28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Use of pharmacological treatments is one possible modifiable risk factor for cognitive disorders. 5 key findings →
Design: case-control study Participants: 282,858 Evidence: moderate
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There is a lower prevalence of diagnosed probable AD in patients taking 2 different 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors-lovastatin and pravastatin.
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A subset of a dementia subgroup with characteristics predominantly associated with DM-related factors may underlie a pathophysiology different from AD, although these patients were clinically diagnosed as having AD. 4 key findings →
Design: longitudinal study Participants: 175 Evidence: moderate
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Among the 30 boxers, 11 were found to be normal (CBI score=0), 12 showed mild deficits (CBI score=1-2), 4 were moderately impaired (CBI score=3-4), and 3 showed signs of severe impairment (CBI score > 4). 3 key findings →
Evidence: low
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Inheritance of the APOE epsilon4 allele is associated with increased risk of late posttraumatic seizures. 5 key findings →
Participants: 106 Evidence: moderate
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Alzheimer disease (AD), a progressive and neurodegenerative disease, is the most common form of dementia with high incidence in elderly people. 1 key finding →
Evidence: low
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Higher phosphatidylcholine intake was associated with lower risk of incident dementia and better cognitive performance in men in eastern Finland. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Age-related hearing loss (ARHL) is the most prevalent sensory deficit in the elderly. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
A link between Alzheimer's disease (AD) and metabolic disorders has been established, with patients with type 2 diabetes at increased risk of developing AD and vice versa. 2 key findings →
Evidence: low
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The amount of attention to age-related hearing loss (ARHL) has been growing, not only from the perspective of being one of the most common health conditions affecting older adults, but also from the perspective of its relation to cognition. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Physical inactivity has recently been identified as a major and independent risk factor for the development of dementia and cognitive decline. 1 key finding →
Evidence: low
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Age-related hearing impairment (ARHI, also known as presbycusis) is potentially a reversible risk factor for dementia and Alzheimer disease (AD). 2 key findings →
Evidence: high
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Western countries are experiencing aging populations and increased longevity; thus, the incidence of dementia and Alzheimer's disease (AD) in these countries is projected to soar. 5 key findings →
Evidence: low
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Delirium is a debilitating form of brain dysfunction frequently encountered in the intensive care unit (ICU). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Noncommunicable disease now contributes to the World Health Organization top 10 causes of death in low-, middle- and high-income countries. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Diabetes is associated with cognitive dysfunction and an increased risk of dementia. 2 key findings →
Evidence: low
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The World Health Organization reports that 47.5 million people are affected by dementia worldwide. 2 key findings →
Evidence: low
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We determined the relationship between apolipoprotein (Apo)E, MRI, and low cognitive scores. 1 key finding →
Evidence: low
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Prevalence, 3-year incidence, and types of dementia are comparable in Black and White elderly in the Piedmont area of North Carolina. 3 key findings →
Participants: 4,136 Evidence: low
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The incidence of obesity in middle age is increasing markedly, and in parallel the prevalence of metabolic disorders including cardiovascular disease and type II diabetes is also rising. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
After adjusting for sex, years of education, smoking status, diabetes, hypertension, apolipoprotein E ε4 carriership, and hearing rehabilitation (defined as hearing aid or cochlear implant use), neither PTA (hazard ratio [HR] per 10-decibels hearing level increase of 0·99 (95% CI 0·89-1·12; p=0·91) nor WRS (HR per 10% decrease of 0·98, 95% CI 0·89-1 ·07; p=0·65) was significantly associated with the development of dementia. 3 key findings →
Evidence: low
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A growing body of evidence supports an intriguing clinical/epidemiological connection between Alzheimer disease (AD) and type 2 diabetes (T2D). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Moderately elevated plasma total homocysteine (tHcy) is a strong modifiable risk factor for vascular dementia and Alzheimer's disease. 2 key findings →
Evidence: low
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Metabolic disorders and aging promote accumulation of amylin amyloid in the cerebrovascular system and gray matter, altering microvasculature and tissue structure. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Macroautophagy/autophagy failure with the accumulation of autophagosomes is an early neuropathological feature of Alzheimer disease (AD) that directly affects amyloid beta (Aβ) metabolism. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
10 of the 3,281 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
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 →