to CN, while CSF p-tau181 and t-tau increased. 3 key findings →
Design: longitudinal study Participants: 430 Evidence: moderate
Full summary, score breakdown and related studies → Original source
This study will establish the precision of TAS Test to identify preclinical AD and estimate risk of cognitive decline and AD. 2 key findings →
Design: cohort study Participants: 300 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The recent development of ultrasensitive technology allows the determination of blood-based biomarkers with high sensitivity, thus facilitating the early detection of AD through the analysis of easily obtained biological samples. 3 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
Digital biomarkers are defined as objective, quantifiable physiological and behavioral data that are collected and measured by means of digital devices. 4 key findings →
Design: longitudinal study Participants: 568 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Vascular risks interact with subthreshold levels of Aβ to promote cognitive decline, partially by accelerating early neocortical tau accumulation. 4 key findings →
Design: longitudinal study Participants: 175 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Compared with Aβ-negative persons, those with regional Aβ binding showed proportionately more APOE ε4 carriers (18 [64%] vs 22 [27%] in PREVENT-AD and 34 [31%] vs 38 [19%] in ADNI), reduced CSF Aβ1-42 levels (F = 24 and 71), and greater longitudinal Aβ-PET accumulation (significant β = 0.019 to 0.056). 3 key findings →
Design: cohort study Participants: 817 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Previous brain-autopsy findings suggest that the myelin levels-which differ substantially between white matter tracts in the brain-are a key modulating factor of region-specific susceptibility to tau deposition. 4 key findings →
Design: longitudinal study Participants: 275 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Inferior cerebellar gray matter SUV did not differ on the basis of diagnosis and amyloid-β status, cross-sectionally and over time. [ 18 F]MK6240 uptake significantly differed between CUY and CU adults in the putamen or pallidum (affecting ∼75% of the region) and in the Braak II region (affecting ∼35%). 5 key findings →
Design: longitudinal study Participants: 125 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.
1,040 records (3.4% of the library) are not peer-reviewed — 965 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