27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
A rare variant in TREM2 (p.R47H, rs75932628) was recently reported to increase the risk of Alzheimer's disease (AD) and, subsequently, other neurodegenerative diseases, i.e. frontotemporal lobar degeneration (FTLD), amyotrophic lateral sclerosis (ALS), and Parkinson's disease (PD). 4 key findings →
Design: meta-analysis Participants: 828 Evidence: high
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Amyloid-beta 42 (Aβ42) and phosphorylated tau (pTau) levels in cerebrospinal fluid (CSF) reflect core features of the pathogenesis of Alzheimer's disease (AD) more directly than clinical diagnosis. 2 key findings →
Participants: 8,074 Evidence: low
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The diabetes attributable risk for dementia of 8.8% suggests that diabetes may have contributed to the clinical syndrome in a substantial proportion of all dementia patients. 2 key findings →
Design: cohort study Participants: 126 Evidence: moderate
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The average life expectancy has increased substantially in the past few decades in most industrialized countries; however, not all of the increased life expectancy is being spent in optimal health, especially among individuals with low socioeconomic status. 4 key findings →
Design: cohort study Participants: 135 Evidence: moderate
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Vascular cognitive impairment is an umbrella term for cognitive dysfunction associated with and presumed to be caused by vascular brain damage. 2 key findings →
Participants: 10,515 Evidence: low
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Vascular risk factors, such as type 2 diabetes, hypertension, obesity and dyslipidaemia often co-occur. 3 key findings →
Design: longitudinal study Participants: 14 Evidence: moderate
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After a median follow-up time of 14.3 (7.9-20.0) years, dementia was recorded in 530 (1.2%) individuals with type 1 diabetes and 1,867 (0.9%) age-, sex-, and county-matched control individuals (mean baseline age 33.0 [14.0] years). 4 key findings →
Design: cohort study Participants: 43,440 Evidence: moderate
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We conducted a genome-wide association study among 2,323 individuals with sporadic amyotrophic lateral sclerosis (ALS) and 9,013 control subjects and evaluated all SNPs with P < 1.0 x 10(-4) in a second, independent cohort of 2,532 affected individuals and 5,940 controls. 1 key finding →
Participants: 2,323 Evidence: moderate
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Sex differences in major cardiovascular risk factors for incident (fatal or non-fatal) all-cause dementia were assessed in the UK Biobank. 4 key findings →
Participants: 502,226 Evidence: low
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Eight candidate predictors entered the prediction model: bulbar versus non-bulbar onset (univariable hazard ratio [HR] 1·71, 95% CI 1·63-1·79), age at onset (1·03, 1·03-1·03), definite versus probable or possible ALS (1·47, 1·39-1·55), diagnostic delay (0·52, 0·51-0·53), forced vital capacity (HR 0·99, 0·99-0·99), progression rate (6·33, 5·92-6·76), frontotemporal dementia (1·34, 1·20-1·50), and presence of a C9orf72 repeat expansion (1·45, 1·31-1·61), all p Interpretation We have developed an externally validated model to predict survival without tracheostomy and non-invasive ventilation for more than 23 h per day in European patients with ALS. 1 key finding →
Participants: 1,936 Evidence: moderate
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Out of 929 patients, 184 (20%) experienced POD. 5 key findings →
Design: cohort study Participants: 929 Evidence: moderate
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Women's reproductive factors have been associated with the risk of dementia; however, these findings remain uncertain. 4 key findings →
Participants: 273,240 Evidence: low
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In this large cohort of older adults, long-term PM2.5 exposure was associated with increased dementia incidence. 3 key findings →
Participants: 541 Evidence: moderate
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An intronic GGGGCC repeat expansion in C9ORF72 is the most common cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), but the pathogenic mechanism of this repeat remains unclear. 3 key findings →
Evidence: low
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Only 11 putative risk factors for delirium are supported by either strong or moderate level of evidence. 1 key finding →
Evidence: low
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The prevalence and the degree of cerebral white matter lesions increased with age. 2 key findings →
Participants: 1,077 Evidence: low
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Amyotrophic lateral sclerosis is characterised by the progressive loss of motor neurons in the brain and spinal cord. 4 key findings →
Evidence: low
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Atherosclerotic lesions are known for their cellular heterogeneity, yet the molecular complexity within the cells of human plaques has not been fully assessed. 4 key findings →
Evidence: low
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White matter hyperintensities (WMHs) are frequently seen on brain magnetic resonance imaging scans of older people. 1 key finding →
Evidence: low
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Long-term exposure to PM 2.5 , NO 2 , and/or BC in Denmark were associated with mortality beyond cardiorespiratory diseases, including diabetes, dementia, psychiatric disorders, asthma, and ALRI. 5 key findings →
Participants: 803,881 Evidence: moderate
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Microglia and complement can mediate neurodegeneration in Alzheimer's disease (AD). 4 key findings →
Evidence: low
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The study included 356,173 participants (median age 56 years; 53.69% female). 5 key findings →
Participants: 356,173 Evidence: low
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Participants were 60 (range 44-74) years old with 38 (30-51) years' T1D duration. 3 key findings →
Participants: 373 Evidence: moderate
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Sex or gender differences in the risk of Alzheimer's disease and related dementias (ADRD) differ by world region, suggesting that there are potentially modifiable risk factors for intervention. 1 key finding →
Evidence: low
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Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease that results in progressive loss of bulbar and limb function. 2 key findings →
Participants: 100,000 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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% 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 →