GFAP was associated with amyloid and tau PET in multivariable models. 4 key findings →
Design: cross-sectional Participants: 200 Evidence: low
Full summary, score breakdown and related studies → Original source
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
GFAP was associated with amyloid and tau PET in multivariable models. 4 key findings →
Design: cross-sectional Participants: 200 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a common neurodegenerative disease characterized by amyloid plaques and impaired brain metabolism. 4 key findings →
Design: cross-sectional Participants: 181 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Using hippocampal atrophy as a quantitative phenotype in a genome-wide scan, we have identified candidate risk genes for sporadic Alzheimer's disease that merit further investigation. 1 key finding →
Design: case-control study Participants: 381 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Higher amyloid beta burden was associated with increasing anxious-depressive symptoms over time in cognitively normal older individuals. 4 key findings →
Design: longitudinal study Participants: 270 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Combining multi-modality brain data for disease diagnosis commonly leads to improved performance. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid positron emission tomography (PET) imaging is being investigated as a screening tool to identify amyloid-positive patients as an enrichment strategy for Alzheimer disease (AD) clinical trial enrollment. 1 key finding →
Participants: 278 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
We developed, replicated, and validated an MRI measure of cerebrovascular and neurodegenerative pathologies that are associated with clinical and neuropathologic diagnosis of AD and related to established biomarkers. 5 key findings →
Design: cross-sectional Participants: 1,175 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In methodologically heterogeneous studies of uncertain applicability to typical clinical settings, amyloid PET, 18 F-FDG PET, and MRI were highly sensitive for neuropathologic AD. 1 key finding →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
To evaluate reverse causation, we assessed whether a polygenic risk score for AD is associated with HGS. 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
A slower rate of hippocampal atrophy in normal APOE2 carriers is consistent with the lower risk of Alzheimer disease in these individuals. 5 key findings →
Design: cohort study Participants: 72 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Cognitive performance in mild AD improved following tACS, with increased FC within cortical networks and between the hippocampus and specific cortical regions. 2 key findings →
Design: randomized controlled trial Participants: 23 Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
One hundred two (37.9%) participants were amyloid positive. 3 key findings →
Design: randomized controlled trial Participants: 269 Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
These findings suggest that (18)F T807 PET could have value as a biomarker that reflects both the progression of AD tauopathy and the emergence of clinical impairment. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We developed an anatomical mapping technique to detect hippocampal and ventricular changes in Alzheimer disease (AD). 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Lean mass was reduced in persons with early AD compared with controls without dementia (F = 7.73; P = .006) after controlling for sex. 2 key findings →
Design: case-control study Participants: 70 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
MRI and CSF provide complimentary predictive information about time to conversion from amnestic mild cognitive impairment to Alzheimer disease and combination of the 2 provides better prediction than either source alone. 3 key findings →
Participants: 399 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
T2DM may promote neurodegeneration independent of AD dementia diagnosis, and its effect may be driven by tau phosphorylation. 4 key findings →
Design: cross-sectional Participants: 816 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
High WMH was a predictor of progression from normal to MCI (adjusted hazard ratio [HR], 3.30; 95% confidence interval [CI], 1.33-8.17; P= .01) but not conversion from MCI to all-cause dementia. 2 key findings →
Design: cohort study Participants: 67 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Imaging patterns of atrophy in CBS vary according to pathologic diagnosis. 4 key findings →
Design: case-control study Participants: 24 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In this study, females exhibited higher tau compared with age-matched males, particularly in the setting of elevated Aβ. 5 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
A framework for multi-centre MRI studies of Alzheimer's disease has been established consisting of a harmonized MRI acquisition protocol across centres, rigorous QC at both the sites and central data analysis hub and an automated image analysis pipeline. 4 key findings →
Design: longitudinal study Participants: 378 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
During a mean follow-up of 12.1 years, 1,520 individuals developed dementia, 1,194 of whom had AD. 4 key findings →
Participants: 12,305 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cerebral white matter of asymptomatic people frequently exhibits circumscribed areas of hyperintensity on magnetic resonance (MR) images and hypodensity on computed tomography scans. 2 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Alzheimer's disease (AD) is characterized by two molecular pathologies: cerebral β-amyloidosis in the form of β-amyloid (Aβ) plaques and tauopathy in the form of neurofibrillary tangles, neuritic plaques, and neuropil threads. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Although beta-amyloid (Abeta) plaques are a primary diagnostic criterion for Alzheimer's disease, this pathology is commonly observed in the brains of non-demented older individuals. 5 key findings →
Participants: 20 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
10 of the 2,885 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 10. The same 10 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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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.
1,034 records (3.7% 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 →