Our analysis encompassed 22 RCTs involving 138,282 participants (mean age 64.8 years, 36.4% female). 5 key findings →
Design: meta-analysis Participants: 138,282 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.
GLP-1 RA therapy did not alter amyloid-β and tau biomarkers nor show improvements in cognition but showed potential metabolic and neuroprotective benefits. 1 key finding →
Design: systematic review Participants: 1,444 Evidence: high
Full summary, score breakdown and related studies → Original source
There was no change in the primary outcome. 5 key findings →
Participants: 32 Evidence: high
Full summary, score breakdown and related studies → Original source
Newer GLDs were associated with a decreased risk of all-cause dementia in people with T2D. Because of the observational nature and significant heterogeneity between studies, the results should be interpreted with caution. 5 key findings →
Design: meta-analysis Participants: 819,511 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
Emerging evidence suggests that treatment with glucagon-like peptide-1 receptor agonists (GLP-1 RAs) could be an interesting treatment strategy to reduce neurological complications such as stroke, cognitive impairment, and peripheral neuropathy. 3 key findings →
Design: systematic review Participants: 19 Evidence: high
Full summary, score breakdown and related studies → Original source
There are fewer than normal glucose transporters at the blood-brain barrier (BBB) in Alzheimer's disease (AD). 2 key findings →
Participants: 18 Evidence: high
Full summary, score breakdown and related studies → Original source
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
This study provides evidence that the effects of GLP-1 receptor agonists may extend beyond their known metabolic and cardioprotective benefits to include neuroprotection, associated with a decreased risk of developing various neurodegenerative disorders. 5 key findings →
Design: cohort study Participants: 102,935 Evidence: moderate
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
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
We concluded that liraglutide improves cognitive decline in patients with type 2 diabetes mellitus. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The positive finding of lower EV Aβ42 supports emerging evidence that plasma neuronal EVs provide an effective platform for demonstrating biomarker responses in clinical trials in AD. 3 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source
Insulin resistance (IR) is a metabolic state preceding development of type 2 diabetes (DM2), cardiovascular disease, and neurodegenerative disorders, including Alzheimer's Disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recent literature shows that GLP-1 and its agonists, DPP-4 inhibitors and combined GLP-1/GIP molecules are effective in partially or fully reversing the effects of neurotoxic compounds, neurovascular complications of diabetes, neuropathological changes related with Alzheimer's disease, Parkinson's disease or vascular occlusion. 4 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
Liraglutide might slow down memory function decline in diabetic patients in early, and possibly preclinical stages of the disease. 2 key findings →
Participants: 20 Evidence: low
Full summary, score breakdown and related studies → Original source
Previous studies have suggested an acutely improving effect of insulin on memory function. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
136 adults with T1D (n=90, age 52 years, 58% female, average HbA1c 7.7%) and without T1D (n=46, age 53 years, 57% female, average HbA1c 5.4%) were included. 5 key findings →
Design: cross-sectional Participants: 90 Evidence: low
Full summary, score breakdown and related studies → Original source
Overall, 214,442 matched individuals initiated GLP-1 RAs or DPP4i (109,731 women, mean age 58.6 years [SD 12], and mean HbA1c 7.7% [1.4]). 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Glucagon-like peptide-1 receptor agonists (GLP-1 RAs), originally developed for type 2 diabetes mellitus and obesity, are increasingly recognized for their significant impact on the central nervous system, leading to reports of both beneficial and adverse mental health effects. 5 key findings →
Design: cohort study Evidence: high
Full summary, score breakdown and related studies → Original source
We also assessed the rates in patients with other significant medical, neurologic, or mental comorbid illness. 3 key findings →
Design: cross-sectional Participants: 652,378 Evidence: low
Full summary, score breakdown and related studies → Original source
The pooled trial included 88,381 participants who received prescriptions for GLP-1 agonists (n = 12,351), DPP-4 inhibitors (n = 43,850), or sulfonylureas (n = 32,216) at baseline and were followed for an average of 4.3 years. 5 key findings →
Participants: 12,351 Evidence: low
Full summary, score breakdown and related studies → Original source
Preclinical evidence in transgenic models of Alzheimer's disease suggests that liraglutide exerts neuroprotective effects by reducing amyloid oligomers, normalising synaptic plasticity and cerebral glucose uptake, and increasing the proliferation of neuronal progenitor cells. 4 key findings →
Participants: 206 Evidence: high
Full summary, score breakdown and related studies → Original source
The global rise in both metabolic syndrome (MetS) and neurodegenerative diseases (NDs), particularly dementia and Alzheimer's disease (AD) poses a growing health and socioeconomic burden. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
In animal models, the incretin hormone GLP-1 affects Alzheimer's disease (AD). 3 key findings →
Participants: 18 Evidence: high
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 →