29,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
In this study, elevated [18F]RO948 SUVRs were most often seen among Aβ-positive cases, which suggests that [18F]RO948 has high specificity for AD-type tau and highlights its potential as a diagnostic marker in the differential diagnosis of AD. 4 key findings →
Design: cross-sectional Participants: 257 Evidence: low
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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
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Neurodegeneration rather than cerebrovascular lesions may play a key role in T2DM-related cognitive impairment. 2 key findings →
Design: cross-sectional Participants: 350 Evidence: low
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GOF indices were highest in normal controls, intermediate in MCI, and lowest in AD (p Conclusions fMRI connectivity indices distinguish patients with MCI who undergo cognitive decline and conversion to AD from those who remain stable over a 2- to 3-year follow-up period. 3 key findings →
Design: cross-sectional Participants: 68 Evidence: moderate
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More-severe diabetes (defined by higher HbA 1c and longer disease duration) but not prediabetes or less-severe diabetes was associated with smaller brain volumes and an increased burden of brain vascular pathology. 3 key findings →
Design: cross-sectional Participants: 1,713 Evidence: low
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These findings suggest a potential vasculoprotective role of vitamin D. 2 key findings →
Design: cross-sectional Participants: 318 Evidence: low
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Preclinical AD is associated with rest-activity rhythm fragmentation, independent of age or sex. 5 key findings →
Design: cross-sectional Participants: 205 Evidence: moderate
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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
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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
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Clinicopathological evidence suggests that the pathology of Alzheimer's disease (AD) begins many years before the appearance of cognitive symptoms. 3 key findings →
Design: cross-sectional 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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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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Symptomatic mutation carriers also demonstrated elevated tau PET binding in the basal ganglia, consistent with prior work with amyloid-β. 2 key findings →
Design: cross-sectional Evidence: low
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CVR was significantly associated with cognitive performance independently of AD pathology. 5 key findings →
Design: cross-sectional Participants: 28 Evidence: low
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In contrast to no change in global cortical SUVR in the CU- and CU+ groups during the 2-y period, global cortical SUVR increased by 0.06 (2.9%) in the MCI+ group and 0.19 (8.0%) in the DEM+ group at follow-up. 5 key findings →
Design: cross-sectional Participants: 107 Evidence: moderate
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Atrophy in FAD is observed early, both in areas commonly associated with sporadic Alzheimer disease and also in the putamen and thalamus, 2 regions associated with early amyloid deposition in FAD mutation carriers. 4 key findings →
Design: cross-sectional Participants: 192 Evidence: low
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CA1 apical neuropil atrophy is apparent in patients with mild AD. 2 key findings →
Design: cross-sectional Participants: 14 Evidence: low
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These findings suggest that DMN fcMRI may prove useful as a biomarker across a wide spectrum of disease, and support the feasibility of DMN fcMRI as a secondary endpoint in upcoming multicenter clinical trials in Alzheimer disease. 2 key findings →
Design: cross-sectional Evidence: moderate
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Plasma A beta levels are affected by age and by systemic and CNS vascular risk factors. 4 key findings →
Design: cross-sectional Participants: 55 Evidence: moderate
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There were detectable WMH, enlarged PVS, infarcts, and microbleeds as early as the 5th decade of life. 2 key findings →
Design: cross-sectional Participants: 138 Evidence: low
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Systemic inflammation is associated with ischemia and Alzheimer disease (AD). 3 key findings →
Design: cross-sectional Evidence: low
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Frontotemporal dementia and Alzheimer disease display different spatial distributions of hypoperfusion on arterial spin labeling MRI. 2 key findings →
Design: cross-sectional Participants: 21 Evidence: low
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PERSI showed superior test-retest reproducibility (1.84%) and group separation ability (cross-sectional Cohen d = 9.45; longitudinal Cohen d = 2.34) compared with other reference regions. 4 key findings →
Design: cross-sectional Participants: 215 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 29,780 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 29,780 records, built mostly from automated pulls of Europe PMC (63.8% of the library) and OpenAlex (17.1%), 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 (3.5% 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 →