The study included 356,173 participants (median age 56 years; 53.69% female). 5 key findings →
Participants: 356,173 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
32,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
The study included 356,173 participants (median age 56 years; 53.69% female). 5 key findings →
Participants: 356,173 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
< 0.01). Using an operationalization of clinical criteria for LATE, 8.2% of participants with MCI or dementia from our tertiary memory clinic were classified as Possible-LATE, Probable-LATE, or LATE-AD. 4 key findings →
Design: longitudinal study Evidence: moderate
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Aging and age-related diseases share convergent pathways at the proteome level. 1 key finding →
Participants: 43,616 Evidence: moderate
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In ARIC (n = 1,736, mean age 63, 58.8% female, 48.7% non-Hispanic White individuals, median follow-up 18.6 years), the dementia incidence rate was 10.4 (95% CI, 9.2-11.6) per 1,000 person-years. 5 key findings →
Design: cohort study Participants: 1,736 Evidence: moderate
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Accurate and automated methods for measuring the thickness of human cerebral cortex could provide powerful tools for diagnosing and studying a variety of neurodegenerative and psychiatric disorders.
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Early microglial accumulation in Alzheimer's disease (AD) delays disease progression by promoting clearance of beta-amyloid (Abeta) before formation of senile plaques.
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Previously derived polygenic risk scores (PRSs) for Alzheimer's disease (AD) perform inconsistently across diverse ancestries. 3 key findings →
Design: cohort Evidence: high
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Disease staging, whereby the spatial extent and load of brain pathology are used to estimate the severity of Alzheimer disease (AD), is pivotal to the gold-standard neuropathological diagnosis of AD. 5 key findings →
Evidence: low
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The extent to which the pathophysiology of autosomal dominant Alzheimer's disease corresponds to the pathophysiology of 'sporadic' late onset Alzheimer's disease is unknown, thus limiting the extrapolation of study findings and clinical trial results in autosomal dominant Alzheimer's disease to late onset Alzheimer's disease. 3 key findings →
Participants: 559 Evidence: low
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D-CAA M + showed greater age-dependent FLR PiB retention (p - , and serially imaged asymptomatic M + demonstrated greater longitudinal increases (p = 0.004). 3 key findings →
Design: longitudinal study Evidence: moderate
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Our results reveal a spatial association between the epileptogenic focus and tau deposition, amyloid deposition, and neurodegeneration in early clinical stages of AD. 5 key findings →
Design: cross-sectional Evidence: low
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Identifying individuals at risk for developing Alzheimer disease (AD) is of utmost importance. 5 key findings →
Evidence: low
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A new secondary prevention trial in older people with amyloid accumulation at high risk for Alzheimer's disease dementia should provide insights into whether anti-amyloid therapy can delay cognitive decline. 1 key finding →
Evidence: low
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The incidence of stroke and dementia are diverging across the world, rising for those in low- and middle-income countries and falling in those in high-income countries. 3 key findings →
Evidence: low
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Neurocognitive disorders--including delirium, mild cognitive impairment and dementia--are characterized by decline from a previously attained level of cognitive functioning. 1 key finding →
Evidence: low
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Systemic inflammation is associated with ischemia and Alzheimer disease (AD). 3 key findings →
Design: cross-sectional Evidence: low
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DCTclock discriminates between diagnostic groups and improves upon traditional cognitive tests for detecting biomarkers of amyloid and tau pathology in CN older adults. 3 key findings →
Participants: 300 Evidence: low
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A hexanucleotide-repeat expansion in C9ORF72 is the most common genetic variant that contributes to amyotrophic lateral sclerosis and frontotemporal dementia 1,2 . 2 key findings →
Evidence: low
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Age-related increases in dementia risk can be attributed to accumulation of multiple pathologies, each of which contributes to dementia risk. 1 key finding →
Evidence: low
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Across Latin American and Caribbean countries (LACs), the fight against dementia faces pressing challenges, such as heterogeneity, diversity, political instability, and socioeconomic disparities. 5 key findings →
Evidence: low
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Trisomy 21, the presence of a supernumerary chromosome 21, results in a collection of clinical features commonly known as Down syndrome (DS). 1 key finding →
Evidence: low
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These results suggest that bvFTD may be characterized by an allostatic-interoceptive overload manifested in ongoing electrophysiological markers, brain atrophy, functional networks, and cognition. 4 key findings →
Participants: 94 Evidence: low
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Characterizing the timing and progression of Alzheimer's disease biomarker onset in Down syndrome (DS) and contrasting potential timing differences with neurotypical adults is needed to identify optimal Alzheimer's disease therapeutic treatment windows in DS. 2 key findings →
Design: longitudinal study Participants: 198 Evidence: moderate
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For both cohorts, the prevalence of mosaicism was 40 and Aβ 42 concentrations. 2 key findings →
Design: longitudinal study Participants: 357 Evidence: moderate
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Studies of post-mortem tissue have shown that the location of fibrillar tau deposits, called neurofibrillary tangles (NFT), matches closely with regions of massive neuronal death, severe cytological abnormalities, and markers of caspase activation and apoptosis, leading to the idea that tangles cause neurodegeneration in Alzheimer's disease and tau-related frontotemporal dementia. 2 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.
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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