Etalanetug presented an adequate safety and immunogenicity profile in healthy adults. 3 key findings →
Evidence: high
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.
Etalanetug presented an adequate safety and immunogenicity profile in healthy adults. 3 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
We conducted a systematic review of research in artificial intelligence (AI) for retinal fundus photographic images. 2 key findings →
Design: systematic review Evidence: high
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Recently, we showed that behavioural variant frontotemporal dementia and Alzheimer's disease cause atrophy within two major networks, an anterior 'Salience Network' (atrophied in behavioural variant frontotemporal dementia) and a posterior 'Default Mode Network' (atrophied in Alzheimer's disease). 3 key findings →
Participants: 12 Evidence: low
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The eRADAR tool uses existing EHR data to detect patients with good accuracy who may have unrecognized dementia. 1 key finding →
Design: cohort study Participants: 4,330 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The study consists of 25,186 patients (mean age = 63.0, interquartile range [IQR] of age = 15.1 years, male = 50%). 3 key findings →
Design: cohort study Participants: 25,186 Evidence: moderate
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Prior work has suggested that obesity and overweight as measured by body mass index (BMI) increases risk of dementia. 4 key findings →
Participants: 10,136 Evidence: moderate
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Midlife serum total cholesterol was associated with an increased risk of AD and VaD. 3 key findings →
Participants: 9,844 Evidence: moderate
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Although previous research has shown that initiation of postmenopausal estrogen hormone therapy (HT) in late life increases risk of dementia, animal studies and some observational studies have suggested that midlife use of HT may be beneficial; however, this has not been rigorously investigated in large population-based studies. 4 key findings →
Participants: 1,524 Evidence: low
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Alzheimer's disease (AD), the most common type of dementia, is a severe neurodegenerative disorder. 4 key findings →
Design: longitudinal study Evidence: moderate
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Our understanding of risk factors for COVID‑19, including pre-existing medical conditions and genetic variations, is limited. 4 key findings →
Participants: 389,620 Evidence: low
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In this large cohort, heavy smoking in midlife was associated with a greater than 100% increase in risk of dementia, AD, and VaD more than 2 decades later. 5 key findings →
Participants: 5,367 Evidence: moderate
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Relationship between alcohol drinking and incident dementia remained uncertain. 2 key findings →
Design: cohort Participants: 296,715 Evidence: early
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The prevalence of ICAS in older adults is high, and it could be a target for primary prevention of stroke and dementia in this population. 3 key findings →
Participants: 1,765 Evidence: moderate
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Eligibility to randomize into the A3 Trial or A45 Trial is based on the screening PET imaging results. 3 key findings →
Design: clinical trial Evidence: moderate
Full summary, score breakdown and related studies → Original source
During lecanemab treatment for AD, it is essential to fully understand the mechanisms, imaging characteristics, and management strategies of ARIA. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Two groups of tau, 3R- and 4R-tau, are generated by alternative splicing of tau exon 10. 1 key finding →
Evidence: low
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Understanding preclinical transitions to impairment in cognitive abilities associated with risks for functional difficulty and dementia. 4 key findings →
Evidence: low
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Overactivated microglia and neuroinflammation are considered to play a crucial role in the progression of Alzheimer's disease (AD). 4 key findings →
Evidence: low
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Postoperative cognitive dysfunction (POCD) is a common postoperative complication involving the central nervous system, but the underlying mechanism is not well understood. 4 key findings →
Evidence: low
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Complement overactivation mediates microglial synapse elimination in neurological diseases such as Alzheimer's disease (AD) and frontotemporal dementia (FTD), but how complement activity is regulated in the brain remains largely unknown. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
We revealed GLP-1's capacity to regulate astrocytic glycolysis, providing mechanistic insight into one of its neuroprotective roles in AD and support for the feasibility of energy regulation treatments for AD. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Clinically, superimposed systemic inflammation generally has significant deleterious effects on the Alzheimer's disease (AD) progression. 4 key findings →
Evidence: low
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BACE1 (beta-site amyloid precursor protein cleaving enzyme 1) was initially cloned and characterized in 1999. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Structural and functional connectivity methods are changing how researchers conceptualize and explore neuropsychiatric disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The insulinotropic hormone glucagon-like peptide-1 (7-36)-amide (GLP-1) has potent effects on glucose-dependent insulin secretion, insulin gene expression, and pancreatic islet cell formation and is presently in clinical trials as a therapy for type 2 diabetes mellitus. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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 →