Plasma biomarkers may aid Alzheimer disease (AD) diagnosis and prognosis. 4 key findings →
Participants: 301 Evidence: moderate
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.
Plasma biomarkers may aid Alzheimer disease (AD) diagnosis and prognosis. 4 key findings →
Participants: 301 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Multimorbidity-the co-occurrence of two or more chronic health conditions-affects > 86% of people with dementia. 1 key finding →
Evidence: low
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Mean age was 83.5 years (delirium 78.7 vs non-delirium 88.4); 13/20 were female; 17/20 had premorbid cognitive decline/impairment or dementia. 5 key findings →
Design: case-control study Evidence: moderate
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By 2040 more people in Scotland are projected to die with palliative care needs, and the complexity of need will increase markedly. 3 key findings →
Participants: 34 Evidence: low
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Microglia are resident macrophages of the central nervous system that have key functions in its development, homeostasis and response to damage and infection. 4 key findings →
Evidence: low
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A European Task Force has recently developed and published the concept and protocols for the setup of the innovative health offer of Brain Health Services for the secondary prevention of dementia and cognitive impairment (dBHS). dBHS are outpatient health care facilities where adult persons can find an assessment of their risk of developing cognitive impairment and dementia, have their risk level and contributing factors communicated using appropriate language supported by adequate communication tools, can decide to participate to programs for personalized risk reduction if at higher risk, and benefit from cognitive enhancement interventions. 1 key finding →
Evidence: low
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Odds ratios for death, dementia, and delirium using anticholinergic-polypharmacy pseudoscales (median = 1.09-1.10) were greater than those of general-polypharmacy pseudoscales (1.05-1.06). 3 key findings →
Design: cohort study Evidence: moderate
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Carriers of the e4 allele may be more vulnerable to conditions that are independent risk factors for cognitive decline, such as cardiometabolic diseases. 4 key findings →
Participants: 111,739 Evidence: low
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Microglia are resident macrophages of the CNS that are involved in its development, homeostasis and response to infection and damage. 4 key findings →
Evidence: low
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Advances in neuroimaging have enabled greater understanding of the progression of cerebral degenerative processes associated with ageing-related dementias. 4 key findings →
Evidence: low
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Our findings suggest that non-economic social deprivation, especially in terms of access to a grocery store, pharmacy, postal office, and bus stop, might be relevant for maintaining cognitive functioning in old age. 4 key findings →
Design: longitudinal study Participants: 91 Evidence: moderate
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Our findings support speech-based cognitive assessments as a promising avenue towards remote MCI screening, with implications for scalable screening in clinical trials and healthcare. 3 key findings →
Participants: 110 Evidence: low
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Among 52 participants recruited, 27 were former caregivers, 16 were current caregivers, and nine were persons with dementia; experiences reflected Alzheimer's (n = 18), sporadic Creutzfeldt-Jakob (n = 12), Lewy body (n = 7), and other dementias (n = 15). 5 key findings →
Participants: 18 Evidence: low
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Cerebral small vessel disease (cSVD) is characterised by white matter hyperintensities (WMH) and contributes to stroke and dementia. 5 key findings →
Design: cross-sectional Participants: 60 Evidence: low
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Cerebral amyloid angiopathy (CAA) is associated with apolipoprotein E (APOE gene, apoE protein) polymorphism: current evidence suggests that the epsilon4 allele is a risk factor for the development of CAA and the epsilon2 allele predisposes to hemorrhage. 3 key findings →
Participants: 62 Evidence: low
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Increasing evidence suggests that vascular risk factors contribute to neurodegeneration, cognitive impairment and dementia. 2 key findings →
Evidence: low
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Subjective memory complaints (SMCs) are common in older people and are often thought to indicate cognitive impairment. 1 key finding →
Evidence: low
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Approximately 2% of those aged ≥60 years had dementia, lower than published estimates. 5 key findings →
Design: retrospective cohort Evidence: moderate
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Thirty-two patients met the inclusion criteria (n=11 moderate-to-severe SVD, mean age 72 ± 10 years, 6 women; n = 21 none-to-minimal SVD, mean age 70 ± 10 years, 12 women). 3 key findings →
Design: cohort study Evidence: moderate
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Dementia risk is influenced by the social conditions in which people live. 5 key findings →
Evidence: low
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A total of 120 people with delirium participated [median age 86.3, range 70-99, 67 (55.8%) female and 55 (45.8%) with dementia]. 5 key findings →
Participants: 120 Evidence: low
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In the fully adjusted model, the cumulative odds ratios (OR) are 1.28 (95% confidence interval [CI]: 1.25–1.31) for any dementia, 1.44 (95% CI: 1.36–1.53) for Alzheimer’s disease and 1.65 (95% CI: 1.48–1.83) for vascular dementia, associated with per unit increase in annual cumulative flooding exposure over lag 0–6 years. 5 key findings →
Design: case-control study Evidence: moderate
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Of 75 221 admissions, 62 188 (82.7%; 33 625 unique patients; mean age 80.2 years; 55.8% female) had a 4AT on admission. 4 key findings →
Evidence: low
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These data are evidence of a gene x environment interaction for cognitive aging. 3 key findings →
Evidence: low
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Both ATH and AD involve inflammation, macrophage infiltration, and occlusion of the vasculature. 1 key finding →
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 →