27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
This study found that a commercially available plasma p-tau217 immunoassay accurately identified biological AD, comparable with results using CSF biomarkers, with reproducible cut-offs across cohorts. 3 key findings →
Design: cohort Participants: 786 Evidence: high
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An unresolved question for the understanding of Alzheimer's disease (AD) pathophysiology is why a significant percentage of amyloid-β (Aβ)-positive cognitively unimpaired (CU) individuals do not develop detectable downstream tau pathology and, consequently, clinical deterioration. 5 key findings →
Design: cohort Participants: 1,016 Evidence: moderate
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Dementia and MCI are associated with neuropsychiatric symptoms in clinical samples. 4 key findings →
Design: cohort study Participants: 138 Evidence: moderate
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We found a sequence to pathological changes, with rates of Aβ deposition in mutation carriers being significantly different from those in non-carriers first (across regions that showed a significant difference, at a mean of 18·9 years [SD 3·3] before expected onset), followed by hypometabolism (14·1 years [5·1] before expected onset), and lastly structural decline (4·7 years [4·2] before expected onset). 2 key findings →
Design: longitudinal study Participants: 346 Evidence: moderate
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The most common anticholinergic classes used were tricyclic antidepressants, first-generation antihistamines, and bladder antimuscarinics. 4 key findings →
Design: cohort study Participants: 3,434 Evidence: moderate
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Compelling experimental evidence suggests that microglial activation is involved in the spread of tau tangles over the neocortex in Alzheimer's disease (AD). 4 key findings →
Design: longitudinal study Participants: 130 Evidence: moderate
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An estimated 8.8 million Indians older than 60 years have dementia. 2 key findings →
Design: longitudinal study Participants: 2,528 Evidence: moderate
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Of 236 eligible participants screened, 43 were excluded. 2 key findings →
Design: longitudinal study Participants: 142 Evidence: high
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The results from utilization of the UDS highlight the possibility for numerous research institutions to successfully collaborate, produce, and use standardized data collection instruments for over a decade. 2 key findings →
Design: longitudinal study Participants: 4,820 Evidence: moderate
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Circulating NfL and GFAP may, independently and jointly, provide useful clinical insight regarding dementia risk and prognosis. 4 key findings →
Design: cohort Participants: 1,712 Evidence: moderate
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Older adults with CVD other than stroke had a higher risk of dementia and AD than did those without CVD. 5 key findings →
Design: cohort study Participants: 3,602 Evidence: moderate
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Compared with abstention, consumption of 1 to 6 drinks weekly is associated with a lower risk of incident dementia among older adults. 5 key findings →
Design: cohort study Participants: 5,888 Evidence: moderate
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Compared with no sensory impairment, DSI was associated with increased risk of all-cause dementia (hazard ratio [HR], 2.60; 95% CI, 1.66-2.06; P Conclusions and relevance In this cohort study, DSI was associated with increased risk of dementia, particularly AD. 5 key findings →
Design: cohort study Participants: 5,888 Evidence: moderate
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Our findings suggest that clinicians should consider sedative-associated, hypoxic, and septic delirium, which often co-occur, as distinct indicators of acute brain injury and seek to identify all potential risk factors that may impact on long-term cognitive impairment, especially those that are iatrogenic and potentially modifiable such as sedation. 2 key findings →
Design: cohort study Participants: 1,048 Evidence: moderate
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EDIC participants had consistently higher brain age values compared with controls without diabetes, indicative of approximately 6 additional years of brain aging (EDIC participants: β, 6.16; SE, 0.71; control participants: β, 1.04; SE, 0.04; P Conclusions and relevance The findings of this study suggest an increase in brain aging among individuals with T1D without any early signs of AD-related neurodegeneration. 4 key findings →
Design: cohort study Participants: 416 Evidence: high
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The analytic cohort included 2488 black and white older adults with repeated depressive symptom assessments from baseline to year 5 who were free of dementia throughout that period. 4 key findings →
Design: prospective cohort Participants: 1,322 Evidence: moderate
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ADNI has demonstrated the feasibility and utility of multicenter PET studies and is helping to clarify the role of biomarkers in the study of aging and dementia. 3 key findings →
Design: longitudinal study Participants: 100 Evidence: moderate
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The APOE*E4 allele of the gene for apolipoprotein E (APOE) has been reported as a risk factor for Alzheimer disease (AD) to varying degrees in different ethnic groups. 1 key finding →
Design: cohort study Participants: 4,450 Evidence: moderate
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Use of NSAIDs was associated with a lower risk of dementia (adjusted hazard ratio or aHR 0.76, 95% CI or CI 0.60-0.96) and, in particular, AD (aHR 0.63, CI 0.45-0.88), but not VaD (aHR 0.92, CI 0.65-1.28). 3 key findings →
Design: cohort study Participants: 3,229 Evidence: moderate
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Over follow-up, 449 (18.3%) participants developed dementia. 2 key findings →
Design: cohort study Evidence: moderate
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This cohort study found that COVID-19 mortality decreased over time during 2020 and that patient demographic characteristics and comorbidities were associated with higher clinical severity. 5 key findings →
Design: cohort study Participants: 174 Evidence: moderate
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Among 112 study participants with MCI, mean (SD) age was 76.6 (6.9) years, 55 were women (49.1%), and 27 progressed to dementia (24.1%), with an incidence rate of 121 per 1000 person-years. 3 key findings →
Design: cohort study Participants: 112 Evidence: moderate
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Brain iron elevation is implicated in Alzheimer's disease (AD) pathogenesis, but the impact of iron on disease outcomes has not been previously explored in a longitudinal study. 3 key findings →
Design: longitudinal study Evidence: moderate
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A total of 716 individuals were included in the analysis: 413 cognitively unimpaired (CU) participants (58.6% female; mean age = 70.6 years, SD = 7.9) and 303 cognitively impaired (CI) participants (54.7% female; mean age = 73.2 years, SD = 7.4). 5 key findings →
Design: longitudinal study Participants: 716 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Across the brain, people with Down syndrome had greater concentrations of tau for a given level of amyloid compared with people with autosomal-dominant Alzheimer's disease. 3 key findings →
Design: cohort study Participants: 137 Evidence: moderate
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 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 →