The 172 total participants had a mean (SD) age of 75.7 (4.8) years, and 108 (62.8%) were women. 4 key findings →
Participants: 172 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
28,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
The 172 total participants had a mean (SD) age of 75.7 (4.8) years, and 108 (62.8%) were women. 4 key findings →
Participants: 172 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
p75 neurotrophin receptor (p75 NTR ) signaling pathways substantially overlap with degenerative networks active in Alzheimer disease (AD). 2 key findings →
Participants: 242 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
With the emergence of Alzheimer's disease (AD) disease-modifying therapies, identifying patients who could benefit from these treatments becomes critical. 1 key finding →
Participants: 1,422 Evidence: moderate
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Fifty-one AD patients enrolled, mean age 73.5. 4 key findings →
Design: clinical trial Evidence: high
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Participants receiving CDCM showed significantly fewer behavioral and psychological symptoms (adjusted mean difference [AMD] in NPI score, -10.26 [95% CI, -16.95 to -3.58]; P = .003; Cohen d, -0.78 [95% CI, -1.09 to -0.46]), better mental health (AMD in SF-12 Mental Component Summary score, 2.26 [95% CI, 0.31-4.21]; P = .02; Cohen d, 0.26 [95% CI, -0.11 to 0.51]), and lower caregiver burden (AMD in BIZA-D score, -0.59 [95% CI, -0.81 to -0.37]; P Conclusions and relevance In this secondary analysis of a cluster randomized clinical trial, CDCM was associated with improved patient, caregiver, and health system-relevant outcomes over 36 months beyond the intervention period. 3 key findings →
Design: RCT Participants: 428 Evidence: high
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GRN mutations cause progranulin haploinsufficiency, which eventually leads to frontotemporal dementia (FTD-GRN). 4 key findings →
Design: clinical trial Evidence: moderate
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At 6 months, compared with usual care, participants receiving the intervention had better QOL (QOL-AD score, 0.09 [95% CI, -0.63 to 0.82] vs -0.88 [95% CI, -1.62 to -0.13]; treatment effect estimate, 0.97; 95% CI, 0.07-1.86; P = .03). 4 key findings →
Participants: 612 Evidence: high
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In the discovery cohort, the mean (SD) age was 70.9 (8.5) years, 191 (58%) were male, the mean (SD) MMSE score was 27.1 (1.9), and 110 individuals with MCI (33%) converted to dementia (71 to AD dementia). 4 key findings →
Design: cohort study Participants: 110 Evidence: moderate
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Brain clocks, which quantify discrepancies between brain age and chronological age, hold promise for understanding brain health and disease. 4 key findings →
Participants: 5,306 Evidence: low
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Neurofilament proteins have been validated as specific body fluid biomarkers of neuro-axonal injury. 5 key findings →
Design: longitudinal study Evidence: moderate
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The study consisted of 20 400 patients (9264 female [45.4%]; 1576 Black [7.7%], 3944 Latinx [19.3%], and 10 480 White [51.4%]), including 5100 patients with mTBI (median [IQR] age, 36.0 [25.0-51.0] years), 5100 patients with msTBI (median [IQR age, 35.0 [25.0-52.0] years), and 10 200 matched patients in the control group (median [IQR] age, 36.0 [25.0-51.0] years). 5 key findings →
Design: cohort study Participants: 400 Evidence: moderate
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In this cohort and MR study of UK Biobank participants, cataracts were associated with increased risk of dementia, especially vascular dementia, and reduced total brain volumes. 5 key findings →
Design: cohort Participants: 304,953 Evidence: moderate
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Anti-amyloid treatments for early symptomatic Alzheimer disease have recently become clinically available in some countries, which has greatly increased the need for biomarker confirmation of amyloid pathology. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Parkinson's disease and dementia with Lewy bodies are currently defined by their clinical features, with α-synuclein pathology as the gold standard to establish the definitive diagnosis. 5 key findings →
Evidence: low
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The epidemiology of Parkinson's disease shows marked variations in time, geography, ethnicity, age, and sex. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In the new AA diagnostic criteria, AD can be defined clinically as encompassing cognitively normal people having a core 1 AD biomarker. 5 key findings →
Evidence: low
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The results underscore the impact of education on brain structure and function in LA, highlighting the importance of incorporating educational factors into diagnosing, care, and prevention, and emphasizing the need for global diversity in research. 5 key findings →
Participants: 1,412 Evidence: low
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Impaired cerebral glucose metabolism is a pathologic feature of Alzheimer's disease (AD), with recent proteomic studies highlighting disrupted glial metabolism in AD. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Phase 3 (NIH stage 1B) is a feasibility randomized controlled trial of the intervention versus the Health Education Program control. 2 key findings →
Design: randomized controlled trial Participants: 28 Evidence: high
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Two of every three persons living with dementia reside in low- and middle-income countries (LMICs). 5 key findings →
Evidence: low
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Among 9239 eligible respondents, 5258 (57.7%) were female and 1210 (9.1%) were Black, 574 (4.7%) were Hispanic, and 7297 (84.4%) were White. 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Disease staging, whereby the spatial extent and load of brain pathology are used to estimate the severity of Alzheimer disease (AD), is pivotal to the gold-standard neuropathological diagnosis of AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) pathology is defined by β-amyloid (Aβ) plaques and neurofibrillary tau, but Lewy bodies (LBs; 𝛼-synuclein aggregates) are a common co-pathology for which effective biomarkers are needed. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Tauopathies are age-associated neurodegenerative diseases whose mechanistic underpinnings remain elusive, partially due to a lack of appropriate human models. 1 key finding →
Evidence: early
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Higher levels of neuroinflammation, neurodegeneration, and synaptic dysfunction in older adults were attenuated in KL-VS HET . 4 key findings →
Participants: 122 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 28,980 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 28,980 records, built mostly from automated pulls of Europe PMC (62.8% of the library) and OpenAlex (17.6%), 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.
1,038 records (3.6% of the library) are not peer-reviewed — 966 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 →