27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Research interest in the application of electroencephalogram (EEG) as a non-invasive diagnostic tool for the automated detection of neurodegenerative diseases is growing. 2 key findings →
Participants: 88 Evidence: moderate
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This study aims to explore the utility of artificial intelligence (AI) in classifying dementia severity based on gait analysis data and to examine how machine learning (ML) can address the limitations of conventional statistical approaches. 1 key finding →
Participants: 34 Evidence: low
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We found that sleep disorders were associated with risk of Alzheimer’s disease (AD), amyotrophic lateral sclerosis, dementia, Parkinson’s disease (PD), and vascular dementia in three national biobanks (hazard ratios from 1.3 (PD) to 5.11 (dementia)). 2 key findings →
Evidence: low
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The association between type 2 diabetes mellitus (T2DM) and cognitive impairment represents a critical public health concern, particularly against the backdrop of the rising global prevalence of diabetes and aging populations. 2 key findings →
Evidence: low
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Biallelic loss-of-function variants in TYROBP and TREM2 cause autosomal recessive presenile dementia with bone cysts known as Nasu-Hakola disease (NHD, alternatively polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy, PLOSL). 3 key findings →
Evidence: low
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Mechanisms regulating human sleep and physiology have evolved in response to rhythmic variation in environmental variables driven by the Earth's rotation around its axis and the Sun. 1 key finding →
Participants: 26 Evidence: low
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The prevalence of CF was 24.3%. Cerebrovascular disease (OR: 2.39, 95% CI: 1.44-3.97) and peripheral arterial disease (OR: 1.74, 95% CI: 1.03-2.95) were significant risk factors, while higher education (OR 0.85, 95% CI 0.76-0.94) and later diabetes onset (OR: 0.93, 95% CI: 0.88-0.98) were protective. 5 key findings →
Design: cross-sectional Evidence: low
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In partial correlations adjusted for age, there was a significant positive association between the cardiovascular composite (r = .156, p = .016) and resistance score; higher cardiovascular composite was associated with greater than expected Aβ for age. 4 key findings →
Participants: 262 Evidence: low
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Vascular dementia (VaD) is a heterogeneous group of brain disorders caused by cerebrovascular pathologies and the second most common cause of dementia, accounting for over 20% of cases and posing an important global health concern. 5 key findings →
Evidence: low
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Cerebrolysin (CBL) is a combination of neurotrophic peptides and amino acids derived from pig brains. 1 key finding →
Evidence: low
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Mutations in the TARDBP gene encoding TDP-43 protein are linked to loss of function in neurons and familial frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS). 5 key findings →
Evidence: low
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Early isolated functional disruptions in salience/visual networks were present in asymptomatic carriers, along with anterior cingulate gray matter reductions. 5 key findings →
Evidence: low
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Surprisingly, levels of strain A and B aSyn species were higher in plasma from individuals with PD compared to DLB in 2 independent cohorts. 5 key findings →
Evidence: low
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Forty bvFTD patients and 40 HC (56.25% female, mean age of 63.55 years) were involved. 5 key findings →
Participants: 36 Evidence: low
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Co-existing neuropathology was frequent, even among individuals without clinical dementia. 5 key findings →
Evidence: moderate
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The majority of individuals at 50% risk of carrying a pathogenic variant causing frontotemporal dementia (FTD) chooses not to undergo presymptomatic genetic testing. 5 key findings →
Participants: 14 Evidence: low
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These findings establish IF as a potent modulator of synaptic resilience in VaD, acting through coordinated preservation of synaptic structure, inhibition of inflammatory synapse loss, and metabolic reprogramming. 2 key findings →
Evidence: low
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In DLB, plasma concentrations of GFAP and NfL were associated with MTA, GCA-F, and Fazekas scale; and the Aβ42/40 ratio was associated with PA and Fazekas. 5 key findings →
Participants: 92 Evidence: low
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Neuropsychiatric symptoms (NPS) are prevalent, emerge early, and are associated with poorer outcomes in Lewy body dementia (LBD). 5 key findings →
Participants: 28 Evidence: low
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Dopamine transporter (DAT) imaging and electroencephalography (EEG) are recommended biomarkers for diagnosing dementia with Lewy bodies (DLB). 4 key findings →
Participants: 120 Evidence: low
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A one‐point ALI increase was associated with MCI conversion odds by 15%. 1 key finding →
Participants: 385 Evidence: low
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-values compared to gait features. Linear regression analysis indicated that turn dynamics had stronger correlations with executive function and working memory, suggesting a more pronounced relationship between cognitive performance and turn features than gait variables. 3 key findings →
Participants: 75 Evidence: low
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The left inferior parietal lobule (IPL)_6_5 (rostroventral area 39) showed the best ability to discriminate between patients with AD and those with CN (AUC = 0.688). 5 key findings →
Participants: 662 Evidence: low
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The CNN-BiLSTM-Attention model demonstrated relatively promising predictive performance (AUC: 0.7317), with moderately high sensitivity (0.6902) and a high negative predictive value (NPV) of 0.9414. 5 key findings →
Participants: 4,626 Evidence: low
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These findings suggest that visual function plays a crucial role in the cognitive and functional abilities of patients with MCI. 2 key findings →
Design: cross-sectional 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 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 →