28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Little is known about the dysbiosis of the gut microbiome in patients with mild cognitive impairment (MCI) potentially at risk for the development of Alzheimer's disease (AD). 5 key findings →
Design: cross-sectional Participants: 14 Evidence: moderate
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< 0.001). Receiver operating characteristic (ROC) analysis identified right hippocampal MD and t-tau as optimal classifiers for AD. 4 key findings →
Design: cross-sectional Evidence: low
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Key markers and mechanisms were identified for each stage: initial neurophysiological deficits in SCD with compensatory metabolomic responses, gut-brain axis dysregulation in MCI, and extensive metabolic disruption and multisystem breakdown in AD. 5 key findings →
Participants: 277 Evidence: low
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We identified 8 brain structural features from 192 MRI features that were associated with the risk of MCI progressing to AD, including: left hippocampus, left inferior lateral ventricle, left amygdala, right middle temporal gyrus, left fusiform gyrus, right amygdala, left cortical total volume, and brain parenchyma total volume. 4 key findings →
Design: longitudinal study Participants: 947 Evidence: moderate
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Neurophysiological activity features and tau pet provided additional information to the clinical model when acquired up to ∼4 years prior to diagnosis, but their accuracy decreased at larger intervals. 5 key findings →
Design: longitudinal study Participants: 102 Evidence: moderate
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This innovative study aims to test the feasibility of iTBS as a cognitive enhancement strategy in MCI. 3 key findings →
Participants: 20 Evidence: high
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In amyloid PET–positive MCI, Ginkgo biloba use was associated with sustained clinical stability, reduced plasma Aβ oligomerization tendency, and attenuation of amyloid PET progression over 18 months. 2 key findings →
Design: cohort study Participants: 21 Evidence: moderate
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Triggering receptor expressed on myeloid cells 2 (TREM2) is a key immunomodulatory receptor broadly expressed on myeloid cells such as macrophages and microglia. 1 key finding →
Evidence: low
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Subgroups with slower versus faster neurodegeneration, despite similar pathological accumulation, were compared to assess associations with genetic/lifestyles. 4 key findings →
Design: longitudinal study Participants: 529 Evidence: moderate
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MDS varied significantly by age, sex, education, and language of administration even among participants with normal cognition. 5 key findings →
Participants: 25,330 Evidence: low
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This study analyzed 871 patients with cognitive impairment, 69.8% of whom were having functional impairment. 5 key findings →
Participants: 871 Evidence: low
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A significant median Centiloid reduction of 30.9 was observed, with a 24.1% amyloid PET negativity rate after six months. 3 key findings →
Participants: 42 Evidence: moderate
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At 3 years, donanemab slowed disease progression on the Clinical Dementia Rating Scale (CDR)-Sum of Boxes (CDR-SB) in early-start participants versus a weighted ADNI control (-1.2 points; 95 % confidence interval [CI], -1.7, -0.7). 5 key findings →
Evidence: high
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Whole-brain bm-CVR values were significantly associated with the diagnosis group of normal, MCI, and early dementia (β = -3.00%/mm Hg, 95% confidence interval (CI) [-5.42, -0.58]), and were lower in the impaired participants relative to participants with normal cognition (β = -2.18, CI [-3.91, -0.45]). 5 key findings →
Design: cohort study Participants: 36 Evidence: moderate
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BackgroundOdor identification deficits predict Alzheimer's disease (AD) in epidemiological studies. 5 key findings →
Design: cross-sectional Participants: 600 Evidence: low
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Long sleep was associated with reduced overall cognitive function (β ± standard error = -0.25 ± 0.07, p < 0.001), with strongest effects in those with depressive symptoms using (-0.74 ± 0.30, p = 0.017) and not using antidepressants (-0.60 ± 0.26, p = 0.024). 5 key findings →
Evidence: low
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High LDL-C (≥160 mg/dL) increased AD risk across all groups {hazard ratio (HR): 1.23 [95% confidence interval (CI): 1.10-1.38],p<0.001;HR: 1.45 (95% CI: 1.08-1.93),p=0.013;HR: 1.25 (95% CI: 1.10-1.42),p<0.001, respectively}, whereas low LDL-C (<70 mg/dL) showed higher VD risk in those not taking cholesterol-lowering medication [HR: 3.02 (95% CI: 1.73-5.27),p<0.001].Low HDL-C (≤40 mg/dL) was associated with increased AD and VD risk in non-users. 2 key findings →
Design: cohort study Evidence: moderate
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Midlife hearing loss was associated with smaller brain volumes, accelerated decline in executive function, accelerated accrual of white matter abnormalities, and a near doubling of dementia risk, suggesting a potential causal or biomarker role for midlife hearing loss in the prevention of late‐life dementia. 4 key findings →
Participants: 1,656 Evidence: low
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Elevated CKM risk level is significantly associated with increased risks of cognitive decline and dementia incidence. 3 key findings →
Participants: 426 Evidence: low
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During a median 13.7 years of follow-up, prediabetes (n=52,693) was associated with higher risks of vascular dementia (hazard ratio (HR):1.36; 95% confidence interval (CI): 1.14-1.61), stroke (HR:1.09; 95% CI: 1.01-1.16), ischemic stroke (HR:1.10; 95% CI: 1.02-1.19), and intracerebral hemorrhage (HR:1.19; 95% CI: 1.01-1.39) compared with normoglycemia, after adjustment for major confounding factors and across extensive sensitivity analyses. 5 key findings →
Participants: 52,693 Evidence: moderate
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Our findings indicate that liver fat mediates associations between cardiometabolic factors and WMHs and that WMHs mediate the association between liver fat and cognitive performance. 5 key findings →
Participants: 32,461 Evidence: moderate
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During a median 13.7 years of follow-up, prediabetes (n=52,693) was associated with higher risks of vascular dementia (hazard ratio (HR):1.36; 95% confidence interval (CI): 1.14-1.61), stroke (HR:1.09; 95% CI: 1.01-1.16), ischemic stroke (HR:1.10; 95% CI: 1.02-1.19), and intracerebral hemorrhage (HR:1.19; 95% CI: 1.01-1.39) compared with normoglycemia, after adjustment for major confounding factors and across extensive sensitivity analyses. 5 key findings →
Participants: 52,693 Evidence: moderate
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Increased phosphorylation of TDP-43 is a pathological hallmark of several neurodegenerative disorders, including amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). 2 key findings →
Evidence: low
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Amyotrophic Lateral Sclerosis (ALS) and Frontotemporal Dementia (FTD) are overwhelmingly linked to TDP-43 dysfunction. 5 key findings →
Evidence: low
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Hippocampal and serum irisin levels were progressively reduced in CCH mice. 5 key findings →
Participants: 212 Evidence: low
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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 →