28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
LSN analysis revealed that interconnectivity patterns of brain regions can be used to classify subjects with AD, those with aMCI, and CN subjects. 5 key findings →
Participants: 20 Evidence: low
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Noninvasive quantitative approaches provide valid estimates of amyloid-β binding. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Although amyloid plaques and neurofibrillary pathology play important roles in Alzheimer disease (AD), our understanding of AD is incomplete, and the contribution of microglia and iron to neurodegeneration is unknown. 1 key finding →
Evidence: low
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Cognitively normal subjects with HTN (n=19) had decreased rCBF in the putamen, globus pallidus, bilaterally, and in the left hippocampus compared with normotensives (n=22). 1 key finding →
Participants: 19 Evidence: low
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The present study indicated that most individuals with the comorbidity of epilepsy and dementia have complex partial seizures that may be adequately controlled on AED therapy. 4 key findings →
Participants: 63 Evidence: low
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Brain changes reminiscent of Alzheimer disease (AD) have been previously reported in a substantial portion of elderly cognitive healthy (HC) subjects. 4 key findings →
Evidence: low
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We report kinetic modeling results of dynamic acquisition data from 0 to 100 min after injection with the tau PET tracer 18 F-AV-1451 in 19 subjects. 2 key findings →
Participants: 19 Evidence: low
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Acupuncture has been used in the therapy of Alzheimer disease (AD); however, its neural mechanisms are still unclear. 2 key findings →
Evidence: low
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Also, patients with MS who engaged in more cognitive leisure were able to withstand more severe brain atrophy at a given cognitive status. 1 key finding →
Participants: 36 Evidence: low
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Alzheimer disease (AD) is the most common form of dementia worldwide. 5 key findings →
Evidence: low
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Prior MR imaging studies, primarily at 1.5T, established hippocampal atrophy as a biomarker for Alzheimer disease. 3T MR imaging offers a higher contrast and signal-to-noise ratio, yet distortions and intensity uniformity are harder to control. 4 key findings →
Participants: 166 Evidence: low
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In this work we use a large scale regularization approach based on penalized logistic regression to automatically classify structural MRI images (sMRI) according to cognitive status. 3 key findings →
Participants: 98 Evidence: low
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The rising incidence of Alzheimer's disease (AD) poses significant challenges to traditional diagnostic methods, which primarily rely on neuropsychological assessments and brain MRIs. 2 key findings →
Evidence: low
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Alzheimer's disease (AD) is a progressive neurodegenerative disorder that significantly impacts cognitive function, posing a major global health challenge. 1 key finding →
Evidence: low
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Thirty-two patients met the inclusion criteria (n=11 moderate-to-severe SVD, mean age 72 ± 10 years, 6 women; n = 21 none-to-minimal SVD, mean age 70 ± 10 years, 12 women). 3 key findings →
Design: cohort study Evidence: moderate
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A total of 13,659 articles were obtained in this study. 5 key findings →
Participants: 13,659 Evidence: low
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The median PPA and NPA were 83.4% and 88.9%, respectively, with lower bounds of 2-sided 95% CIs being 50% or greater for all readers. 4 key findings →
Design: clinical trial Participants: 140 Evidence: low
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(18)F-THK5351 is a useful PET tracer for the early detection of neurofibrillary pathology in AD patients. 3 key findings →
Evidence: low
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SUVR at 60-90 min after injection gave robust quantitation of (18)F-GE180, which correlated well with distribution volume ratios calculated from the entire recording and using a white matter reference region. 2 key findings →
Evidence: low
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Over the course of most common neurodegenerative diseases the amygdala accumulates pathologically misfolded proteins. 2 key findings →
Evidence: moderate
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The structural brain network of patients showed reduced local efficiency compared to controls. 2 key findings →
Evidence: low
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ANOVA revealed significant group differences in lateral ventricular SUVR across the Alzheimer, mild cognitive impairment, and healthy control groups ( P = 0.004). 5 key findings →
Evidence: low
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Implicit memory, including priming, can be preserved in aging and dementia despite impairment of explicit memory. 1 key finding →
Evidence: low
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Our data suggest that genetically-modified NSCs could provide a powerful combinatorial approach to not only enhance synaptic plasticity but to also target and modify underlying Alzheimer's disease pathology. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The paired helical filaments (PHF) formed by the intrinsically disordered human protein tau are one of the pathological hallmarks of Alzheimer disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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 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 →