27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Two longitudinal studies with different populations demonstrated that loneliness was a risk factor for the development of the pain, depression, and fatigue symptom cluster over time. 4 key findings →
Design: longitudinal study Participants: 115 Evidence: moderate
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Higher Abeta deposition is associated with greater longitudinal decline in mental status and verbal memory in the preceding years. 5 key findings →
Design: longitudinal study Participants: 57 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Slow gait speed has been shown to predict incident dementia and cognitive decline in older individuals. 1 key finding →
Design: longitudinal study Participants: 57,456 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The CHS has developed a methodology for longitudinal studies of dementia in large cohorts and represents the largest study of dementia including cognitive testing, MRI and genetic markers. 1 key finding →
Design: longitudinal study Participants: 5,888 Evidence: moderate
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Factors influencing survival in Alzheimer disease include race/ethnicity and comorbid diabetes and hypertension. 5 key findings →
Design: longitudinal study Participants: 323 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Growing evidence suggests that fine particulate matter (PM 2.5 ) likely increases the risks of dementia, yet little is known about the relative contributions of different constituents. 5 key findings →
Design: cohort study Evidence: moderate
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Study objectives Sleep duration has been associated with risk of dementia and stroke, but few studies have investigated the relationship between sleep duration and brain MRI measures, particularly in middle age. 3 key findings →
Design: prospective cohort Evidence: moderate
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MCI criteria perform poorly when applied to a representative population sample. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD), the most common cause of dementia, has long been associated with bacterial infections and inflammation-causing immunosenescence. 5 key findings →
Design: longitudinal study Participants: 108 Evidence: moderate
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Persistent pain was associated with accelerated memory decline and increased probability of dementia. 5 key findings →
Design: cohort study Evidence: moderate
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In persons with multimorbidity, there exists co-occurrence of diseases beyond chance, which clinicians need to take into account in their daily practice. 2 key findings →
Design: prospective cohort Participants: 1,099 Evidence: moderate
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Currently available literature shows limited information on aging in RGNDs, with relatively many reports of young-onset dementia. 2 key findings →
Design: longitudinal study Participants: 25 Evidence: moderate
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These findings add to the growing literature to suggest that the degree of functional impairment at baseline is an important predictor of conversion to dementia and may help explain differences in findings between epidemiological and clinic-based studies. 4 key findings →
Design: longitudinal study Participants: 28 Evidence: moderate
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These results demonstrate an important role of clusterin in the pathogenesis of AD and suggest that alterations in amyloid chaperone proteins may be a biologically relevant peripheral signature of AD. 4 key findings →
Design: longitudinal study Evidence: moderate
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Significantly more patients with MCI than without MCI at baseline (10 of 37 [27.0%] vs 1 of 145 [0.7%]; relative risk, 39.2 [95% CI, 5.2-296.5]; P Conclusions and relevance Mild cognitive impairment at PD diagnosis predicts a highly increased risk for early dementia. 1 key finding →
Design: cohort study Participants: 182 Evidence: moderate
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Low daytime SBP was independently associated with a greater progression of cognitive decline in older patients with dementia and MCI among those treated with AHDs. 5 key findings →
Design: cohort study Participants: 172 Evidence: moderate
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The prevalence of A+T+N+F+ profile was 66.24% in clinically diagnosed AD dementia patients; similarly, the majority of individuals with reduced FDG-PET were AD dementia subjects. 1 key finding →
Design: longitudinal study Participants: 551 Evidence: moderate
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Recent genetic and proteomic studies demonstrate that clusterin/apolipoprotein-J is associated with risk, pathology, and progression of Alzheimer's disease (AD). 5 key findings →
Design: longitudinal study Participants: 139 Evidence: moderate
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Identifying a clinical distinction between the invariably lethal prion disease Creutzfeldt-Jakob disease (CJD) and nonprion rapidly progressive dementias is important and sometimes difficult; thus, reliable tools for diagnosis are in great demand. 4 key findings →
Design: cohort study Participants: 30 Evidence: moderate
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The amyloid/tau/neurodegeneration (A/T/N) framework uses cerebrospinal fluid (CSF) levels of total tau (tTau) as a marker of neurodegeneration and CSF levels of phosphorylated tau 181 (pTau181) as a marker of tau tangles. 4 key findings →
Design: cohort study Participants: 465 Evidence: moderate
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This study aimed to examine whether baseline CSF measures of Alzheimer disease (AD)-related pathology are associated with the time to onset of mild cognitive impairment (MCI) and whether these associations differ by age, sex, Apolipoprotein E ( ApoE4 ) status, and proximal (≤7 years) vs distal (>7 years) time to symptom onset. 4 key findings →
Design: longitudinal study Participants: 273 Evidence: moderate
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The trajectories of core Alzheimer disease (AD) cerebrospinal fluid (CSF) biomarkers and the concurrent cognitive changes across the clinical spectrum remain unclear yet are important for clinical trial design. 4 key findings →
Design: cohort study Participants: 197 Evidence: moderate
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Prion diseases can mimic Alzheimer disease (AD) at presentation. 4 key findings →
Design: cohort study Participants: 345 Evidence: moderate
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To assess age-, sex-, and subtype-specific incidence rates of dementia and to calculate the risk of dementia, the authors performed a large, community-based, prospective cohort study on dementia as part of the Rotterdam Study. 4 key findings →
Design: cohort study Participants: 7,046 Evidence: moderate
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Atherosclerosis has been implicated in the development of dementia and its major subtypes, Alzheimer's disease and vascular dementia. 4 key findings →
Design: cohort study Participants: 6,647 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. 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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 →