27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Targeting of tau pathology has long been proposed as a potential therapeutic strategy for Alzheimer's disease (AD). 5 key findings →
Design: clinical trial Evidence: high
Full summary, score breakdown and related studies → Original source
From 10,037 records, 82 studies were included. 5 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
Mean age was 65 years and 43% were female. 5 key findings →
Design: cohort study Participants: 158 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We determined the demographics and social drivers of health associated with utilization and initial adherence of these medications. 5 key findings →
Participants: 1,198,362 Evidence: low
Full summary, score breakdown and related studies → Original source
Mary Poppins famously asserted that "a spoonful of sugar helps the medicine go down," but this bon mot is likely wrong in almost every way. 1 key finding →
Design: meta-analysis Participants: 74,148 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Among 1,528,885 adults with type 2 diabetes (mean age, 58 years; 49.2% women), GLP-1 receptor agonists plus metformin were associated with lower incidence of vascular dementia (HR, 0.46; 95% CI, 0.37-0.57), mild cognitive disorder (HR, 0.79; 95% CI, 0.66-0.95), and Alzheimer disease (HR, 0.46; 95% CI, 0.31-0.70). 5 key findings →
Design: cohort study Participants: 1,528,885 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
These convergent data support a prospective clinical trial of low-dose lithium orotate to slow disease progression in MCI. 3 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source
The long-term efficacy of amyloid-targeting therapies hinges on their ability to slow downstream neuropathologic change, but little is known about the influence of amyloid clearance on tau pathology and neurodegeneration. 4 key findings →
Design: longitudinal study Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Glucagon-like peptide-1 receptor agonists (GLP-1RAs) have shown promise in preclinical models of neurodegeneration, with emerging evidence suggesting these effects may be driven by modulation of neuroinflammation. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
GLP-1RA use was associated with a significantly lower risk of dementia [hazard ratio (HR) 0.80, 95% confidence interval (CI) 0.71-0.91, P = .001] and Alzheimer's disease (HR 0.76, 95% CI 0.59-0.98, P = .033) compared with DPP4i use. 4 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Glucagon-like peptide-1 receptor (GLP-1R) activation is widely assumed to regulate the metabolic disorder in Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The intersection of metabolic disease and neurodegeneration represents one of the most consequential frontiers in translational neuroscience. 3 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
The aggregation of the 42-residue form of the amyloid-β peptide (Aβ42) is important in Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Fifty-three sources were included. 2 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Considering the overall sci-entific evidence presented, it is important to note that GLPs are no longer just antihyperglycemic drugs but are remarkably versatile, with a future in almost every field of medicine. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
All recently approved monoclonal antibodies (eg, aducanumab, lecanemab, and donanemab) for Alzheimer disease (AD) were shown to increase the risks of amyloid-related imaging abnormalities (ARIA) in randomized clinical trials, which can include brain swelling or hemorrhage. 4 key findings →
Participants: 240 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Glucagon-like peptide-1 receptor agonists (GLP-1 RAs), particularly semaglutide, have demonstrated substantial efficacy for glycemic control and weight management and are increasingly prescribed across diverse populations. 4 key findings →
Design: narrative review Evidence: high
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Stroke and dementia are leading causes of death and disability worldwide, requiring enhanced preventive strategies. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Glucagon-like peptide-1 receptor agonists (GLP-1RAs) have expanded beyond glycemic control to include cardiovascular and renal risk reduction, with recent approval for reducing major adverse cardiovascular events in individuals with obesity or overweight and established cardiovascular disease. 1 key finding →
Design: clinical trial Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
To the Editor: MC1 is a monoclonal anti-tau antibody developed by the Peter Davies laboratory in the 1990s to aid the neuropathological diagnosis of Alzheimer disease (AD).1 Raised against Alz-50-immunopurified paired helical filaments (PHFs) from an AD brain, MC1 recognizes a conformational, discontinuous epitope involving residues 7-9 in the N-terminus and 313-322 in the third repeat domain of tau (Figure 1A). 1 key finding →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Neurodegenerative disorders (NDDs), primarily alzheimer, dementia, parkinson, and rare NDD disease, present an escalating global health crisis, currently affecting over 55 million older adults worldwide. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Our findings reveal various concerns about Aduhelm involving efficacy, safety, and affordability. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We estimated associations of educational attainment and Alzheimer disease genetic risk with treatment initiation and incident dementia and compared GLP-1 receptor agonist initiators with initiators of non-sodium-glucose cotransporter 2 inhibitor second-line therapies, with a separate sodium-glucose cotransporter 2 inhibitor compa 4 key findings →
Design: cohort study Participants: 14,364 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Haploinsufficiency of progranulin (resulting from mutations in the GRN gene) is a major genetic cause of frontotemporal dementia (FTD), which is characterized by profound changes in personality and behavior, progressive impairments in executive function, speech, language and/or movement, TDP-43 pathology, lysosomal dysfunction, and neuroinflammation. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Electrochemical biosensors offer a promising route for the rapid, non-invasive detection of disease biomarkers by converting biochemical interactions into measurable electrical signals. 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 →