27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
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
Increased levels of triglycerides at midlife predict brain Aβ and tau pathology 20 years later in cognitively healthy individuals. 5 key findings →
Design: cohort study Participants: 134 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
There were 838 BioFINDER-2 participants (mean age, 73.9 [SD, 7.3] years; 431 women [51%]; 407 men [49%]) and 380 ADNI participants (average age, 72.9 [SD, 7.0] years; 194 women [51%]; 186 mean [49%]) included. 3 key findings →
Design: cross-sectional Participants: 838 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Most neuroinflammatory CSF biomarkers were associated with WML in individuals without dementia. 5 key findings →
Design: longitudinal study Participants: 247 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
We found that amyloid-β-positive cognitively unimpaired individuals were mainly characterized by decreased functional connectivity between the medial temporal lobe and regions in the anterior-temporal system, most prominently between left perirhinal/entorhinal cortices and medial prefrontal cortex. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Implementation of amyloid biomarkers in clinical practice would be accelerated if such biomarkers could be measured in blood. 4 key findings →
Participants: 719 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Pericyte damage, reflected by CSF PDGFRβ, may be involved in age-related BBB disruption together with neuroinflammation, but is not related to Alzheimer-related pathologic changes. 2 key findings →
Participants: 408 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The CSF Aβ42/Aβ40 and Aβ42/Aβ38 ratios are significantly better than CSF Aβ42 to detect brain amyloid deposition in prodromal AD and to differentiate AD dementia from non-AD dementias. 5 key findings →
Participants: 1,182 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
EPVS are related to SVD, also in early disease stages, but the lack of correlation with cognition suggests that their importance is limited. 5 key findings →
Participants: 240 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Our data suggest that structural MRI can be used to identify biologically and clinically meaningful subtypes of AD. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
A growing body of evidence suggests that the dysregulation of neuronal iron may play a critical role in Alzheimer's disease. 3 key findings →
Participants: 236 Evidence: low
Full summary, score breakdown and related studies → Original source
Patients with CBS without typical AD pathology exhibited AV-1451 retention in the motor cortex, corticospinal tract, and basal ganglia contralateral to the affected body side, clearly different from controls and patients with AD dementia or PSP. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Dominance of 4R over three-repeat (exon 10-) tau isoforms contrasts with earlier reports of R406W patients and was not sufficiently explained by the presence of H1/H2 haplotypes in two of the autopsied patients. 3 key findings →
Design: systematic review Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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 →