Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Three blood gene expression datasets of high dimensionality and low sample size (HDLSS) have been utilized in this study, with one dataset exhibiting significant class imbalance. 5 key findings →
Evidence: low
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Obstructive sleep apnoea (OSA) is increasingly recognised as a significant risk factor for cognitive decline and dementia. 1 key finding →
Evidence: low
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A total of eight studies were included from 1,384 search results, reviewing data from 10,449 cognitively unimpaired older adults. 5 key findings →
Evidence: low
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Type 1 diabetes (T1D) is a serious disease which affects millions of people worldwide and is a major factor for vascular contributions to cognitive impairment and dementia (VCID). 3 key findings →
Evidence: low
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We observed higher within‐ and between‐DMN FC in the CS‐OSA compared to the CI‐OSA group; however, this difference was not observed between the CS‐nonOSA and CI‐nonOSA groups. 5 key findings →
Evidence: low
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The enzyme pair PINK1 and PRKN together orchestrates a cytoprotective mitophagy pathway that selectively tags damaged mitochondria with phospho-serine 65 ubiquitin (pS65-Ub) and directs them for autophagic-lysosomal degradation (mitophagy). 4 key findings →
Evidence: low
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Graph theory has proven to be useful in studying brain dysfunction in Alzheimer’s disease using MagnetoEncephaloGraphy (MEG) and fMRI signals. 5 key findings →
Evidence: low
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This is the first reported case of AIWS in a patient with DLB. 5 key findings →
Evidence: low
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Alzheimer’s disease (AD) remains a significant global health challenge with limited FDA-approved treatments, necessitating the search for novel preventive strategies. 3 key findings →
Evidence: low
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Hypertensive patients also had significantly lower thiol levels compared to those without hypertension (p < 0.05).Conclusion Our findings suggest that total and native thiol levels decline with cognitive deterioration and advancing age. 4 key findings →
Participants: 128 Evidence: low
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The amyloid precursor protein intracellular domain (AICD), a cleavage product of amyloid precursor protein implicated in Alzheimer disease and amyloid lateral sclerosis, is a functionally important but structurally elusive intrinsically disordered protein. 2 key findings →
Evidence: low
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Clinical investigations have suggested a potential link between cataracts and Alzheimer's disease (AD). 2 key findings →
Evidence: low
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Bridging Integrator 1 (BIN1) is a genetic risk factor for late-onset Alzheimer disease. 2 key findings →
Evidence: low
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Intramembrane proteolysis by γ-secretase is critically implicated in Alzheimer disease pathogenesis by processing of its amyloid precursor protein substrate C99 into harmful amyloid-β peptide (Aβ) species. 2 key findings →
Evidence: low
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In 1906, Alois Alzheimer first described the neuropathological hallmarks of the disease that now bears his name. 2 key findings →
Participants: 62 Evidence: moderate
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Neurodegenerative dementias with behavioral clinical presentation are a diverse group of diseases. 4 key findings →
Participants: 20 Evidence: moderate
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Early and accurate diagnosis of dementia is essential to improving patient outcomes and reducing societal burden. 1 key finding →
Participants: 164 Evidence: low
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Our studies showed that DC and DRs in VD and AD groups were significantly lower than those in controls, while AC values were significantly higher. 5 key findings →
Evidence: low
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The observation group had significantly lower Self-Rating Anxiety Scale (SAS) and Self-Rating Depression Scale (SDS) scores than the control group (both P<0.001). 5 key findings →
Participants: 45 Evidence: low
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DNA methylation, mRNA and protein levels, and cognitive performance using the Mini-Mental State Examination (MMSE) and Clock Drawing Test (CDT). 3 key findings →
Evidence: low
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This study (RCT) investigated the impact of Expressive Therapies Continuum (ETC)-based art therapy on cognitive function and quality of life among older adults with dementia living in a complex care setting. 3 key findings →
Evidence: low
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Neurodegeneration in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) results from both gain of toxicity and loss of normal function of the RNA-binding protein TDP-43, but their mechanistic connection remains unclear. 3 key findings →
Evidence: low
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87 DLB patients (77.5 ± 7.2yo; 34.5 % females) were included. 4 key findings →
Evidence: low
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Cerebral amyloid angiopathy (CAA) is a common age-related disorder, a prominent comorbidity of Alzheimer disease (AD), and causes vascular cognitive impairment and dementia. 3 key findings →
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 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 →