28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
• Brain health depends on certain environmental resources of which socioeconomically disadvantaged people in particular are deprived. • Resource deprivation may increase dementia risk due to reduced attainment for deprived populations. • Improving attainment across the lifetime for disadvantaged individuals should be a public health priority for dementia prevention. 1 key finding →
Evidence: low
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The unprecedented rise of artificial intelligence (AI) in recent times is unparalleled in history.AI 1 seemingly possesses cognitive abilities that hitherto only humans could boast of -reason, an inimitable, embodied, and finite existence. 47Nonetheless, the ubiquitous abilities of AI can help to enhance treatment and care for PLWDs in 48 enabling early diagnosis, continuous monitoring and personalized support. 1 key finding →
Evidence: low
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Conventional dementia screening tools, whether paper tests or static artificial intelligence (AI) models, capture only a snapshot of cognition and need to be adminstered periodically. 5 key findings →
Evidence: low
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The approval of disease-modifying treatments for Alzheimer's disease demands a rethinking of cognitive screening. 4 key findings →
Evidence: low
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Participants reported routine screening for cognitive impairment only in the context of the Medicare annual wellness visit and generally avoided routine screening because of limited treatment options to support patients, such as poor access to geriatrics/neuropsychiatric services. 5 key findings →
Evidence: low
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Dementia is a progressive condition that affects cognitive and functional abilities. 2 key findings →
Evidence: low
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This approach predicts clinical progression (2-year Clinical Dementia Rating Sum of Boxes change > 1) with an area under the curve of 0.836. 4 key findings →
Evidence: low
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Data from the qualitative interviews will provide dyad preferences for intervention development. 4 key findings →
Evidence: low
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During alteplase administration, the patient experienced clinical deterioration. 5 key findings →
Evidence: low
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BackgroundAlzheimer's disease (AD) exhibits significant clinical and pathological heterogeneity, particularly during the mild cognitive impairment (MCI) transitional stage. 1 key finding →
Evidence: low
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Mild Cognitive Impairment (MCI) is marked by a measurable decline in cognitive function that exceeds typical age-related changes but does not yet qualify as dementia. 2 key findings →
Evidence: low
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We found that orientation, memory, and irritability scores were useful in predicting AD dementia onset, while daily living, depression, and executive function scores were identified as strong predictors in the LB cohort. 3 key findings →
Evidence: moderate
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Amnestic mild cognitive impairment (aMCI) represents a critical prodromal stage of Alzheimer's disease (AD), yet effective therapeutic interventions to prevent or delay this conversion remain an unmet clinical need. 5 key findings →
Evidence: low
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We consider the recent publication by Ornish and colleagues and the rigor expected for interventional clinical trials. 1 key finding →
Evidence: low
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BackgroundWhile transcranial alternating current stimulation (tACS) shows therapeutic promise for neurological and psychiatric disorders when applied repeatedly, its potential is constrained by multiple laboratory visits. 2 key findings →
Evidence: low
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Mild cognitive impairment (MCI) is primarily characterized by a gradual decline in cognitive function, where early detection and intervention are crucial to preventing Alzheimer's disease progression. 3 key findings →
Evidence: low
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BackgroundEpigenetic mechanisms, particularly histone modifications at gene promoters, are crucial for controlling gene transcription. 4 key findings →
Evidence: low
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MTX46943-mediated TREM2 activation leads to TREM2/DAP12 receptor complex formation and stabilizes surface location required for downstream signaling and microglia activation. 5 key findings →
Evidence: low
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Alzheimer's disease (AD) is a progressive and complicated neurodegenerative disorder that mostly affects the elderly and is characterized by memory loss, cognitive dysfunction, accumulation of amyloid beta (Aβ) plaques, neurofibrillary tangles, and cholinergic deficits. 1 key finding →
Evidence: low
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The most notable effect sizes were observed in entropy for Beta1 and Beta3 bands in frontal regions for the DTS7 and DTS1 tasks, Beta2 relative power in C4 during DTAN, Theta modulation in the Theta and alpha-1 bands in frontal regions during DTS7, and Alpha2 modulations in the same task. 5 key findings →
Participants: 37 Evidence: low
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The most notable effect sizes were observed in entropy for Beta1 and Beta3 bands in frontal regions for the DTS7 and DTS1 tasks, Beta2 relative power in C4 during DTAN, Theta modulation in the Theta and alpha-1 bands in frontal regions during DTS7, and Alpha2 modulations in the same task. 5 key findings →
Participants: 37 Evidence: low
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Trans-active response DNA-binding protein-43 (TDP-43) is the major pathological protein in motor neuron disease and TDP-43 pathology has been described in the brains of up to 50% of patients with Alzheimer disease (AD). 5 key findings →
Evidence: low
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It is now widely accepted that the development of neurodegenerative diseases depends on and affects many pathological processes, both in the brain and the periphery. 1 key finding →
Evidence: low
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The Mini-Mental State Examination (MMSE) is widely used in cognitive screening, including in primary care settings. 4 key findings →
Evidence: low
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The results of this study identified important relationships between cognitive features in the ADAS-Cog and provide a clear example of the value of data-driven machine learning approaches in the identification of markers that indicate disease progression in dementia. 3 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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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.
1,034 records (3.7% 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 →