28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
We demonstrated significant elevations in blood GFAP and YKL-40 levels in patients on the AD continuum compared with CU individuals. 5 key findings →
Design: systematic review Participants: 3,366 Evidence: high
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The main findings demonstrated an association between serum GFAP level and post-mortem tau pathology (β = 12.85; P < 0.001) that was independent of amyloid deposits (β = 13.23; P = 0.02). 5 key findings →
Design: cohort Participants: 139 Evidence: moderate
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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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Glymphatic failure may precede amyloid pathology, and predicts amyloid deposition, neurodegeneration, and clinical progression in AD. 2 key findings →
Design: cohort Participants: 419 Evidence: moderate
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This randomized clinical trial demonstrated the positive effects of rTMS on cognitive and functional performance, and the plastic changes in the hippocampal-cortical network. 5 key findings →
Participants: 30 Evidence: high
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These findings suggest medication-specific educational mailings targeting patients with AD or ADRD and their clinicians are not effective in reducing the use of high-risk medications. 4 key findings →
Design: open-label trial Participants: 787 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Differential diagnosis of dementia remains a challenge in neurology due to symptom overlap across etiologies, yet it is crucial for formulating early, personalized management strategies. 1 key finding →
Participants: 51,269 Evidence: low
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Variants of the gene triggering receptor expressed on myeloid cells-2 (TREM2) increase the risk of Alzheimer's disease (AD) and other neurodegenerative disorders. 4 key findings →
Design: clinical trial Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
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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Of 92 383 participants, 60 582 (65.6%) were women and the mean (SD) age was 56.4 (8.0) years. 3 key findings →
Design: cohort Participants: 92,383 Evidence: moderate
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US clinical practice guidelines for the diagnostic evaluation of cognitive impairment due to Alzheimer's disease (AD) or AD and related dementias (ADRD) are decades old and aimed at specialists. 5 key findings →
Design: systematic-review Evidence: high
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In this nationwide population-based study, SGLT2i use significantly reduced the risks of neurodegenerative disorders in patients with type 2 diabetes independent of various factors including comorbidities and bioclinical parameters. 5 key findings →
Design: cohort Participants: 358,862 Evidence: moderate
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The results of this cohort study suggest that hearing loss was associated with increased dementia risk, especially among people not using hearing aids, suggesting that hearing aids might prevent or delay the onset and progression of dementia. 5 key findings →
Design: cohort Participants: 573,088 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 this 3-year randomized clinical trial, ω-3 treatment was safe and well-tolerated but failed to reach significant reductions in WML accumulation or neuronal integrity breakdown among all participants, which may be attributable to sample size limitations. 5 key findings →
Participants: 102 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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Identifying concomitant Lewy body (LB) pathology through seed amplification assays (SAA) might enhance the diagnostic and prognostic work-up of Alzheimer's disease (AD) in clinical practice and trials. 2 key findings →
Design: cohort Participants: 795 Evidence: moderate
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Biological staging of individuals with Alzheimer's disease (AD) may improve diagnostic and prognostic workup of dementia in clinical practice and the design of clinical trials. 4 key findings →
Design: longitudinal study Participants: 426 Evidence: moderate
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This study aimed to evaluate the impact of APOE4 homozygosity on Alzheimer's disease (AD) by examining its clinical, pathological and biomarker changes to see whether APOE4 homozygotes constitute a distinct, genetically determined form of AD. 2 key findings →
Participants: 3,297 Evidence: low
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Peripheral glial fibrillary acidic protein (GFAP) and neurofilament light chain (NfL) are sensitive markers of neuroinflammation and neuronal damage. 4 key findings →
Design: cohort study Participants: 48,542 Evidence: moderate
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Alzheimer's disease is the leading cause of dementia worldwide, but the cellular pathways that underlie its pathological progression across brain regions remain poorly understood 1-3 . 4 key findings →
Participants: 48 Evidence: low
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Many coronavirus disease 2019 (COVID-19) positive individuals exhibit abnormal electroencephalographic (EEG) activity reflecting "brain fog" and mild cognitive impairments even months after the acute phase of infection. 5 key findings →
Design: systematic review Participants: 19 Evidence: high
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Our study suggests a possible utility of plasma Aβ42/40, P-tau181, and P-tau231 as a noninvasive biomarkers to assess amyloid copathology in DLB, and plasma GFAP and NfL as monitoring biomarkers for cognitive symptoms in DLB. 4 key findings →
Design: cohort study Participants: 89 Evidence: moderate
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Baseline plasma VEGFA and PGF each showed a significant interaction with amyloid burden on prospective cognitive decline. 5 key findings →
Design: longitudinal study Participants: 317 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.
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 →