30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
The LBD-present group had higher QSM values in the SNc (P = 0.008) than the LBD-absent group with no differences in SNr. 5 key findings →
Design: cohort study Participants: 13 Evidence: moderate
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Four progression pathways were concluded from our analyses, cognitive stability (32.8 %), sequential MCI-only decline (34.9 %), accelerated MCI-to-dementia progression (15.8 %), and rapid direct conversion (16.5 %). 5 key findings →
Design: longitudinal study Participants: 1,136 Evidence: moderate
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Females had higher rates of positive amyloid PET visual reads (63% vs. 59%, P < 0.001) and higher Centiloids (CLs; median 48.7 vs. 36.8, p < 0.001). 5 key findings →
Participants: 10,361 Evidence: moderate
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At baseline, Aβ+ participants showed higher CP FWf, increased white matter hyperintensity (WMH) volume, and decreased diffusion tensor image analysis along the perivascular space (DTI-ALPS). 5 key findings →
Design: cohort study Participants: 216 Evidence: moderate
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It is not known exactly where amyloid-β (Aβ) fibrils begin to accumulate in individuals with Alzheimer's disease (AD).
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This cross-sectional evaluation of the NIA-AA criteria for preclinical AD indicates that the 1-3 staging criteria coupled with stage 0 and SNAP categories classify 97% of CN subjects from a population-based sample, leaving only 3% unclassified. 2 key findings →
Design: cross-sectional Evidence: moderate
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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
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This roughly 15-year interval where the slope of the amyloid SUVR vs time curve is greatest and roughly linear represents a large therapeutic window for secondary preventive interventions. 1 key finding →
Participants: 246 Evidence: low
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Clinical phenotypes are associated with differential patterns of tau but not amyloid pathology. 3 key findings →
Participants: 119 Evidence: low
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Furthermore, neuroimaging analysis identified 2 additional loci of high interest for further study. 1 key finding →
Design: case-control study Participants: 168 Evidence: moderate
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This advantage may represent a sex-specific form of cognitive reserve delaying verbal memory decline until more advanced disease stages. 1 key finding →
Design: cross-sectional Participants: 379 Evidence: low
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While prior work reliably demonstrates that the APOE ɛ4 allele has deleterious group level effects on Alzheimer disease pathology, the homogeneity of its influence across the lifespan and spatially in the brain remains unknown. 1 key finding →
Design: longitudinal study Evidence: moderate
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MI failed to show an effect on metabolism in FDG-based AD biomarker, but exploratory analysis suggested positive effect on limbic system metabolism. 4 key findings →
Participants: 67 Evidence: high
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Of 3894 participants, 1671 underwent PET imaging and were included in the study; 2198 did not undergo imaging, and 25 were excluded for other reasons. 2 key findings →
Participants: 3,894 Evidence: low
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Ultimately, we hope this project will provide the groundwork for future development of prevention and treatment strategies for delirium, designed to minimize the long term negative impact of delirium in older adults. 1 key finding →
Design: cohort study Participants: 550 Evidence: moderate
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Patients with behavioural Alzheimer's disease showed worse memory scores than behavioural variant frontotemporal dementia and did not differ from typical Alzheimer's disease, while executive function composite scores were lower compared to behavioural variant frontotemporal dementia and typical Alzheimer's disease. 3 key findings →
Participants: 17 Evidence: low
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Different biomarkers for Alzheimer disease provide different information from one another that is likely to be complementary. 1 key finding →
Participants: 34 Evidence: low
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We aimed to determine the regional pattern of brain atrophy associated with the C9ORF72 gene mutation, and to determine which regions best differentiate C9ORF72 from subjects with mutations in tau and progranulin, and from sporadic frontotemporal dementia. 5 key findings →
Participants: 76 Evidence: low
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Preclinical AD as detected by PET PiB is not benign, as it is associated with progression to symptomatic AD. 4 key findings →
Design: cohort study Evidence: moderate
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As expected, the MENO group was older than the PERI and CNT groups. 3 key findings →
Evidence: moderate
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We found no significant correlation between CSF biomarkers and cognitive scores in any of the 3 clinical groups individually. 2 key findings →
Design: cross-sectional Participants: 399 Evidence: low
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In a middle-aged, at-risk cohort, a physically active lifestyle is associated with an attenuation of the deleterious influence of age on key biomarkers of AD pathophysiology. 3 key findings →
Design: cross-sectional Participants: 186 Evidence: high
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Compared with noncarriers, cognitively unimpaired mutation carriers had elevated mean cortical Pittsburgh Compound B distribution volume ratio levels in their late 20s, and 7 of 9 carriers older than 30 years reached the threshold for amyloidosis (distribution volume ratio level > 1.2). 4 key findings →
Design: cross-sectional Participants: 24 Evidence: low
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Increased WMHs are associated with aging, decreased glucose metabolism, and decline in executive function but do not affect AD-specific pathologic progression, suggesting that the vascular contribution to dementia is probably additive although not necessarily independent of the amyloid pathway. 5 key findings →
Design: longitudinal study Evidence: moderate
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Resting-state functional connectivity magnetic resonance imaging changes with progressing AD severity are similar between ADAD and LOAD. 2 key findings →
Design: cross-sectional Participants: 79 Evidence: moderate
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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.
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 30,580 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 30,580 records, built mostly from automated pulls of Europe PMC (64.7% of the library) and OpenAlex (16.6%), 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.
1,037 records (3.4% of the library) are not peer-reviewed — 964 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