28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
The presence of tangles of abnormally phosphorylated tau is a characteristic of Alzheimer's disease (AD), and the loss of synapses correlates with the degree of dementia. 4 key findings →
Evidence: low
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Alzheimer's disease (AD) is the most common dementia in the elderly. 4 key findings →
Evidence: low
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There is increasing appreciation that non-neuronal cells contribute to the initiation, progression and pathology of diverse neurodegenerative disorders. 4 key findings →
Evidence: low
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Alzheimer's disease (AD) is a major contributor of dementia leading to the degeneration of neurons in the brain with major symptoms like loss of memory and learning. 4 key findings →
Evidence: low
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Alzheimer's disease (AD) is a complex neurodegenerative disease in the elderly and the most common cause of human dementia. 4 key findings →
Evidence: low
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Microglial-mediated neuroinflammation plays an important role in vascular dementia, and modulating neuroinflammation has emerged as a promising treatment target. 4 key findings →
Evidence: low
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Alzheimer's Disease (AD) is a chronic neurodegenerative disorder and the most common type of dementia (60-80% of cases). 4 key findings →
Evidence: low
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Dysfunction of immune and vascular systems has been implicated in aging and Alzheimer disease; however, their interrelatedness remains poorly understood. 4 key findings →
Evidence: low
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Human lumbar CSF patterns of Abeta peptides were analysed by urea-based beta-amyloid sodium dodecyl sulphate polyacrylamide gel electrophoresis with western immunoblot (Abeta-SDS-PAGE/immunoblot). 4 key findings →
Participants: 12 Evidence: low
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Alzheimer disease (AD) is associated with an increase in the brain of the 18-kDa translocator protein (TSPO), which is overexpressed in activated microglia and reactive astrocytes. 4 key findings →
Evidence: low
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Dysbiosis of intestinal microbiota in the elderly can cause a leaky gut, which may result in silent systemic inflammation and promote neuroinflammation - a relevant pathomechanism in the early course of Alzheimer's disease. 4 key findings →
Participants: 18 Evidence: low
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Anti-inflammatory drugs have been suggested as a possible treatment for Alzheimer's disease (AD). 4 key findings →
Participants: 32 Evidence: low
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Here we elucidate the effect of Alzheimer disease (AD)-predisposing genetic backgrounds, APOE4, PSEN1ΔE9, and APPswe, on functionality of human microglia-like cells (iMGLs). 4 key findings →
Evidence: low
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Mitochondrial dysfunction and oxidative stress occur in vascular dementia (VaD), but the specific molecular mechanism regulating these events remains unclear. 4 key findings →
Evidence: low
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of 74,486 decedents (60.5% women; mean age 87.1 years (standard deviation: 7.1)), 82.6% had at least one ED visit in their last year of life. 3 key findings →
Design: cohort study Evidence: moderate
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The 32 796 872 Medicare beneficiaries in the cohort had a mean (SD) age of 74.0 (12.5) years and included 18 228 513 females (55.6%). 5 key findings →
Design: cross-sectional Participants: 18 Evidence: moderate
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From both commercial and Medicare Advantage perspectives, mirabegron was the most clinically effective treatment, while oxybutynin was the least expensive. 4 key findings →
Design: meta-analysis Evidence: high
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Patients with CLTI undergoing peripheral vascular intervention from 2017 to 2018 were derived from the Medicare-linked VQI (Vascular Quality Initiative) registry. 5 key findings →
Participants: 114 Evidence: moderate
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In 2012, the national prevalence of antipsychotic drug use was 20.7% for elderly patients with dementia, with a national incidence of 3.9%. 4 key findings →
Design: cross-sectional Participants: 34,536 Evidence: low
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The prevalence of cognitive impairment, MCI, and dementia among participants aged 60 years and older were 21.48% (95% CI, 19.90-23.10), 15.70% (95% CI, 14.30-17.10), and 5.77 (95% CI, 4.90-6.70), respectively. 5 key findings →
Design: cross-sectional Participants: 3,233 Evidence: low
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= 0.041). Socioeconomic status and residential area are associated with long-term survival in patients with EOD. 2 key findings →
Design: cohort study Participants: 3,825 Evidence: moderate
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The number of people living with dementia worldwide is growing. 3 key findings →
Design: meta-analysis Participants: 1,636 Evidence: high
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ADI groups differed by sex, ethnoracial background, and MMSE scores. 5 key findings →
Design: cohort study Participants: 755 Evidence: moderate
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High correlations between plasma and serum were observed for most assays (ρ > 0.8), though plasma often yielded higher concentrations. 5 key findings →
Participants: 100 Evidence: low
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The final study sample comprised 8,797 participants (53.5% women, mean age at HUNT4 77.8 [SD 6.2]). 5 key findings →
Participants: 8,797 Evidence: low
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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 →