30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
Given the impact of discrepant thresholds on tau positivity rates, biomarker staging, and eligibility for future clinical treatment trials, recommendations are offered to select cut-point derivations based on the unique goals and priorities of different studies. 1 key finding →
Design: systematic review Participants: 6,536 Evidence: high
Full summary, score breakdown and related studies → Original source
In both amyloid-positive cohorts (ADNI [age = 75.99±7.69] and A05 [age = 74.03±9.03]), cognitive-domain-specific tau-PET outperformed global and temporal-lobe tau-PET for predicting future cognitive decline in episodic memory, language, executive functioning, and visuospatial abilities. 3 key findings →
Design: meta-analysis Participants: 121 Evidence: high
Full summary, score breakdown and related studies → Original source
Generalised linear regressions showed significant quadratic associations between amyloid age and cognitive performance and cubic associations between amyloid age and tau, both at baseline and at the 32-month follow-up. 1 key finding →
Design: cohort study Participants: 167 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Deposition of amyloid and tau pathology can be quantified in vivo using positron emission tomography (PET). 5 key findings →
Design: longitudinal study 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
The site and rate of atrophy are different across the tau-PET patterns. 1 key finding →
Design: longitudinal study Participants: 366 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
LEADS data emphasizes the importance of biomarkers to enhance diagnostic accuracy in EOAD. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Aβ-positive individuals can remain tau-negative for at least 5 years. 2 key findings →
Design: case-control study Participants: 45 Evidence: moderate
Full summary, score breakdown and related studies → Original source
When discriminating between preclinical Aβ status, the area under the curve (AUC) for plasma pTau181 (0.83) and tau PET (entorhinal, 0.87; temporal, 0.85; neocortical, 0.67) were equally high (all DeLong P > 0.05), but tau PET outperformed plasma pTau181 in discriminating MCI/AD from SCD (AUC for plasma pTau181: 0.74; AUCs for tau PET: entorhinal, 0.89; temporal, 0.92; neocortical, 0.89) (all P < 0.01). 4 key findings →
Design: cross-sectional Participants: 40 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The effects of sex and APOE ε4 must be considered when studying these populations. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
To date, there is no validated fluid biomarker for tau pathology in Alzheimer's disease, with contradictory results from studies evaluating the correlation between phosphorylated tau in CSF with tau PET imaging. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
We identified several demographic, clinical, and neurobiological factors that are important to explain the variance in tau PET retention observed across the AD pathological continuum, non-AD neurodegenerative disorders, and cognitively unimpaired persons. 1 key finding →
Participants: 1,944 Evidence: low
Full summary, score breakdown and related studies → Original source
We identified a significant association between witnessed apneas in CU elderly and elevated tau-PET signal in tau-susceptible brain regions. 5 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
Age is an important determinant of severity of cortical tau uptake in atypical AD, with young participants more likely to show widespread and severe cortical tau uptake. 3 key findings →
Participants: 42 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease and other neurodegenerative dementias belong to the family of tauopathies. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
The regional relationships between tau positron emission tomography (PET) imaging and cognitive impairment in Alzheimer's disease (AD) remain uncertain. 3 key findings →
Design: cross-sectional Participants: 71 Evidence: low
Full summary, score breakdown and related studies → Original source
In MCI/AD patients, [ 18 F]flortaucipir binding in entorhinal, limbic, and neocortical regions was associated with cortical atrophy. 5 key findings →
Participants: 100 Evidence: low
Full summary, score breakdown and related studies → Original source
A next generation of tau PET tracers for the imaging of Alzheimer's disease and other dementias has recently been developed. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
18 F-AV1451 prominently specific binding was found in the amygdala, entorhinal cortex, parahippocampus, fusiform, posterior cingulate, temporal, parietal, and frontal brain regions. 5 key findings →
Participants: 115 Evidence: low
Full summary, score breakdown and related studies → Original source
Optimized tau PET classifiers may diagnose AD with high accuracy, but both tau PET and structural brain MRI capture partly unique information relevant for the clinical deterioration in AD. 2 key findings →
Participants: 32 Evidence: low
Full summary, score breakdown and related studies → Original source
Higher tau-PET in the presence of low amyloid-PET is associated with abnormally increased glucose metabolism that is accompanied by episodic memory impairment. 3 key findings →
Participants: 70 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) patients are known to have heterogeneous clinical presentation and pathologic patterns. 5 key findings →
Participants: 83 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is associated with reduced temporo-parietal cerebral blood flow (CBF). 4 key findings →
Participants: 156 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma p217+tau levels elevate early in the AD continuum and correlate well with Aβ and tau PET. 4 key findings →
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.
1,040 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