Distinct gut microbial compositions are associated with dementia. 2 key findings →
Design: systematic review Participants: 896 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Distinct gut microbial compositions are associated with dementia. 2 key findings →
Design: systematic review Participants: 896 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Low baseline Aβ42/Aβ40 was significantly associated with increased amyloid accumulation (β = 0.257, 95% confidence interval (CI) 0.177-0.336, P < 0.001), and with higher risk of conversion to Aβ-PET positivity (Hazard ratio (HR) = 2.84, 95% CI 1.14-7.04, P = 0.025) and to MCI due to AD (HR = 3.25, 95% CI 1.17-9.01, P = 0.024). 5 key findings →
Design: longitudinal study Participants: 200 Evidence: moderate
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Among 1,528,885 adults with type 2 diabetes (mean age, 58 years; 49.2% women), GLP-1 receptor agonists plus metformin were associated with lower incidence of vascular dementia (HR, 0.46; 95% CI, 0.37-0.57), mild cognitive disorder (HR, 0.79; 95% CI, 0.66-0.95), and Alzheimer disease (HR, 0.46; 95% CI, 0.31-0.70). 5 key findings →
Design: cohort study Participants: 1,528,885 Evidence: moderate
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Alzheimer's disease (AD) is the leading cause of dementia and is characterized by progressive amyloid accumulation followed by tau-mediated neurodegeneration. 1 key finding →
Evidence: low
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The viral-inflammatory hypothesis of Alzheimer's disease offers a new paradigm, yet interventions like antivirals and vaccination present a paradox that challenge therapeutic development. 1 key finding →
Design: randomized controlled trial Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Aggregation of the protein tau defines tauopathies, the most common age-related neurodegenerative diseases, which include Alzheimer's disease and frontotemporal dementia. 1 key finding →
Evidence: low
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LIGHT will provide insight into the implementation and (cost-)effectiveness of a lifestyle intervention for indicated prevention in a memory clinic setting. 2 key findings →
Design: randomized controlled trial Evidence: high
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Across several cohorts, delirium is emerging as an important prognostic signal, independent of chronic markers of baseline morbidity, that identifies patients at markedly increased risk of death or future dementia. 5 key findings →
Design: cohort study Participants: 2,556 Evidence: moderate
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The clinical utility of plasma phosphorylated tau at threonine 217 (p-tau217) levels as a diagnostic tool for cognitive disorders in real-world settings remains uncertain. 5 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
Major depressive disorder (MDD) has been associated with an increased risk of cognitive decline and neurodegenerative disorders like Alzheimer's disease (AD), prompting interest in peripheral biomarkers related to amyloid metabolism as well as neuroaxonal and astroglial injury. 5 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
Baseline NfL and GFAP did not differ between patients with or without ARIA (ln[NfL] ECLIA 1.24 ± 0.38 pg/mL vs 1.25 ± 0.40 pg/mL, p = 0.77; ln[NfL] Simoa 2.87 ± 0.47 pg/mL vs 2.98 ± 0.40 pg/mL, p = 0.30, ln[GFAP] ECLIA 4.95 ± 0.36 pg/mL vs 4.88 ± 0.47 pg/mL, p = 0.69). 4 key findings →
Participants: 15 Evidence: low
Full summary, score breakdown and related studies → Original source
Comparing those having MCI, both CU and SCD participants had significantly lower amyloid PET standardized uptake value ratio (SUVR) (p < 0.001; p = 0.005). 4 key findings →
Participants: 66 Evidence: low
Full summary, score breakdown and related studies → Original source
Centiloid values significantly decreased from 52.3 ± 23.4 at baseline to - 5.6 ± 16.5 at follow-up, with a mean change of - 58.0 (p < 0.001). 5 key findings →
Participants: 12 Evidence: moderate
Full summary, score breakdown and related studies → Original source
These convergent data support a prospective clinical trial of low-dose lithium orotate to slow disease progression in MCI. 3 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source
Undiagnosed dementia is common and associated with increased mortality, identifying a vulnerable population missed by current diagnostic pathways. 3 key findings →
Design: cohort Participants: 13,142 Evidence: moderate
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Despite reductions in plasma p-tau217 with donanemab treatment, this biomarker cannot currently be used to accurately detect TRAC by PET (< 24.1 CL) in individuals with early symptomatic AD. 1 key finding →
Design: phase-3-trial Participants: 830 Evidence: null result
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Guidelines recommend limiting antipsychotic treatment to short-term use ( Methods Using UK primary care data from the Clinical Practice Research Datalink, linked with hospital and mortality data from Jan 1, 1998, to March 31, 2021, we emulated two sets of target trials, one after 12 weeks of antipsychotic treatment and another after 24 weeks of antipsychotic treatment, to compare continuing treatment versus tapering treatment and continuing treatment versus abrupt discontinuation of treatment. 3 key findings →
Design: cohort Participants: 24,822 Evidence: moderate
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The long-term efficacy of amyloid-targeting therapies hinges on their ability to slow downstream neuropathologic change, but little is known about the influence of amyloid clearance on tau pathology and neurodegeneration. 4 key findings →
Design: longitudinal study Evidence: high
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For VA and Medicare cohorts, dementia diagnosis was absent in 88.7% and 80.5%, respectively, of follow-up encounters in the other system. 5 key findings →
Design: cohort study Participants: 68,092 Evidence: moderate
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Overall, 92.7% of the original cohort members participated in at least one follow-up round and 87.2% participated in at least two (balanced by deworming treatment status). 4 key findings →
Design: longitudinal study Participants: 7,527 Evidence: high
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This cross-sectional study evaluates the performance of the US Food and Drug Administration–cleared phosphorylated tau 217 (p-tau217) to β-amyloid 42 ratio cut points used to detect amyloid pathology associated with Alzheimer disease. 1 key finding →
Design: cross-sectional Evidence: low
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A total of 322 participants with p-tau217, GFAP, and NfL analyses were stratified into the EOAD or FTD group based on their diagnosis. 5 key findings →
Design: cohort study Participants: 245 Evidence: moderate
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Baseline 18F-MK-6240 PET showed a minimal signal in CU participants, localized signal to the medial temporal lobe in participants with MCI, and a signal spanning the inferolateral temporal lobe and extending posteriorly along the ventral cortex in participants with AD. 5 key findings →
Design: longitudinal study Participants: 27 Evidence: moderate
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For detecting AD-dementia, the ensemble model achieved the area under the receiver operating characteristic curve (AUROC) of 0.943 (95% confidence interval, 0.906-0.980), 0.786 (95% confidence interval, 0.673-0.899), and 0.795 (95% confidence interval, 0.716-0.874) in the internal validation, External-1, and External-2, respectively. 4 key findings →
Design: case-control study Participants: 190 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
This study included 17,182 participants with a mean age of 69.2 ± 10.6 years, 59.2% of which were women. 5 key findings →
Design: cohort study Participants: 17,182 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. 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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% 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 →