30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
Better cognitive outcome and higher synaptic density in PS2APP mice was predicted by higher TSPO expression at 8 mo. The progression of TSPO activation to 13 mo also showed a moderate association with spared cognition, but amyloidosis did not correlate with the cognitive outcome, regardless of the time point. 3 key findings →
Design: longitudinal study Evidence: moderate
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Forty-six clinically normal older adults (mean age = 70 years; 43% female) were included. 2 key findings →
Design: longitudinal study Evidence: moderate
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Heterogeneity in progression to Alzheimer's disease (AD) poses challenges for both clinical prognosis and clinical trial implementation. 3 key findings →
Design: longitudinal study Evidence: moderate
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Insulin resistance (IR) is the main pathological condition underlying vascular disorders, such as diabetes and cardiovascular disease, which are well established risk factors for cognitive decline and Alzheimer disease (AD). 3 key findings →
Design: longitudinal study Evidence: moderate
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SUVr(60-90) and SUVr(40-60) overestimated binding with 13% and 10%, respectively, compared with RPM2. 1 key finding →
Design: longitudinal study Evidence: moderate
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Until now, data on the longitudinal trajectories of amyloid accumulation, tau pathology, and brain atrophy over multiple time points remain scarce in DS. 1 key finding →
Design: longitudinal study Evidence: moderate
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Alzheimer disease (AD) is a growing problem for aging populations worldwide. 4 key findings →
Design: longitudinal study Evidence: moderate
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This study aims to quantify microglial activation in individuals with Alzheimer disease (AD) using the 18-kDa translocator protein (TSPO) PET imaging in the hippocampus and precuneus, the 2 AD-vulnerable regions, and to evaluate the association of baseline neuroinflammation with amyloidosis, tau, and longitudinal cognitive decline. 4 key findings →
Design: longitudinal study Evidence: moderate
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Associations of physical exercise with Alzheimer disease (AD) biomarkers and cognitive functioning have been observed cross-sectionally. 4 key findings →
Design: longitudinal study Participants: 181 Evidence: moderate
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Accumulating data suggest cerebrospinal fluid (CSF) neurogranin (Ng) as a potential biomarker for cognitive decline and neurodegeneration in Alzheimer disease (AD). 4 key findings →
Design: longitudinal study Evidence: moderate
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This cohort study examines rates of new diagnosis of Alzheimer disease and related dementias among beneficiaries of Medicare Advantage plans vs traditional Medicare from 2016 through 2020. 1 key finding →
Design: cohort study Evidence: moderate
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The study cohort included 1 415 265 long-stay nursing home residents with dementia who died between 2013 and 2022. 5 key findings →
Design: cohort study Evidence: moderate
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Surrogates were accurate in the majority of cases, made errors in 12% to 22% of cases, and were uncertain in 11% to 16% of cases. 4 key findings →
Design: longitudinal study Evidence: moderate
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Exposure to high neighborhood‐level socioeconomic disadvantage is associated with negative health outcomes. 5 key findings →
Design: longitudinal study Participants: 645 Evidence: moderate
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We found that both state of birth and state of residence account for a modest portion of ADRD mortality variation. 5 key findings →
Design: longitudinal study Evidence: moderate
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Our study included 74,275 weeks of driving data (2015-2024, average follow-up 6.1 years). 5 key findings →
Design: longitudinal study Participants: 36 Evidence: moderate
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A significant ADI × dementia interaction was observed for global atrophy (p = .005) and several other outcomes. 5 key findings →
Design: longitudinal study Participants: 14 Evidence: moderate
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The empirical language composite showed superior and consistent sensitivity (faster decline rate) with all three biomarkers. 5 key findings →
Design: longitudinal study Evidence: moderate
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This cohort study examines the association of serum hyperphosphorylated tau and neurofilament light chain concentrations with psychosis in Alzheimer disease. 1 key finding →
Design: cohort study Evidence: moderate
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In their study, Chen et al 1 examined the association between apolipoprotein E (APOE) genotype and longitudinal cognitive trajectories among middle-aged and older East Asian adults participating in the Healthy Aging Longitudinal Study of Taiwan (HALST).Although sporadic late-onset Alzheimer disease (AD) is polygenic, APOE remains the strongest genetic determinant of AD risk, with carriers of the APOE ε4 allele having increased odds of developing AD dementia in a dose-dependent manner compared with APOE ε3 homozygotes. 1 key finding →
Design: longitudinal study Participants: 21 Evidence: moderate
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Three trajectory classes were identified: stable, slow decliners, and fast decliners. 4 key findings →
Design: longitudinal study Evidence: moderate
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The study included 685 patients who underwent MDS-cognitive and 3,630 patients assessed using OASIS. 5 key findings →
Design: cohort study Participants: 685 Evidence: moderate
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Clinical stages showed a progressively increased prevalence of Aβ-positivity and higher entorhinal tau PET pathology from cognitively normal (CN) to SOCD, MCI, and dementia in both tracers. 5 key findings →
Design: longitudinal study Participants: 446 Evidence: moderate
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The AI-powered pipeline achieved robust performance with intraclass correlation coefficients exceeding 0.97 for regional uptake estimation compared with MR-based ground truth. 5 key findings →
Design: longitudinal study Participants: 666 Evidence: moderate
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Data indicated that participants' needs fluctuated, with 3 key time points of heightened need: dementia diagnosis, in-home care, and transition into residential care. 3 key findings →
Design: longitudinal study Evidence: moderate
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 30,980 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 30,980 records, built mostly from automated pulls of Europe PMC (65.2% of the library) and OpenAlex (16.4%), 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.
1,042 records (3.4% of the library) are not peer-reviewed — 967 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