Alzheimer's disease (AD), the leading cause of dementia, has an estimated heritability of approximately 70% 1 . 3 key findings →
Participants: 32,558 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.
Alzheimer's disease (AD), the leading cause of dementia, has an estimated heritability of approximately 70% 1 . 3 key findings →
Participants: 32,558 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In this genetic association study, a novel variant associated with AD was identified: R251G always coinherited with ε4 on the APOE gene, which mitigates the ε4-associated AD risk. 5 key findings →
Design: case-control study Participants: 37 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Characterization of the genetic landscape of Alzheimer's disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
A number of new recommendations and good practice points are made, namely in CSF, neuropsychology, neuroimaging and reviewing non-evidence based therapies. 2 key findings →
Design: meta-analysis Evidence: high
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Slow gait speed has been shown to predict incident dementia and cognitive decline in older individuals. 1 key finding →
Design: longitudinal study Participants: 57,456 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
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
The MD is a scientifically supported dietary intervention with broad preventive and therapeutic benefits. 2 key findings →
Design: systematic review Participants: 84 Evidence: high
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Ageing and a sedentary lifestyle are associated with declines in muscle function and cardiorespiratory fitness, resulting in an impaired capacity to perform daily activities and maintain independent functioning. 2 key findings →
Evidence: high
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Increased BPSD was reported in 59.6% of patients as worsening of preexisting symptoms (51.9%) or as new onset (26%), and requested drug modifications in 27.6% of these cases. 4 key findings →
Participants: 4,913 Evidence: low
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Immune-regulatory mechanisms of drug-free remission in rheumatoid arthritis (RA) are unknown. 4 key findings →
Evidence: low
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An estimated 40% of dementia is potentially preventable by modifying 12 risk factors throughout the life course. 4 key findings →
Participants: 39 Evidence: moderate
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Copy-number variants (CNVs) are major contributors to human disease. 2 key findings →
Design: case-control Participants: 22,319 Evidence: moderate
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Individuals with neuropsychiatric, cardiovascular, and sensory impairment/cancer patterns are at increased risk for dementia and APOE ε4, and inflammation may further increase the risk. 3 key findings →
Participants: 2,478 Evidence: low
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Although the discovery of the critical role of α-synuclein (α-syn) in the pathogenesis of Parkinson's disease (PD) is now twenty-five years old, it still represents a milestone in PD research. 5 key findings →
Evidence: low
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Concluding, this innovative EEG analysis, in combination with a genetic test (both low-cost and widely available), could evaluate on an individual basis with great precision the risk of MCI progression. 3 key findings →
Participants: 97 Evidence: low
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Among the more than 90 identified genetic risk loci for late-onset Alzheimer's disease (AD) and related dementias, the apolipoprotein E (APOE) gene ɛ2/ɛ3/ɛ4 polymorphisms remain the longstanding benchmark for genetic disease risk with a consistently large effect across studies 1-10 . 5 key findings →
Design: case-control Evidence: high
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The alteration of the insulin-signaling/mTOR pathways represents an early event in DS brain and likely contributes to the cerebral dysfunction and intellectual disability observed in this unique population. 1 key finding →
Participants: 17 Evidence: low
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This manuscript is the second part of a two-part description of the current status of understanding of the network function of the brain in health and disease. 5 key findings →
Evidence: low
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We explored the potential link between chronic inflammatory arthritis and COVID-19 pathogenic and resolving macrophage pathways and their role in COVID-19 pathogenesis. 4 key findings →
Evidence: low
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From 356 participants, 104 were MCI-C, whereas 252 were MCI-NC. 5 key findings →
Participants: 356 Evidence: low
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Dementia developed in 104 individuals (29.6%), including 85 (22.4%) who met core clinical criteria for probable and possible Alzheimer's disease dementia. 3 key findings →
Participants: 398 Evidence: low
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The aim of this study is to validate the Italian version of the Pittsburgh Sleep Quality Index (PSQI), comparing five different groups of individuals (healthy young and elderly, sleep apnoea syndrome patients, depressed patients, individuals with dementia) by both questionnaire scores and polysomnographic measures. 4 key findings →
Evidence: low
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Increasing evidences support the notion that the impairment of intracellular degradative machinery is responsible for the accumulation of oxidized/misfolded proteins that ultimately results in the deposition of protein aggregates. 5 key findings →
Evidence: low
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Neurodegenerative processes of various types of dementia start years before symptoms, but the presence of a "neural reserve", which continuously feeds and supports neuroplastic mechanisms, helps the aging brain to preserve most of its functions within the "normality" frame. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The human brain contains about 100 billion neurons forming an intricate network of innumerable connections, which continuously adapt and rewire themselves following inputs from external and internal environments as well as the physiological synaptic, dendritic and axonal sculpture during brain maturation and throughout the life span. 5 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. 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 →