28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Vascular health had quantifiably greater impact on neurodegeneration in AD regions than on amyloid deposition. 3 key findings →
Design: longitudinal study Participants: 430 Evidence: moderate
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More-severe diabetes (defined by higher HbA 1c and longer disease duration) but not prediabetes or less-severe diabetes was associated with smaller brain volumes and an increased burden of brain vascular pathology. 3 key findings →
Design: cross-sectional Participants: 1,713 Evidence: low
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Our main findings were: (i) FDG-PET uptake in the bilateral anterior cingulate cortex and anterior temporal pole was associated with baseline global cognition in cognitively stable 80+ (the resilience signature); (ii) established Alzheimer's disease imaging biomarkers did not predict baseline global cognition in this subset of participants; (iii) in the full MCSA 80+ and ADNI cohorts, amyloid burden and FDG-PET in the resilience signature were the stronger predictors of baseline global cognition; (iv) sex and systemic vascular health predicted FDG-PET in the resilience signature, suggesting vascular health maintenance as a potential pathway to preserve the metabolism of these areas; and (v) the resilience signature provided significant information about global longitudinal cognitive change even when considering amyloid status in both the MCSA and ADNI cohorts. 1 key finding →
Design: longitudinal study Participants: 192 Evidence: moderate
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CSF Aβ42 levels are tightly coupled with cortical amyloid load in the earliest stages of preclinical AD, and begin to decrease dramatically prior to the point when an abnormal threshold of cortical accumulation is detected with amyloid imaging. 1 key finding →
Design: longitudinal study Participants: 164 Evidence: moderate
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Among the 174 participants (81 men [46.6%]; 93 women [53.4%]; mean [SD] age, 65.7 [8.9] years), a proportion (14%-17%) of individuals with neurodegeneration alone (SNAP) later demonstrated Aβ+. 1 key finding →
Design: cohort study Participants: 174 Evidence: moderate
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In 303 participants (mean [SD] age, 73.16 [5.19] years, 181 [60%] women, 96 [32%] non-Hispanic White, 113 [37%] Non-Hispanic Black, 94 [31%] Hispanic), baseline WMH volumes were associated with cortical thinning in medial temporal and frontal/parietal regions. 4 key findings →
Design: cohort study Participants: 303 Evidence: moderate
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White matter hyperintensities are associated with increased risk of dementia and cognitive decline. 5 key findings →
Participants: 2,367 Evidence: low
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The mean age was 70.9 years (standard deviation, 5.9), 57.2% were women, 40.6% were illiterate, and 88.3% were farmers. 2 key findings →
Participants: 5,765 Evidence: high
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Hearing impairment in older adults is independently associated in longitudinal studies with accelerated cognitive decline and incident dementia, and in cross-sectional studies, with reduced volumes in the auditory cortex. 5 key findings →
Design: cross-sectional Participants: 126 Evidence: moderate
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The prevalence of A+T+N+F+ profile was 66.24% in clinically diagnosed AD dementia patients; similarly, the majority of individuals with reduced FDG-PET were AD dementia subjects. 1 key finding →
Design: longitudinal study Participants: 551 Evidence: moderate
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Recent genetic and proteomic studies demonstrate that clusterin/apolipoprotein-J is associated with risk, pathology, and progression of Alzheimer's disease (AD). 5 key findings →
Design: longitudinal study Participants: 139 Evidence: moderate
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The amyloid/tau/neurodegeneration (A/T/N) framework uses cerebrospinal fluid (CSF) levels of total tau (tTau) as a marker of neurodegeneration and CSF levels of phosphorylated tau 181 (pTau181) as a marker of tau tangles. 4 key findings →
Design: cohort study Participants: 465 Evidence: moderate
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A total of 20 relevant studies involving 44,893 individuals were included in the analysis. 5 key findings →
Design: systematic review Participants: 42,955 Evidence: high
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An international working group from the Centres of Excellence in Neurodegeneration completed a structured process to develop definitions and imaging standards for markers and consequences of cerebral small vessel disease (SVD). 3 key findings →
Evidence: low
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Overall, memory worsened from age 30 years through the 90s. The HVa worsened gradually from age 30 years to the mid-60s and more steeply beyond that age. 5 key findings →
Design: cross-sectional Participants: 1,246 Evidence: low
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These factors should be investigated in longitudinal studies for their role in detecting onset of symptoms in AD. 1 key finding →
Design: longitudinal study Participants: 749 Evidence: moderate
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Amyloid accumulation was evaluated in 236 individuals who underwent >1 amyloid PET scan. 1 key finding →
Design: longitudinal study Participants: 236 Evidence: moderate
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This study suggests that early tau deposition may follow multiple trajectories during preclinical AD and may involve several cortical regions. 3 key findings →
Design: cross-sectional Participants: 447 Evidence: moderate
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Pericyte damage, reflected by CSF PDGFRβ, may be involved in age-related BBB disruption together with neuroinflammation, but is not related to Alzheimer-related pathologic changes. 2 key findings →
Participants: 408 Evidence: moderate
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We constructed models for MCI and mild dementia that predict MMSE over time. 1 key finding →
Design: longitudinal study Participants: 961 Evidence: moderate
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Vascular care in patients with Alzheimer disease with cerebrovascular lesions slows progression of WMLs. 2 key findings →
Participants: 123 Evidence: high
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44 participants were included: 20 PSEN1 E280A mutation carriers and 24 non-carriers. 2 key findings →
Participants: 44 Evidence: moderate
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Alzheimer's disease is the primary cause of dementia worldwide, with an increasing morbidity burden that may outstrip diagnosis and management capacity as the population ages. 5 key findings →
Participants: 417 Evidence: low
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Autosomal-dominant AD is associated with increased WMH well before expected symptom onset. 4 key findings →
Participants: 299 Evidence: low
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Brain atrophy with aging was observed in supratentorial and infratentorial areas, as well in primary motor, sensory, and heteromodal association regions. 1 key finding →
Design: longitudinal study Participants: 33 Evidence: moderate
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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.
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 →