30,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
This meta-analysis included cross-sectional amyloid PET scans acquired with 5 radiotracers from 49 227 participants across 53 studies from 15 countries (mean age, 71 years; 54% female, 62% cognitively impaired). 5 key findings →
Design: meta-analysis Participants: 48 Evidence: high
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Selected clinical features may identify patients with suspected RPD who are likely to continue to decline. 2 key findings →
Participants: 248 Evidence: low
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In both cohorts, CSF MTBR-tau243 was associated with tau-PET temporal meta-ROI burden (BioFINDER-2: β = 1.1, p = < 0.0001 and Knight-ADRC: β = 0.7, p = < 0.0001), and this association did not differ by sex (BioFINDER-2 β = 0.04, p = 0.6 and Knight-ADRC: β = 0.009, p = 0.9). 3 key findings →
Design: cross-sectional Participants: 446 Evidence: low
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These analyses suggest that CenTauR harmonization increases the comparability of tau‐PET data acquired with different tracers. 2 key findings →
Design: longitudinal study Participants: 1,089 Evidence: moderate
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Accelerated atrophy of medial temporal lobe subregions was evident already during preclinical AD. 5 key findings →
Participants: 363 Evidence: low
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Both visual read methods exhibited strong concordance with semiquantitative SUVRs. 5 key findings →
Design: cohort study Participants: 1,654 Evidence: moderate
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This study included 3540 participants with RVC data and 489 with WMH data (median [IQR] age: 73.2 [71.4-76.3] and 72.5 [71.2-75.4] years; female: 52.9% and 47.6%) over a median follow-up of 7.4 [IQR 5.5-8.5] and 3.8 [IQR 2.9-5.3] years, respectively. 5 key findings →
Design: cross-sectional Participants: 3,540 Evidence: moderate
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This study summarizes the existing literature on TSPO expression in specific regions of the brain in patients with dementia, and also provides some preliminary evidence on the possible association between neuroinflammation and dementia. 5 key findings →
Design: meta-analysis Evidence: high
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Rates of hippocampal atrophy match both baseline cognitive status and the change in cognitive status over time in elderly persons who lie along the cognitive continuum from normal to MCI to AD.
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PiB and florbetapir retention ratios were strongly associated in the same individuals, and this relationship was consistent across several data analysis methods, despite scan-rescan intervals of more than a year.
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Amyloid imaging is currently introduced to the market for clinical use. 5 key findings →
Design: cross-sectional Evidence: moderate
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Infections have been associated with the incidence of Alzheimer disease and related dementias, but the mechanisms responsible for these associations remain unclear. 4 key findings →
Evidence: low
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After disclosure, 27 patients with amyloid-positive SCD+ (median [IQR] age, 70 [66-74] years; gender: 14 men [52%]; median [IQR] education: 15 [13 to 17] years, median [IQR] Mini-Mental State Examination [MMSE] score, 29 [28 to 30]) had higher median (IQR) IES-R total score (10 [2 to 14] vs 0 [0 to 2]; P Conclusions and relevance The disclosure of a positive amyloid-PET result to patients with SCD+ was associated with a bigger psychological change, yet such change did not reach the threshold for clinical concern. 5 key findings →
Participants: 27 Evidence: low
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Our results support the utility of CSF VEC as a marker of endothelial injury in AD and highlight the importance of endothelial injury as an early pathology that contributes to cognitive impairment in even the earliest preclinical stages. 3 key findings →
Participants: 700 Evidence: moderate
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Across 3 study samples, combining the functional connectome and molecular properties substantially enhanced the explanatory power compared to single modalities, providing a valuable tool to explain regional susceptibility to tau deposition in AD. 3 key findings →
Participants: 1,000 Evidence: low
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Our results indicate that assessing regional changes in amyloid, particularly in posterior cortical regions, can aid in the early detection of subclinical amyloid-related decline in episodic memory as early as middle age. 2 key findings →
Evidence: low
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Our data suggest that vascular abnormalities, independently of blood pressure levels, may play a role in the setting of subjective memory complaints as well as of WMH in elderly hypertensive patients. 4 key findings →
Design: cross-sectional Evidence: low
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None of the participants were diabetics, smokers, or met criteria for obesity. 4 key findings →
Design: cross-sectional Evidence: moderate
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The regions of loss observed in subjects with amnestic mild cognitive impairment (aMCI) who progressed to Alzheimer disease (AD) within 18 months of the MRI are typical of subjects with AD. 3 key findings →
Evidence: low
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Hippocampal atrophy (HA) is usually attributed to the neurofibrillary tangles and neuritic plaques of Alzheimer disease. 5 key findings →
Evidence: low
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Susceptibility-weighted imaging (SWI) evolved from simple two-dimensional T2*-weighted sequences to three-dimensional sequences with improved spatial resolution and enhanced susceptibility contrast. 5 key findings →
Evidence: low
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Revised diagnostic criteria for Alzheimer disease (AD) acknowledge a key role of imaging biomarkers for early diagnosis. 5 key findings →
Evidence: low
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[F-18]-MK-6240, a novel tau positron emission tomography (PET) tracer recently discovered for the in vivo detection of neurofibrillary tangles, has the potential to improve diagnostic accuracy in the detection of Alzheimer disease. 2 key findings →
Evidence: low
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These findings support the idea that vascular amyloid burden directly contributes to chronic cerebral ischemia and highlights the possible utility of amyloid imaging as a marker of CAA severity. 2 key findings →
Evidence: low
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Loss of cholinergic neurons is associated with impaired cognitive function, particularly memory loss and Alzheimer disease (AD). 3 key findings →
Participants: 1,391 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 30,180 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 30,180 records, built mostly from automated pulls of Europe PMC (64.2% of the library) and OpenAlex (16.9%), 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 →