27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
These findings suggest that a hearing intervention might reduce cognitive change over 3 years in populations of older adults at increased risk for cognitive decline but not in populations at decreased risk for cognitive decline. 5 key findings →
Design: randomized controlled trial Participants: 858 Evidence: high
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Dementia and MCI are associated with neuropsychiatric symptoms in clinical samples. 4 key findings →
Design: cohort study Participants: 138 Evidence: moderate
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We tested the hypothesis that plasma neurofilament light chain (NfL) identifies asymptomatic carriers of familial frontotemporal lobar degeneration (FTLD)-causing mutations at risk of disease progression. 4 key findings →
Design: longitudinal study Participants: 277 Evidence: moderate
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Hearing loss is independently associated with incident all-cause dementia. 4 key findings →
Design: longitudinal study Participants: 639 Evidence: moderate
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Periventricular white matter hyperintensities (WMH; PVWMH) and deep WMH (DWMH) are regional classifications of WMH and reflect proposed differences in cause. 4 key findings →
Design: meta-analysis Participants: 26,654 Evidence: high
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In patients with sporadic ALS, we identified the repeat expansion in 236 (7·0%) of 3377 white individuals from the USA, Europe, and Australia, two (4·1%) of 49 black individuals from the USA, and six (8·3%) of 72 Hispanic individuals from the USA. 1 key finding →
Participants: 4,448 Evidence: low
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Of the 14 685 participants (7355 female [50%] and 7330 male [50%]; mean [SD] age, 73.8 [8.5] years) who met the inclusion criteria, 221 participants (1.5%) developed LOE during follow-up. 5 key findings →
Design: longitudinal study Participants: 713 Evidence: moderate
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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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Variants of UNC13A, a critical gene for synapse function, increase the risk of amyotrophic lateral sclerosis and frontotemporal dementia 1-3 , two related neurodegenerative diseases defined by mislocalization of the RNA-binding protein TDP-43 4,5 . 2 key findings →
Evidence: low
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The genetic basis of Lewy body dementia (LBD) is not well understood. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Studies of long-term cognitive change should account for the potential effects of education on the outcome, since some studies have demonstrated an association of education with dementia risk. 4 key findings →
Design: cohort study Participants: 14,020 Evidence: moderate
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Neither targeted lecanemab treatment nor treatment unrestricted by APOE ε4 genotype is cost-effective vs SoC alone for patients with MCI or mild dementia due to AD. 2 key findings →
Design: modelling Evidence: moderate
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Using exome sequencing, we identified a p.R191Q amino acid change in the valosin-containing protein (VCP) gene in an Italian family with autosomal dominantly inherited amyotrophic lateral sclerosis (ALS). 1 key finding →
Evidence: moderate
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The genetic variant rs72824905-G (minor allele) in the PLCG2 gene was previously associated with a reduced Alzheimer's disease risk (AD). 4 key findings →
Participants: 53,627 Evidence: low
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On the basis of their findings in this large community population of elderly people, the authors conclude that a wide range of dementia-associated mental and behavioral disturbances afflict the majority of individuals with dementia. 3 key findings →
Participants: 5,092 Evidence: low
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MATR3 is an RNA- and DNA-binding protein that interacts with TDP-43, a disease protein linked to amyotrophic lateral sclerosis (ALS) and frontotemporal dementia. 4 key findings →
Evidence: low
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Sensory impairments were common: 28% had visual impairment, 35% had hearing loss, 22% had poor smell, 12% had touch insensitivity; 26% had more than two impairments, and 5.6% had more than three sensory impairments. 2 key findings →
Participants: 1,810 Evidence: low
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During follow-up, 203 cases of hospitalisation with dementia were identified. 5 key findings →
Participants: 151 Evidence: moderate
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Even before dementia becomes apparent, cognitive decline may contribute to deterioration in oral health. 4 key findings →
Design: cohort study Participants: 10,050 Evidence: moderate
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An (18)F-labeled PET amyloid-beta (Abeta) imaging agent could facilitate the clinical evaluation of late-life cognitive impairment by providing an objective measure for Alzheimer disease (AD) pathology. 4 key findings →
Design: open-label trial Participants: 16 Evidence: low
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Nuclear depletion and cytoplasmic aggregation of the RNA-binding protein TDP-43 are cellular hallmarks of amyotrophic lateral sclerosis (ALS). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In this multi-cohort study of older adults without cognitive impairment, we show that WMH and lacunes independently predict increased risk of MCR, after adjusting for key confounders. 5 key findings →
Design: cohort study Participants: 1,772 Evidence: moderate
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However, many did not adjust for important confounders or did not include women and non-whites. 4 key findings →
Participants: 10,975 Evidence: moderate
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In order to determine the meaning of cognitive impairment in community dwelling elderly, 3,481 adults were interviewed in their homes using the Mini-Mental State Examination. 5 key findings →
Participants: 3,481 Evidence: low
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The prevalence of ICAS in older adults is high, and it could be a target for primary prevention of stroke and dementia in this population. 3 key findings →
Participants: 1,765 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 →