30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
This fifteen-year study provides a large database of highly characterized individuals with longitudinal cognitive, imaging and lifestyle data and biofluid collections, to aid in the development of interventions to delay onset, prevent or treat AD. 1 key finding →
Design: cohort study Participants: 1,112 Evidence: moderate
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Dementia has been associated with COVID-19 prevalence, but whether this reflects higher infection, older age of patients, or disease severity remains unclear. 4 key findings →
Participants: 1,814 Evidence: moderate
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Data were drawn from the UK Biobank cohort study with a total of 228 223 participants with Hospital Episodes Statistics and primary care linkage health records. 4 key findings →
Design: cohort study Participants: 2,378 Evidence: moderate
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In this largely presymptomatic population, these results suggest subtle differences across plasma p-tau species and platforms for the prediction of amyloid and tau PET and magnetic resonance imaging measures of cerebrovascular and Alzheimer-related pathology. 5 key findings →
Participants: 1,329 Evidence: low
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We found that longitudinal changes in cognitive function measured by the cognitive composite decreased at low and high values of total sleep time (P < 0.001), time in non-REM (P < 0.001) and REM sleep (P < 0.001), sleep efficiency (P < 0.01) and <1 Hz and 1-4.5 Hz non-REM slow wave activity (P < 0.001) even after adjusting for age, CSF total tau/amyloid-β42 ratio, APOE ε4 carrier status, years of education and sex. 2 key findings →
Design: cross-sectional Participants: 100 Evidence: moderate
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Apolipoprotein E (APOE) ε4 is the single most important genetic risk factor for cognitive impairment and Alzheimer disease (AD), while lifestyle factors such as smoking, drinking, diet, and physical activity also have impact on cognition. 3 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In this Seminar, we highlight the main developments in the field of Alzheimer's disease. 2 key findings →
Evidence: low
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We found that severe COVID-19 infection, associated with a high mortality rate, might develop in a minority of fully vaccinated individuals with multiple co-morbidities. 5 key findings →
Design: cohort study Participants: 152 Evidence: moderate
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Plasma p-tau217 and p-tau181 were correlated (r=0·90, p diff =0·31) and in pathology-confirmed Alzheimer's disease (n=15, mean age 73 years [SD 12]) versus pathologically confirmed FTLD (n=68, mean age 67 years [SD 8]; AUC=0·96 [0·92-1·00] for p-tau217, AUC=0·91 [0·82-1·00] for p-tau181; p diff =0·22). 4 key findings →
Participants: 15 Evidence: low
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The category of neocortical LP according to the LPC system was associated with a 5.9 OR (p < 0.0001) of dementia in the 134 NBTR cases and a 3.14 OR (p = 0.0001) in the 202 UPBB cases. 2 key findings →
Participants: 202 Evidence: low
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Most studies have focused on dementia and suicidal behavior, with inconsistent results. 5 key findings →
Design: cohort study Participants: 21 Evidence: moderate
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Although the performance of the different methods still has room for improvement, the results are promising and this methodology has a great potential as a support tool for clinicians and healthcare professionals. 3 key findings →
Design: systematic review Evidence: high
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Older adults with cognitive disorders can learn smartphone-based memory strategies and doing so benefits prospective memory functioning and independence. 2 key findings →
Design: randomized controlled trial Evidence: high
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In this longitudinal study, we included 396 cognitively normal to dementia subjects with 18 F-Florbetapir/ 18 F-Florbetaben-amyloid-PET, 18 F-Flortaucipir-tau-PET and ~ 2-year cognitive follow-up. 1 key finding →
Design: longitudinal study Participants: 396 Evidence: moderate
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Patients with Alzheimer dementia from the Swedish Dementia Registry starting on ChEIs within 3 months of the dementia diagnosis were included and compared to nontreated patients with Alzheimer dementia. 4 key findings →
Participants: 11,652 Evidence: moderate
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Previous studies have suggested that the APOE ɛ4 allele plays a role in the risk and age at onset of dementia in DS; however, data on in vivo biomarkers remain scarce. 5 key findings →
Design: cohort study Evidence: moderate
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The 4417 participants in the study included 2618 women (59%) and had a mean (SD) age of 71.3 (4.7) years. 5 key findings →
Design: cross-sectional Participants: 2,618 Evidence: low
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Importantly, they suggest that these associations might be explained by a decrease of amyloidosis and tau-pathology. 2 key findings →
Design: cross-sectional Participants: 512 Evidence: moderate
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Worldwide, the prevalence of dementia is increasing and diet as a modifiable factor could play a role. 3 key findings →
Participants: 493,888 Evidence: moderate
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In 303 participants (mean [SD] age, 73.16 [5.19] years, 181 [60%] women, 96 [32%] non-Hispanic White, 113 [37%] Non-Hispanic Black, 94 [31%] Hispanic), baseline WMH volumes were associated with cortical thinning in medial temporal and frontal/parietal regions. 4 key findings →
Design: cohort study Participants: 303 Evidence: moderate
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These findings highlight substantial disparities in the timeliness and comprehensiveness of dementia diagnosis. 4 key findings →
Design: cross-sectional Participants: 993 Evidence: low
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Forty-eight studies from 18,456 screened abstracts (Dementia: n = 2,516, Control: n = 1,224) met inclusion criteria for the systematic review. 5 key findings →
Design: systematic review Participants: 2,516 Evidence: high
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The genetic basis of Lewy body dementia (LBD) is not well understood. 4 key findings →
Evidence: low
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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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Advanced glycation end products (AGEs) and their receptor (RAGE) are implicated in the pathophysiological processes of dementia and potentially underlie the association of diabetes with neurodegeneration. 4 key findings →
Design: cohort study Participants: 1,021 Evidence: moderate
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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.
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 30,580 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 30,580 records, built mostly from automated pulls of Europe PMC (64.7% of the library) and OpenAlex (16.6%), 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.
1,037 records (3.4% of the library) are not peer-reviewed — 964 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