28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
All concurrent validity correlations followed the expected directionality, with 19/21 inter-scale correlations in the total sample reaching statistical significance (p<0.05), and 17/21 reaching at least a low correlation (0.3). 4 key findings →
Participants: 100 Evidence: low
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In 2021, global mortality from AD and other dementias among individuals aged 60 and older reached approximately 1,922,970.75 cases (95% CI: 480,348.08 to 5,104,315.95), and the prevalence was 52,560,253.51 cases (95% CI: 41,399,948.84 to 65,633,448.71). 5 key findings →
Evidence: moderate
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Thirty-three studies were included, most published after 2019 (72.7%). 5 key findings →
Design: cross-sectional Evidence: moderate
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Despite comprising the largest segment of the sexual minority population and experiencing unique stressors and health disparities, bi+ dementia caregivers remain underrepresented in health and caregiving research. 3 key findings →
Design: cross-sectional Participants: 125 Evidence: low
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Participants in the study had an average age of 85.4 ± 7.1 years. 5 key findings →
Design: cross-sectional Evidence: low
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In 2022, among a total of 2 189 231 Medicare beneficiaries aged 45 to 64 years, 71 092 (3.25%) received a diagnosis of YOD. 5 key findings →
Design: cross-sectional Evidence: low
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Higher offspring education (> 12 years) was associated with higher baseline cognitive scores and faster cognitive decline. 5 key findings →
Participants: 17,484 Evidence: low
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Among a cohort comprising 109,778 individuals, the use of GLP-1RA demonstrated a reduced risk of dementia compared with its non-use (aHR, 0.90; 95% CI, 0.83-0.97). 4 key findings →
Participants: 109,778 Evidence: moderate
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The global age-standardized prevalence of AD and other dementias increased from 672 (95% uncertainty interval: 589 to 764) per 100,000 population in 1990 to 694 (603 to 794) per 100,000 population in 2021, with AAPCs of 0.09% (95% confidence interval: 0.06% to 0.11%). 5 key findings →
Evidence: low
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The early and accurate diagnosis of Alzheimer's Disease and Frontotemporal Dementia remains a critical challenge, particularly with traditional machine learning models which often fail to provide transparency in their predictions, reducing user confidence and treatment effectiveness. 5 key findings →
Evidence: low
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Lewy body dementia is the second most common form of neurodegenerative dementia, following Alzheimer's disease. 5 key findings →
Evidence: low
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At baseline, participants were aged 70-95 years (mean: 75.2 ± 4.3), with 54% being women. 5 key findings →
Evidence: moderate
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This review covers recent advances (2023-2024) in neuroimaging research into the pathophysiology, progression, and treatment of Alzheimer's disease (AD) and related dementias (ADRD). 5 key findings →
Evidence: low
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During wakefulness, neuromodulators operate largely independently to support behavior and cognition. 5 key findings →
Evidence: low
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Plasma from individuals with a higher WMH burden was associated with increased BBB disruption in hBMEC. 5 key findings →
Participants: 155 Evidence: low
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In mid-life, the sample sizes ranged from 4100 in 2022 to 5589 in 2017-18 and in late-life from 2799 in 2011-12 to 3762 in 2017-18. 5 key findings →
Design: cross-sectional Evidence: low
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Higher GCA was associated with lower dementia risk (hazard ratio = 0.865, 95% confidence interval = 0.756 to 0.990). 5 key findings →
Evidence: low
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Novel insights into Alzheimer's disease through the study of individuals with Down syndromePeople with Down syndrome (DS) represent the largest genetically defined population at risk for Alzheimer's disease (AD). 1 Virtually all adults with DS develop AD neuropathology by midlife due to triplication of the amyloid precursor protein (APP) gene on chromosome 21.As medical advances and social integration have extended life expectancy into the 60s, AD has emerged as the major determinant of cognitive decline, morbidity, and mortality in this DS population. 2 What was once viewed as an inevitable consequence of aging in DS is now recognized as a unique scientific opportunity to uncover the earliest events that drive AD.The predictable and accelerated course of DS-associated AD (DSAD) provides an unparalleled window into the molecular and cellular origins of amyloid and tau pathology, neuroinflammation, cerebrovascular pathology, and neurodegeneration. 1 key finding →
Design: longitudinal study Evidence: moderate
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These findings provide no evidence of a group-level Alzheimer-related p-tau217 elevation in young people with DSRD and support DSRD as a condition distinct from Alzheimer’s disease. 5 key findings →
Design: longitudinal study Participants: 132 Evidence: moderate
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In bvFTD patients, longer interoceptive-ACWs than controls were observed in the bilateral fronto-temporal and parietal regions. 5 key findings →
Evidence: low
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We show reduced fiber cross-section in LBD versus PD, and increased concentrations of plasma neurofilament light chain and p-tau217; with p-tau217 and fiber cross-section associated with cognition. 5 key findings →
Participants: 47 Evidence: low
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Of the 1388 studies identified, 70 met the inclusion criteria for this review. 5 key findings →
Design: cohort study Evidence: high
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• SCD patients showed attenuation of sensory (P1, N1, P2) and cognitive (P300, P600, P900) components, with performance-related gains. • MCI patients exhibited neural compensations, reversing the downward trend observed in SCD, which resulted in a non-monotonic pattern of ERPs. • The progression of cognitive decline was linked to electrophysiological discontinuity, suggesting resilience mechanisms in both low and higher order cognitive regions. 5 key findings →
Participants: 178 Evidence: moderate
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Of the participants, 25, 92, and 61 were classified as cognitively normal, with mild cognitive impairment, and with dementia, respectively. 5 key findings →
Design: cohort study Evidence: moderate
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SSRI treatment showed no significant effect on AD dementia progression (hazard ratio = 1.64, 95% confidence interval: 0.61 to 4.38) or cognitive trajectories, regardless of AD pathology. 5 key findings →
Design: longitudinal study 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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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 →