Treatment with GLP-1 RAs may provide a new opportunity to reduce the incidence of dementia in patients with type 2 diabetes. 2 key findings →
Participants: 15,820 Evidence: high
Full summary, score breakdown and related studies → Original source
Research
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Seventeen studies were identified: thirteen cohort studies, two case-control studies, and two nested case-control studies. 5 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
Glucagon-like peptide-1 (GLP-1) is a human incretin hormone derived from the proglucagon molecule. 1 key finding →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
70/100
The results showed that intestinal expression of GLP-1 1 could reduce the intestinal pathogenic genus such as Enterobacteriaceae and was obviously associated with a greater number of beneficial genera such as Lactobacillus and Akkermansia. 4 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
Reversal genes and the candidate compounds were identified by the leave-one-out cross-validation procedure. 3 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
The PubMed and Embase databases were searched for clinical trials of anti-Aβ immunotherapy published on or before January 12, 2022. 4 key findings →
Design: clinical trial Participants: 9,429 Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Genetic variation in sulfonylurea targets was associated with a lower risk of AD, and future studies are warranted to clarify the underlying mechanistic pathways between sulfonylureas and AD. 5 key findings →
Participants: 326,885 Evidence: low
Full summary, score breakdown and related studies → Original source
ATN (β-amyloid [Aβ], tau, neurodegeneration) system categorizes individuals based on their core Alzheimer disease (AD) biomarkers. 4 key findings →
Design: cross-sectional Participants: 410 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Therefore, respective software was developed in-house.8,9 Segmentation results are then analysed for potential associations with disease risks and to establish reference intervals of organ size and function.10 SHIP is also used as a basis for meta-research with a particular focus on incidental MRI findings and their effects on study participants.11,12 With its large amount of standardized data and the option to internally replicate findings from SHIP-START using data of the independent SHIP-TREND, the project offers good opportunities to apply new bioinformatical tools to mine the data and gain new insights into risk factors and pathomechanisms. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
We sought to identify cognitive measures associated with the earliest detectable signs of emerging Aβ and tau pathology. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Many drugs that target amyloid-β (Aβ) in Alzheimer disease (AD) have failed to demonstrate clinical efficacy. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The AD drug development pipeline has agents representing a substantial array of treatment mechanisms and targets. 1 key finding →
Design: clinical trial Participants: 31 Evidence: low
Full summary, score breakdown and related studies → Original source
Comparison of SUVR in different brain regions demonstrated significant differences in the temporal, occipital and cerebellar cortices. 4 key findings →
Participants: 830 Evidence: low
Full summary, score breakdown and related studies → Original source
Among 157 subjects with a mean age of 71.8 (±7.7) included in this study, 76 individuals were stratified as metformin users. 5 key findings →
Participants: 157 Evidence: low
Full summary, score breakdown and related studies → Original source
49/100
Aducanumab was granted accelerated approval with a conflicting evidence base, near-unanimous Food and Drug Administration Advisory Committee vote to reject approval, and a widely criticized launch price of $56,000 per year. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
47/100
Despite an ever-growing prevalence and increasing economic burden of Alzheimer's disease (AD) and Parkinson's disease (PD), recent advances in drug development have only resulted in minimally effective treatment. 1 key finding →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Alois Alzheimer first described in a patient "a peculiar severe disease process of the cerebral cortex", people suffering from this pathology have been waiting for a breakthrough therapy. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Recent studies show that incretin hormone analogues effectively control blood glucose while producing major weight losses and reducing the risk of all-cause mortality, myocardial infarction, stroke and kidney function impairment. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
45/100
Insulin resistance (IR) contributes to the pathophysiology of diabetes, dementia, viral infection, and cardiovascular disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is a neurodegenerative disease that accounts for most of the 50-million dementia cases worldwide in 2018. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Lack of Klotho or FGF23 results in hyperphosphatemia and hypervitaminosis D. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
43/100
Since type 2 diabetes mellitus (T2DM) is a risk factor for Alzheimer's disease (AD) and both have the same pathogenesis (e.g., insulin resistance), drugs used to treat T2DM have been gradually found to reduce the progression of AD in AD models. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Significant weight reduction ability of semaglutide has been demonstrated in various phase-3 clinical trials, for which recently semaglutide became the first long-acting GLP-1 receptor agonist to be approved by the United States Food and Drug Administration for management of obesity. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recent clinical guidelines have emphasized the importance of screening for cognitive impairment in older adults with diabetes, however, there is still a lack of understanding about the drug therapy. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Obesity in women of reproductive age has a number of adverse metabolic effects, including Type II Diabetes (T2D), dyslipidemia, and cardiovascular disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Where “Free full text” comes from
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
How the 0–100 score works — and why some entries are capped
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.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
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.
What this library is — and isn't
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 →