30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
Mounting evidence in adults without AD indicates that females exhibit higher tau deposition than age-matched males, particularly in the setting of elevated β-amyloid (Aβ), but the evidence for sex differences in tau accumulation rates is inconclusive. 5 key findings →
Design: meta-analysis Participants: 1,376 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
The study team reported a significant change in diagnoses and patient medication when tau PET was added to an already extensive diagnostic workup that included cerebrospinal fluid AD biomarkers. 5 key findings →
Design: cohort study Participants: 878 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Neuroinflammation and cerebrovascular dysfunction are early events occurring already at presymptomatic stages of AD and contribute to disease progression. 5 key findings →
Design: longitudinal study Participants: 508 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Our findings suggest that tau PET is more sensitive than Aβ PET and measures of cortical thickness for detecting early cognitive changes in preclinical AD. 2 key findings →
Design: cross-sectional Participants: 106 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
For amyloid PET, 7 scenarios were rated as appropriate, 2 as uncertain, and 8 as rarely appropriate. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In this study, we investigated associations between neuropsychiatric symptoms (i.e., apathy, anxiety, and depression) and cerebral atrophy, white matter lesions (WML), beta-amyloid (Aβ) deposition, and cognitive decline in a nondemented sample. 104 cognitively unimpaired and 53 subjects with mild cognitive impairment were followed for up to 4 years within the Swedish BioFINDER study. 1 key finding →
Design: longitudinal study Participants: 53 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Mean squared displacement revealed widespread microstructural differences already between Aβ-negative/tau-negative and Aβ-positive/tau-negative participants with a spatial distribution that closely resembled the pattern of Aβ accumulation. 4 key findings →
Participants: 292 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The current literature provides overall preliminary evidence on the establishment of the second-generation tau PET tracers into the clinical context, thereby successfully addressing some methodological issues from the tau PET tracer of the first generation. 2 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
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
The advent of PET ligands that bind tau pathology has enabled the quantification and visualization of tau pathology in aging and in Alzheimer disease (AD). 2 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In Alzheimer's diseases (AD), tau pathology is strongly associated with cognitive decline. 5 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
Tau is a hallmark pathology of Alzheimer's disease, and animal models have suggested that tau spreads from cell to cell through neuronal connections, facilitated by β-amyloid (Aβ). 3 key findings →
Participants: 312 Evidence: low
Full summary, score breakdown and related studies → Original source
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
In this patient, the clinical disease symptoms progressed rapidly in life, paralleled with an annual increase of tau PET retention of 20% to 40% in many cortical regions. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Mixed pathologies of α-synuclein, β-amyloid and tau are relatively common in Parkinson's disease (PD) and Dementia with Lewy Bodies (DLB). 5 key findings →
Participants: 18 Evidence: low
Full summary, score breakdown and related studies → Original source
The abnormal accumulation of amyloid-β and tau targets specific spatial networks in Alzheimer's disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tau positron emission tomography ligands provide the novel possibility to image tau pathology in vivo However, little is known about how in vivo brain uptake of tau positron emission tomography ligands relates to tau aggregates observed post-mortem. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The recent development of several tau positron emission tomography (PET) tracers represents a major milestone for the Alzheimer's disease (AD) field. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Increases in tau and cognitive dysfunction occur years before commonly used thresholds for Aβ-positivity. 1 key finding →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Current literature provides partial evidence for clinical utility of [ 18 F]flortaucipir PET. 1 key finding →
Design: clinical trial Evidence: low
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