Neuronal active Caspase-6 (Casp6) is associated with Alzheimer disease (AD), cognitive impairment, and axonal degeneration. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Neuronal active Caspase-6 (Casp6) is associated with Alzheimer disease (AD), cognitive impairment, and axonal degeneration. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Immunization with preaggregated amyloid beta-peptide (Abeta(1-42)) and administration of antibodies against Abeta into amyloid precursor protein APP(V717F)- transgenic mice (an animal model of AD) have recently been reported to dramatically reduce amyloid plaque deposition, neuritic dystrophy, and astrogliosis, most likely by enhancing Abeta clearance from brain. 4 key findings →
Evidence: low
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A total of 145 342 adults met inclusion criteria; 10.5% had ADRD and were likely to be older, female, and have more comorbid conditions. 4 key findings →
Participants: 342 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In this article, the challenges faced by several noted population studies for Alzheimer dementia in operationalizing current clinical diagnostic criteria for Alzheimer's disease (AD) have been reviewed. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) has been genetically and pathologically associated with neuroinflammation. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The mean (SD) age of participants was 70.57 (8.00) years, with 179 (42.9 %) females. 5 key findings →
Design: cross-sectional Participants: 123 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Our findings suggest that disease progression follows a stage-dependent MVD pattern that can identify at-risk regions. 5 key findings →
Participants: 403 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
After controlling for the level of cognitive impairment, we found a double dissociation between AD clinical phenotype and localization/magnitude of atrophy, characterized by predominant neocortical involvement in EOAD and more focal anterior medial temporal involvement in LOAD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Since the original publication describing the illness in 1907, the genetic understanding of Alzheimer's disease (AD) has advanced such that it is now clear that it is a genetically heterogeneous condition, the subtypes of which may not uniformly respond to a given intervention. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
A non-coding variant (rs35349669) in INPP5D increases the risk for Alzheimer's disease (AD), and elevated INPP5D expression is associated with increased plaque deposition. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The Trem2 variant R47H, confers substantially elevated risk of developing late onset Alzheimer's disease, while NHD-linked Trem2 variants like Y38C, are associated with development of early onset dementia with white matter pathology. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The intervention engaged 69 (63.8%) of 108 clinicians across the 7 clinics. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The rising prevalence of mild cognitive impairment (MCI) and dementia, combined with persistent underdiagnosis, is driving an increased need for scalable cognitive assessment tools. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Inheritance of apoE4 is a strong risk factor for the development of late-onset sporadic Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The increasing prevalence of cognitive impairment among the older adult population warrants attention to the identification of practices that may minimize the progression of early forms of cognitive impairment, including the transitional stage of mild cognitive impairment (MCI), to permanent stages of dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Education was independently associated with cognitive impairment and dementia among a representative community-based sample of African Americans and the association remains significant across a variety of sensitivity analyses designed to control for measurement and confounding biases. 5 key findings →
Evidence: low
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Alzheimer disease (AD) results, in part, from the excess accumulation of the amyloid-β (Aβ) peptide as neuritic plaques in the brain. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Toll-like receptors (TLR) are transmembrane pattern recognition receptors that recognize microbial ligands and signal for production of inflammatory cytokines and type I interferon in macrophages and dendritic cells (DC). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Variants in the microglial receptor TREM2 confer risk for multiple neurodegenerative diseases. 4 key findings →
Evidence: low
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Microglia-mediated neuroinflammation is widely associated with seizures and epilepsy. 4 key findings →
Evidence: low
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Among 421,131 MA beneficiaries, telehealth use increased sharply in Q2 2020 for both ADRD and non-ADRD groups, peaking at 33.9 and 30.6% respectively. 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Saturation and competition binding studies of (3)H-THK5117 in post-mortem AD brain tissue showed the presence of multiple binding sites. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Aβ is the main component of amyloid deposits in Alzheimer disease (AD) and its aggregation into oligomers, protofibrils and fibrils is considered a seminal event in the pathogenesis of AD. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Immunohistochemical analysis of brains of patients with Alzheimer disease (AD) revealed that the cysteine proteinase inhibitor cystatin C colocalizes with amyloid beta-protein (Abeta) in parenchymal and vascular amyloid deposits. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
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 →