27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
We have characterized a cluster of single immunoglobulin variable (IgV) domain receptors centromeric of the major histocompatibility complex (MHC) on human chromosome 6. 4 key findings →
Evidence: low
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Microglia are brain macrophages that mediate neuroinflammation and contribute to and protect against neurodegeneration. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Intervention and treatment in Alzheimer's disease dementia (AD-dementia) can be cost effective but the majority of patients are not diagnosed in a timely manner. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Functional and cognitive impairments were markedly higher for those who died aged 90 and older- predominantly women-than for those who died aged 85 to 89. 5 key findings →
Participants: 321 Evidence: moderate
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Dementia is a leading health policy challenge, with cases expected to triple by 2050, particularly in low- and middle-income countries. 2 key findings →
Evidence: low
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The increasing age of the population around the world has meant that greater attention is being paid to disorders that mainly affect older people. 4 key findings →
Evidence: low
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Incident stroke has long been recognized to cause dementia shortly after the event. 3 key findings →
Evidence: low
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Resting state functional magnetic resonance imaging (fMRI) was used to measure whole brain functional connectivity within specific networks hypothesised to be more affected in dementia with Lewy bodies (DLB) (a disease characterised by prominent attentional deficits, spontaneous motor features of parkinsonism and depression) than in Alzheimer׳s disease (AD) and controls. 4 key findings →
Participants: 68 Evidence: low
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Progressive and non-progressive patients are difficult to differentiate on the basis of current clinical diagnostic criteria for FTD but a combination of general cognitive, executive dysfunction and impaired ADL measures appear to be the most promising discriminators. 2 key findings →
Participants: 71 Evidence: low
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Genetic variation in the APOE gene and variation in chromosome 21 genotypes, including the APP locus, may influence age-associated cognitive decline in adults with Down syndrome. 3 key findings →
Design: longitudinal study Evidence: moderate
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The findings from this study add to the anatomical knowledge of hippocampal subregions in PD, allowing us to understand the unique functional contribution of each subfield. 4 key findings →
Evidence: low
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Neuroinflammation and activation of innate immunity are early events in neurodegenerative diseases including Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
= 49.17) had a higher incidence of psychotic disorder (p = .028) compared to non-progressors and progressors. 5 key findings →
Design: longitudinal study Evidence: moderate
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The risk of delirium admissions was elevated for the first 1-30 days of prescriptions [IRR 1.54 (95% CI 1.30-1.82) for men, 1.44 (1.22-1.70) for women] and whilst reducing over time for women [1.10 (0.94-1.29) for 91-365 days of prescriptions], it remained elevated for men [1.38 (1.17-1.64)]. 5 key findings →
Participants: 293 Evidence: low
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In a population-based sample, increasing gliosis precedes development of Alzheimer lesions. 3 key findings →
Evidence: moderate
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Cardiovascular risk factors and lifestyle factors are associated with an increased risk of cognitive decline and dementia in observational studies, and have been targeted by multidomain interventions. 5 key findings →
Participants: 4,162 Evidence: low
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Tau filaments with distinct morphologies and/or isoform compositions underlie a large number of human neurodegenerative diseases. 2 key findings →
Evidence: low
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Delirium is a common cause and complication of hospitalization in the elderly and is associated with higher risk of future dementia and progression of existing dementia, of which 70% is Alzheimer's disease (AD). 3 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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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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Within one week after dcLVA, 64.3% of patients demonstrated MMSE improvement, with further functional gains observed in continence, emotional regulation, motor coordination, and feeding independence. 5 key findings →
Evidence: moderate
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Unmet PC needs were highly prevalent (78.2%). 4 key findings →
Participants: 359 Evidence: low
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Participants with Lewy body dementia described losses associated with communication, continence, and energy leading to a progressive loss of independence. 5 key findings →
Design: longitudinal study Evidence: moderate
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It has been claimed that semantic dementia (SD), the temporal variant of fronto-temporal dementia, is characterized by an across-the-board deficit affecting all types of conceptual knowledge. 2 key findings →
Evidence: low
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This method differentiated eight tauopathies, including Alzheimer's disease, Pick disease, progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), argyrophilic grain disease (AGD), frontotemporal dementia with parkinsonism associated with chromosome 17 with N279K mutation (FTDP-17 N279K), and globular glial tauopathies types II and III. 5 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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 →