32,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Participants age 60-85 years deemed cognitively unimpaired were disclosed an elevated or not elevated brain amyloid result by a certified clinician. 5 key findings →
Participants: 3,686 Evidence: high
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Cerebral amyloid deposition is associated with APOE4 carrier status in older healthy control subjects and symptomatic AD patients, and increases with age in older cognitively normal individuals. 3 key findings →
Participants: 245 Evidence: low
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From a total sample of 559 older adults from the Massachusetts Alzheimer's Disease Research Center longitudinal cohort, 454 were included in the primary analysis: 283 with clinically normal cognition (CN), 115 with mild cognitive impairment (MCI), and 56 with subjective cognitive concerns (SCC) but no objective impairment, a proposed transitional group between CN and MCI. 1 key finding →
Design: longitudinal study Evidence: moderate
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This study was designed to evaluate whether subjects with amyloid beta (Aβ) pathology, detected using florbetapir positron emission tomorgraphy (PET), demonstrated greater cognitive decline than subjects without Aβ pathology. 4 key findings →
Evidence: low
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ADNI participants (921 dyads) had a mean (SD) age of 71 (7) years and mean (SD) of 17 (3) years of education; 485 (53%) were female, 30 (3%) were Asian, 105 (11%) were Black, and 756 (82%) were White. eVAL participants (279 dyads) had a mean (SD) age of 71 (8) years and mean (SD) of 17 (2) years of education; 151 (54%) were female, 17 (6%) were Asian, 12 (4%) were Black, and 245 (88%) were White. 5 key findings →
Design: cross-sectional Participants: 921 Evidence: moderate
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Our objective was to investigate cross-sectional associations between odor identification ability and imaging biomarkers of neurodegeneration and amyloid deposition in clinically normal (CN) elderly individuals, specifically testing the hypothesis that there may be an interaction between amyloid deposition and neurodegeneration in predicting odor identification dysfunction. 1 key finding →
Design: cross-sectional Evidence: low
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The average detection rates for mild cognitive impairment is 0.08 (interquartile range=0.00-0.02) for both clinicians and practices, suggesting that only about 8% of expected cases were diagnosed on average. 3 key findings →
Participants: 25 Evidence: low
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The choroid plexus (ChP) is a major source of cerebrospinal fluid (CSF) production, with a direct and indirect role in protein clearance, and pathogenesis of Alzheimer's disease (AD). 3 key findings →
Participants: 509 Evidence: low
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Sex differences in Alzheimer's disease (AD) biology and progression are not yet fully characterized. 2 key findings →
Evidence: low
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Pathological hallmarks of Alzheimer's disease (AD) are deposits of amyloid beta (Aβ) and hyper-phosphorylated tau aggregates in brain plaques. 4 key findings →
Participants: 13 Evidence: low
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This approach to the detection of individuals at high risk for preclinical AD-identified in single CN individuals using this quantitative ADsig MRI biomarker-may provide investigators with a population enriched for AD pathobiology and with a relatively high likelihood of imminent cognitive decline consistent with prodromal AD. 3 key findings →
Evidence: low
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Older adults with subjective cognitive decline (SCD) in the absence of objective neuropsychological dysfunction are increasingly viewed as at risk for non-normative cognitive decline and eventual progression to Alzheimer's disease (AD) dementia. 3 key findings →
Evidence: low
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Cross-sectional data, including CSF analytes, molecular imaging of cerebral fibrillar β-amyloid (Aβ) with PET using the [ 11 C] benzothiazole tracer Pittsburgh compound B (PiB), MRI-based brain structures, and clinical/cognitive outcomes harmonized from 8 studies, collectively involving 3,284 cognitively normal individuals 18 to 101 years of age, were analyzed. 4 key findings →
Design: cross-sectional Evidence: low
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The AS task is a useful measure of executive function across the AD spectrum. 1 key finding →
Participants: 182 Evidence: low
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Research increasingly suggests that subjective cognitive decline (SCD) in older adults, in the absence of objective cognitive dysfunction or depression, may be a harbinger of non-normative cognitive decline and eventual progression to dementia. 3 key findings →
Evidence: low
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Tests of both episodic memory and executive function are predictors of time to progression from mild impairment to a clinical diagnosis of Alzheimer disease. 1 key finding →
Participants: 235 Evidence: low
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These results highlight the need to increase the overall detection rates of MCI and of dementia particularly in socioeconomically disadvantaged groups. 4 key findings →
Evidence: low
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Alzheimer's disease (AD) is a progressive age-related neurodegenerative disease. 1 key finding →
Evidence: low
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HRU and payments were overall similar between A4 and LEARN Medicare. 5 key findings →
Design: cohort Participants: 367 Evidence: early
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Affective symptoms are of prognostic utility, but interventions to prevent dementia syndromes are limited. 1 key finding →
Evidence: low
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In the Alzheimer's disease (AD) continuum, the prodromal state of mild cognitive impairment (MCI) precedes AD dementia and identifying MCI individuals at risk of progression is important for clinical management. 4 key findings →
Evidence: low
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Transcranial magnetic stimulation (TMS) is a powerful tool to probe in vivo brain circuits, as it allows to assess several cortical properties such asexcitability, plasticity and connectivity in humans. 1 key finding →
Evidence: low
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Three trajectory classes were identified: stable, slow decliners, and fast decliners. 4 key findings →
Design: longitudinal study Evidence: moderate
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Four thousand four hundred eighty-six participants were included (mean age 71.3 ± 4.7 years, 30% participants Aβ+, 59% female). 5 key findings →
Design: cross-sectional Evidence: moderate
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A decline in instrumental activities of daily living (IADL) correlates with the progression from mild cognitive impairment (MCI) to Alzheimer's disease (AD) dementia and has been associated with frontal and parietal hypometabolism, lower cerebrospinal fluid amyloid β 1-42 , and inferior temporal cortical thinning. 4 key findings →
Design: cross-sectional Evidence: low
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 32,180 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 32,180 records, built mostly from automated pulls of Europe PMC (66.5% of the library) and OpenAlex (15.8%), 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.
1,045 records (3.2% 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events
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