27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
An increasing number of midlife vascular risk factors was significantly associated with elevated amyloid SUVR; this association was not significant for late-life risk factors. 5 key findings →
Design: cohort study Participants: 20 Evidence: moderate
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In this community-based cohort without dementia, florbetapir uptake is associated with older age and APOE genotype. 5 key findings →
Design: longitudinal study Participants: 329 Evidence: moderate
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Glia have been implicated in Alzheimer's disease (AD) pathogenesis. 4 key findings →
Evidence: low
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Higher Abeta deposition is associated with greater longitudinal decline in mental status and verbal memory in the preceding years. 5 key findings →
Design: longitudinal study Participants: 57 Evidence: moderate
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Persons with severe CAA compared with those without CAA were more likely to carry an APOE ε4 allele (64.9% vs 42.8%, respectively; P Conclusions and relevance Being Hispanic and having had a transient ischemic attack-like episode were predictors of CAA in persons with AD. 1 key finding →
Design: longitudinal study Participants: 193 Evidence: moderate
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Arterial stiffness, measured by PWV, is an emerging risk factor for dementia through its repeated relationships with cognition, cSVD, and Aβ deposition. 4 key findings →
Design: cross-sectional Evidence: low
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International hospital-based studies have indicated a high risk of cognitive impairment after stroke, evidence from community-based studies in China is scarce. 2 key findings →
Design: cross-sectional Participants: 599 Evidence: low
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Tauopathies, including frontotemporal dementia (FTD) and Alzheimer's disease (AD), are neurodegenerative diseases in which tau fibrils accumulate. 5 key findings →
Evidence: low
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Elevated risk of developing Alzheimer's disease (AD) is associated with hypomorphic variants of TREM2, a surface receptor required for microglial responses to neurodegeneration, including proliferation, survival, clustering, and phagocytosis. 4 key findings →
Evidence: low
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Genetic studies have highlighted microglia as pivotal in orchestrating Alzheimer's disease (AD). 4 key findings →
Evidence: low
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In older adults, variable agreement between in vivo imaging and CERAD NP score was observed. 3 key findings →
Design: longitudinal study Evidence: moderate
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Alzheimer's disease (AD) is a neurodegenerative disease that causes late-onset dementia. 4 key findings →
Evidence: low
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Sepsis is a leading cause of death in critical illness, and its pathophysiology varies depending on preexisting medical conditions. 4 key findings →
Evidence: moderate
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Chronic musculoskeletal pain has been linked to dementia; however, chronic pain typically occurs in multiple sites; therefore, this study was to investigate whether greater number of chronic pain sites is associated with a higher risk of dementia and its subtypes. 4 key findings →
Participants: 356,383 Evidence: low
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An (18)F-labeled PET amyloid-beta (Abeta) imaging agent could facilitate the clinical evaluation of late-life cognitive impairment by providing an objective measure for Alzheimer disease (AD) pathology. 4 key findings →
Design: open-label trial Participants: 16 Evidence: low
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Despite differences in prevalence of APOE-ε4, its association with dementia risk was similar across Chinese, Japanese, Filipino, and non-Latino White participants. 2 key findings →
Design: cohort Participants: 46,325 Evidence: moderate
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Neurodegenerative tauopathies characterized by hyperphosphorylated tau include frontotemporal dementia and Parkinsonism linked to chromosome 17 (FTDP-17) and Alzheimer's disease (AD). 3 key findings →
Evidence: low
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The AD drug development pipeline is advancing agents directed at a variety of target processes. 1 key finding →
Design: clinical trial Participants: 36 Evidence: low
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Alzheimer's disease (AD), the most common form of dementia, is characterized by the abnormal accumulation of amyloid plaques and hyperphosphorylated tau aggregates, as well as microgliosis. 4 key findings →
Evidence: low
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TREM2 is a pattern recognition receptor, expressed on microglia and myeloid cells, detecting lipids and Aβ and inducing an innate immune response. 4 key findings →
Evidence: low
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Accumulating evidence suggests that neurodegeneration induced by pathogenic proteins depends on contributions from surrounding glia. 4 key findings →
Evidence: low
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The high failure rate of clinical trials in Alzheimer's disease (AD) and AD-related dementia (ADRD) is due to a lack of understanding of the pathophysiology of disease, and this deficit may be addressed by applying artificial intelligence (AI) to "big data" to rapidly and effectively expand therapeutic development efforts. 5 key findings →
Evidence: low
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We have characterised the proteolytic cleavage events responsible for the shedding of triggering receptor expressed on myeloid cells 2 (TREM2) from primary cultures of human macrophages, murine microglia and TREM2-expressing human embryonic kidney (HEK293) cells. 4 key findings →
Evidence: low
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Rare coding variants in the triggering receptor expressed on myeloid cells 2 (TREM2) are associated with increased risk for Alzheimer's disease (AD), but how they confer this risk remains uncertain. 4 key findings →
Evidence: low
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The TREM2-DAP12 receptor complex sustains microglia functions. 4 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.
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 →