28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
We aim to investigate the relationships between the population characteristics of patients with Alzheimer's Disease (AD) and their Healthcare Utilization (HU) during the COVID-19 pandemic. 1 key finding →
Design: longitudinal study Evidence: moderate
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Researchers examined brains obtained at autopsy from nondemented and demented individuals to study extracellular amyloid deposits and intraneuronal neurofibrillary changes. 3 key findings →
Evidence: low
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Although amyloid imaging with PiB-PET ([C-11]Pittsburgh Compound-B positron emission tomography), and now with F-18-labeled tracers, has produced remarkably consistent qualitative findings across a large number of centers, there has been considerable variability in the exact numbers reported as quantitative outcome measures of tracer retention. 4 key findings →
Evidence: low
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The researchers isolated and sequenced an apparently full-length complementary DNA clone coding for the A4 polypeptide. 3 key findings →
Evidence: low
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Rapid progress in deciphering the biological mechanism of Alzheimer's disease (AD) has arisen from the application of molecular and cell biology to this complex disorder of the limbic and association cortices. 5 key findings →
Evidence: low
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The positron emission tomography (PET) radiotracer Pittsburgh Compound-B (PiB) binds with high affinity to beta-pleated sheet aggregates of the amyloid-beta (Abeta) peptide in vitro. 2 key findings →
Evidence: low
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Early and accurate diagnosis of Alzheimer's disease (AD) has a major impact on the progress of research on dementia. 5 key findings →
Participants: 37 Evidence: low
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Dementia is marked by progressive cognitive decline linked to oxidative stress, neuroinflammation, and synaptic dysfunction. 4 key findings →
Design: systematic review Participants: 29 Evidence: high
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The AD set included 23,092 cases and 30,920 controls, the ALS set included 7391 cases and 12,442 controls, and the PD set included 8498 patients and 9161 controls. 3 key findings →
Design: meta-analysis Participants: 23,092 Evidence: high
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Less-invasive biomarkers for early Alzheimer disease (AD) are urgently needed. 3 key findings →
Design: randomized controlled trial Participants: 109 Evidence: low
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Amyloid beta (Aβ) peptides are the major components of senile plaques, one of the main pathological hallmarks of Alzheimer disease (AD). 4 key findings →
Design: meta-analysis Evidence: high
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This study provides a comprehensive review of the last 10 years of research on neuroinflammation and AD, including the number and impact of research findings, research hotspots, and future trends. 2 key findings →
Design: systematic review Participants: 3,833 Evidence: low
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Simufilam did not meet co-primary or secondary endpoints in these Phase 3 trials. 3 key findings →
Design: post-hoc analysis Evidence: high
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A diverse and stable microbiota promotes a healthy state, nevertheless, an imbalance in gut or oral bacterial composition, called dysbiosis, can cause gastrointestinal disorders, systemic inflammatory states and oxidative stress, among others. 5 key findings →
Design: systematic review Evidence: high
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Research evidence indicating common metabolic mechanisms through which type 2 diabetes mellitus (T2DM) increases risk of late-onset Alzheimer's dementia (LOAD) has accumulated over recent decades. 2 key findings →
Design: systematic review Evidence: high
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Our results support the positive cognitive effects of boswellic acids by reducing the systemic inflammation. 5 key findings →
Design: randomized controlled trial Evidence: high
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Recent functional imaging studies have revealed coactivation in a distributed network of cortical regions that characterizes the resting state, or default mode, of the human brain.
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To investigate earlier pathologies preceding filamentous tau inclusions, researchers studied wild-type and P301S mutant human tau transgenic mice. 3 key findings →
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The apolipoprotein E (APOE) ε4 allele is the strongest genetic risk factor for late-onset, sporadic Alzheimer's disease (AD).
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This review discusses time-dependent models of Alzheimer's disease (AD) that track the temporal evolution of validated pathophysiological biomarkers relative to age of onset, aging, and co-occurring brain pathologies. 4 key findings →
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The major cell classes of the brain differ in their developmental processes, metabolism, signaling, and function.
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The study used network-sensitive neuroimaging methods to test whether neurodegenerative diseases target large-scale neural networks in living humans. 3 key findings →
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Alzheimer's disease (AD) is associated with neurodegeneration in vulnerable limbic and heteromodal regions of the cerebral cortex, detectable in vivo using magnetic resonance imaging.
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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. 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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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.
1,034 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 →