28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Resting-state functional connectivity magnetic resonance imaging changes with progressing AD severity are similar between ADAD and LOAD. 2 key findings →
Design: cross-sectional Participants: 79 Evidence: moderate
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Lower plasma β-amyloid 42 and 42/40 levels have been associated with incident dementia, but results are conflicting and few have investigated cognitive decline among elders without dementia. 4 key findings →
Participants: 550 Evidence: low
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Poorer OI in older adults without dementia was associated with increased risk of dementia. 5 key findings →
Participants: 2,428 Evidence: low
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Twenty-two percent of the participants aged 75 years or older had MCI. 2 key findings →
Participants: 927 Evidence: moderate
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Among adults with Down syndrome, the striatum consistently accumulates amyloid earlier than the cortex when measured with PiB. 2 key findings →
Design: longitudinal study Participants: 175 Evidence: moderate
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There were insufficient data to make any recommendations regarding cognitive screening of asymptomatic individuals. 4 key findings →
Evidence: low
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We investigated the effects of matrix type and reagent batch changes on diagnostic performances and longitudinal trajectories of brain-derived tau (BD-tau). 4 key findings →
Design: longitudinal study Participants: 26 Evidence: moderate
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Interestingly, we found no consistent differences in learning and memory performance between high versus low PiB cognitively normal or amnestic MCI subjects. 5 key findings →
Evidence: low
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Among the 12 biomarkers, only pTau was higher in frail individuals than in their not-frail peers (471.3 ± 58.1 pg/mL vs. 451.9 ± 61.1 pg/mL, p = 0.022). 4 key findings →
Design: longitudinal study Participants: 313 Evidence: moderate
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Psychotic symptoms occur in ~40% of subjects with Alzheimer's disease (AD) and are associated with more rapid cognitive decline and increased functional deficits. 3 key findings →
Evidence: low
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HI is associated with increased risk of developing dementia in older adults. 3 key findings →
Evidence: high
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These results should be confirmed with a randomized clinical trial of a centrally active ACE inhibitor in the prevention of cognitive decline and dementia. 5 key findings →
Participants: 1,054 Evidence: high
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Symptomatic mutation carriers also demonstrated elevated tau PET binding in the basal ganglia, consistent with prior work with amyloid-β. 2 key findings →
Design: cross-sectional Evidence: low
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A biological research framework to define Alzheimer' disease with dichotomized biomarker measurement was proposed by National Institute on Aging-Alzheimer's Association (NIA-AA). 3 key findings →
Design: longitudinal study Evidence: moderate
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Here, we investigated if TAR-DNA-binding protein-43 (TDP-43), the disease protein in frontotemporal lobar degeneration and ubiquitin inclusions with or without motor neuron disease as well as amyotrophic lateral sclerosis, also formed inclusions in Lewy body (LB) disorders including Parkinson's disease (PD) without or with dementia (PDD), and dementia with LBs (DLB) alone or in association with Alzheimer's disease (AD). 3 key findings →
Evidence: low
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These results suggest that all adults with Down syndrome should be screened for Alzheimer's disease pathology starting shortly before age 40 years and considered for clinical trials. 1 key finding →
Design: longitudinal study Participants: 328 Evidence: moderate
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Well-authenticated biomarkers can provide critical insights into the biological basis of Alzheimer disease (AD) to enable timely and accurate diagnosis, estimate future burden and support therapeutic trials. 5 key findings →
Evidence: low
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These observations suggest that brain amyloid deposition results in low CSF Abeta(42), and that amyloid imaging and CSF Abeta(42) may potentially serve as antecedent biomarkers of (preclinical) AD. 2 key findings →
Evidence: low
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Plasma A beta levels are affected by age and by systemic and CNS vascular risk factors. 4 key findings →
Design: cross-sectional Participants: 55 Evidence: moderate
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Cerebrovascular disease is the second most common cause of acquired cognitive impairment and dementia and contributes to cognitive decline in the neurodegenerative dementias. 5 key findings →
Evidence: low
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Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are age-related neurodegenerative disorders with shared genetic etiologies and overlapping clinical and pathological features. 2 key findings →
Evidence: low
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Physicians noted impairment in a minority of impaired patients. 3 key findings →
Design: cross-sectional Participants: 1,107 Evidence: low
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In these older adults, associations of risk factors with a given cause of death were related to specific deficits in that same organ system. 2 key findings →
Design: cohort study Participants: 5,888 Evidence: moderate
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Among ACHIEVE participants in the top quartile of predicted risk, 3-year cognitive decline in the hearing intervention was 61.6% (95% confidence interval [CI]: 33.7%-94.1%) slower than the control. 5 key findings →
Participants: 2,692 Evidence: moderate
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Although amyloid imaging with PiB-PET ([C-11]Pittsburgh Compound-B positron emission tomography), and now with F-18-labeled tracers, has produced remarkably consistent qualitative findings across a large number of centers, there has been considerable variability in the exact numbers reported as quantitative outcome measures of tracer retention. 4 key findings →
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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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 (3.7% 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 →