Aβ1-42, tTau and pTau (but not Aβ1-40) and the ratios with Aβ1-42 had good diagnostic agreement with 18 F-Florbetapir PET. 4 key findings →
Participants: 35 Evidence: moderate
Full summary, score breakdown and related studies → Original source
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Aβ1-42, tTau and pTau (but not Aβ1-40) and the ratios with Aβ1-42 had good diagnostic agreement with 18 F-Florbetapir PET. 4 key findings →
Participants: 35 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Amyloid-PET presented higher diagnostic accuracy, sensitivity, and NPV than CSF Aβ1-42 but not Aβ42/40 ratio. 5 key findings →
Participants: 148 Evidence: low
Full summary, score breakdown and related studies → Original source
In the negative images of the HS group, the contrast between the white matter and the gray matter was high in the FMM PET images, while striatal uptake was relatively higher in the FPN PET images. 5 key findings →
Participants: 605 Evidence: low
Full summary, score breakdown and related studies → Original source
Twenty-five/38 (65.8%) amyloid PET/CT scans resulted positive for amyloid deposition. 5 key findings →
Participants: 38 Evidence: low
Full summary, score breakdown and related studies → Original source
Cross-sectional positron emission tomography (PET) studies find that cognitively normal carriers of the apolipoprotein E (APOE) epsilon4 allele, a common Alzheimer's susceptibility gene, have abnormally low measurements of the cerebral metabolic rate for glucose (CMRgl) in the same regions as patients with Alzheimer's dementia. 1 key finding →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
The mean values of SUVr were higher in AD patients (median 1.20, Q1-Q3 1.16-1.30) than in HC subjects (median 1.05, Q1-Q3 1.04-1.08; p = 0.0001) in the overall cortex and all cortical regions (precuneus, anterior and posterior cingulate, and frontal median, temporal, parietal and occipital cortex). 5 key findings →
Participants: 46 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma p‐tau181 differentiated pathology‐confirmed AD from NC with negative amyloid PET scans with an AUC of 0.93. 5 key findings →
Participants: 91 Evidence: moderate
Full summary, score breakdown and related studies → Original source
[18F]flutemetamol PET scans were positive in 133 out of 211 (63%) patients, of whom 110 out of 144 (76%) patients had a pre-PET Alzheimer's disease (AD) diagnosis and 23 out of 67 (34%) patients had a non-AD diagnosis. 5 key findings →
Participants: 211 Evidence: low
Full summary, score breakdown and related studies → Original source
Elevated FTP-PET reflects Braak IV or greater neuropathology. 3 key findings →
Participants: 26 Evidence: low
Full summary, score breakdown and related studies → Original source
This evaluation shows an [ 18 F]MK-6240 distribution in concordance with postmortem studies and that simplified quantitative approaches such as the SUVR offer valid estimates of neurofibrillary tangle load 90 min post injection. [ 18 F]MK-6240 is a promising tau tracer with the potential to be applied in the disease diagnosis and assessment of therapeutic interventions. 2 key findings →
Participants: 14 Evidence: low
Full summary, score breakdown and related studies → Original source
Patients with Alzheimer's disease can present with different clinical phenotypes. 3 key findings →
Participants: 20 Evidence: low
Full summary, score breakdown and related studies → Original source
Future longitudinal studies examining the association of more severe depressive symptoms and cerebral tau accumulation are needed to substantiate this finding and to guide prevention and treatment in AD. 4 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
[ 18 F]flutemetamol data can now be expressed in Centiloid units, enhancing its utility in clinical and research applications for β-amyloid imaging. 2 key findings →
Participants: 74 Evidence: low
Full summary, score breakdown and related studies → Original source
The novel tau-PET tracer [18F]PI-2620 detects the 3/4-repeat-(R)-tauopathy Alzheimer's disease (AD) and the 4R-tauopathies corticobasal syndrome (CBS) and progressive supranuclear palsy (PSP). 2 key findings →
Participants: 29 Evidence: low
Full summary, score breakdown and related studies → Original source
Older participants had lower hippocampal volumes and overall flortaucipir uptake. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
18 F-Flortaucipir, as a classical Tau protein visualizer, has been widely used in the diagnosis of neurodegenerative diseases, especially Alzheimer disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Posterior cortical atrophy (PCA) and logopenic progressive aphasia (LPA) are clinical syndromes that commonly have underlying Alzheimer's disease (AD), although non-AD pathologies have also been reported. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Among 565 veterans, 34.9% of received an amyloid PET scan and 98.0% of these were consistent with appropriate use criteria. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The cortical SUVR (R2 = 0.97) and striatal SUVR (R2 = 0.95) demonstrated an excellent linear correlation between FBB and FMM using a WC as reference region. 5 key findings →
Participants: 107 Evidence: low
Full summary, score breakdown and related studies → Original source
This study evaluated performance of a commercially available standardized software program for calculation of florbetapir PET standard uptake value ratios (SUVr) in comparison with an established research method. 1 key finding →
Participants: 183 Evidence: low
Full summary, score breakdown and related studies → Original source
Positive correlations were found between eFBP/eFMM and 18F-FDG-PET SUVR independently of Aβ status and Aβ radiotracer (R>0.72, p<0.001). eFBP/eFMM single-subject analysis revealed clusters of significant hypoperfusion with good correspondence to hypometabolism topographies, independently of the underlying neurodegenerative patterns. 5 key findings →
Participants: 94 Evidence: low
Full summary, score breakdown and related studies → Original source
In the 98 participants with long follow-up, Centiloid = 26 provided the highest overall predictive value = 87% (NPV = 85%, PPV = 88%). 5 key findings →
Participants: 37 Evidence: low
Full summary, score breakdown and related studies → Original source
It is currently unclear how amyloid-β and tau deposition are linked to changes in synaptic function and axonal structure over the course of Alzheimer's disease. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Animal studies demonstrate that hyperactive neurons facilitate early accumulation and spread of tau and amyloid-β proteins in the pathological cascade of Alzheimer's disease (AD). 3 key findings →
Participants: 120 Evidence: low
Full summary, score breakdown and related studies → Original source
Clear divergence in tauopathy between the sexes are apparent approximately 20 years earlier than previously reported. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
9 of the 319 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 9. The same 9 appear here every time.
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 →