28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Apolipoprotein E (apoE), a chaperone for the amyloid beta (Abeta) peptide, regulates the deposition and structure of Abeta that deposits in the brain in Alzheimer disease (AD). 3 key findings →
Evidence: low
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The term "aging-related tau astrogliopathy" (ARTAG) describes pathological accumulation of abnormally phosphorylated tau protein in astrocytes. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The ATP-binding cassette transporter A7 (ABCA7) has been identified as a susceptibility factor of late onset Alzheimer disease in genome-wide association studies. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
APOE-epsilon4 is associated with small vessel arteriolosclerosis, microinfarcts of the deep nuclei, neuritic senile plaque density, and amyloid angiopathy in patients with autopsy-proven Alzheimer disease (AD). 5 key findings →
Evidence: low
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Except for autosomal dominant early-onset families, genetic testing in asymptomatic individuals is unwarranted. 5 key findings →
Participants: 20 Evidence: low
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One of the major histopathological hallmarks of Alzheimer's disease (AD) is redundant senile plaques mainly composed of beta-amyloid (Abeta) aggregates. 5 key findings →
Participants: 19 Evidence: low
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These CSF A beta 42 findings are consistent with acceleration by the APOE*4 allele of pathogenic A beta 42 brain deposition starting in later middle age in persons with normal cognition. 2 key findings →
Evidence: low
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A generally similar pattern of cerebral hypometabolism was detected in APOE epsilon4-positive and -negative patients with Alzheimer disease. 4 key findings →
Evidence: low
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Among 124 876 cases and controls, genome-wide conjunction analyses of ALS, FTD, PD, AD, CBD, and PSP revealed significant genetic overlap between ALS and FTD at known ALS loci: rs13302855 and rs3849942 (nearest gene, C9orf72; P = .03 for rs13302855 and P = .005 for rs3849942) and rs4239633 (nearest gene, UNC13A; P = .03). 3 key findings →
Evidence: low
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Several studies, including genome wide association studies (GWAS), have strongly suggested a central role for the ATP-binding cassette transporter subfamily A member 7 (ABCA7) in Alzheimer's disease (AD). 3 key findings →
Evidence: low
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This study provides evidence to support that high Lp(a) concentrations was causally associated with an increased risk of large artery stroke but a decreased risk of small vessel stroke and Alzheimer disease. 5 key findings →
Participants: 696 Evidence: low
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Reproductive history events signaling more estrogen exposure such as premenopausal status, longer reproductive span, higher number of children, and use of HT and HC were associated with larger GMV in women in midlife. 4 key findings →
Evidence: low
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Lecanemab cleared amyloid-β in two-thirds and reduced the rate of cognitive and functional worsening in people with mild cognitive impairment and mild dementia due to Alzheimer disease in an 18-month double-blinded randomized placebo-controlled trial reported by van Dyck et al. 1 key finding →
Evidence: high
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A comparison of a randomized clinical trial of donepezil in AD patients and this observational study indicates that if appropriate methodological and statistical precautions are undertaken, then results from randomized clinical trials can be predictive with AD patients in clinical practice. 5 key findings →
Participants: 91 Evidence: high
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Recent trials of repetitive transcranial magnetic stimulation (rTMS) have reported encouraging results for improving or stabilizing cognition in patients diagnosed with Alzheimer dementia. 5 key findings →
Participants: 523 Evidence: high
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We hypothesize that the experimental group will be more effective in managing caregiver burden and coping strategies and that this will improve the perception of well-being, anxiety, and depression among caregivers. 4 key findings →
Design: randomized controlled trial Evidence: high
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As a safe and effective medicine, akatinol memantine, which has a similar effect as donepezil for AD, can remarkably improve the cognition, behavior, and mood of AD patients. 1 key finding →
Participants: 50 Evidence: low
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Alzheimer's disease is the leading cause of dementia. 5 key findings →
Evidence: low
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Increasing evidence suggests that vascular risk factors contribute to neurodegeneration, cognitive impairment and dementia. 2 key findings →
Evidence: low
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In an aging population with increasing incidence of dementia and cognitive impairment, strategies are needed to slow age-related decline and reduce disease-related cognitive impairment in older adults. 1 key finding →
Evidence: low
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Age-related hearing loss (ARHL) is a common problem for older adults, leading to communication difficulties, isolation, and cognitive decline. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Current evidence suggests that vascular factors, such as midlife hypertension, diabetes, and cerebrovascular disease, contribute significantly to the development of dementia and Alzheimer's disease, and that active engagement in mental, physical, and social activities may postpone the onset of dementia by providing cognitive reserve. 1 key finding →
Evidence: low
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Growing evidence supports a strong and likely causal association between cardiovascular disease (CVD), and its risk factors, with incidence of cognitive decline and Alzheimer's disease. 1 key finding →
Evidence: low
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Impaired exercise tolerance during formal testing is predictive of perioperative complications. 1 key finding →
Evidence: low
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Keeping these concentrations below the tolerance values prevents the development of manifest and subclinical signs of aluminum toxicity. 2 key findings →
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. 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 →