27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
The systematic review and NMA includes 493 168 participants from 869 trials (adding 53 trials since October 2022) reporting data for 13 drug classes (63 drugs) and 26 outcomes of interest. 5 key findings →
Design: systematic review Participants: 168 Evidence: high
Full summary, score breakdown and related studies → Original source
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
There was no change in the primary outcome. 5 key findings →
Participants: 32 Evidence: high
Full summary, score breakdown and related studies → Original source
Understanding the neuropathological effects of amyloid β (Aβ)-targeting therapies and amyloid-related imaging abnormalities (ARIA) in Alzheimer's disease is critical for optimising treatment efficacy and patient outcomes. 4 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
This article summarizes the top 20 research studies of 2024 identified as POEMs (patient-oriented evidence that matters). 4 key findings →
Design: meta-analysis Evidence: high
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
Despite the increasing approval of antiamyloid antibodies for Alzheimer disease (AD), their clinical relevance and risk-benefit profile remain uncertain. 4 key findings →
Design: meta-analysis Participants: 21,236 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Our two-sample MR analysis indicated that T2D is not associated with the risk of AD (OR: 1.03, CI: 0.99-1.08, P = 0.128). 5 key findings →
Participants: 455,017 Evidence: low
Full summary, score breakdown and related studies → Original source
We identified GLP-1 receptor agonist initiation compared to DPP-4 inhibitors initiation was associated with a reduced risk of AD (hazard ratio [HR] ≤ 0.69 and P value < 0.001) and SGLT-2 inhibitor initiation compared to DPP-4 inhibitor initiation was associated with a reduced risk of AD (HR ≤ 0.67 and P value < 0.001). 5 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source
Among 275,144 initiators of DPP-4 inhibitors or sulfonylureas, followed for 750,846 person-years, DPP-4 inhibitors were associated with a reduced dementia risk compared with sulfonylureas (4.4 vs. 5.7 events per 1000 person-years; HR 0.77, 95% CI 0.71-0.85). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This case suggests that mirtazapine may be beneficial in mitigating GLP-1 RA-induced gastrointestinal side effects, thereby improving adherence and therapeutic efficacy. 4 key findings →
Design: case report Evidence: low
Full summary, score breakdown and related studies → Original source
Metformin is the most widely used oral insulin-sensitizing agent. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
GLP-1RA use was associated with lower risk of dementia (HR 0.80, 95% CI 0.71–0.91) and Alzheimer’s disease (HR 0.76, 95% CI 0.59–0.98) compared to DPP4is. 5 key findings →
Design: cohort study Participants: 12,351 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
As Alzheimer's disease (AD) research advances, tau has emerged as both a critical biomarker and a promising therapeutic target, central to understanding disease mechanisms, tracking progression, and guiding treatment development. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In Alzheimer's disease, tau pathology spreads across brain regions as the disease progresses. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Clinical trials for Alzheimer's disease (AD) must be registered on clinicaltrials.gov. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Repurposed drugs provide a rich source of potential therapies for Alzheimer's disease (AD) and other neurodegenerative disorders (NDD). 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
The AMPK/SIRT1/PGC-1α pathway represents a cornerstone target at the intersection of metabolism, aging, and disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
A marked evolution in Alzheimer's disease (AD) therapy research is ongoing. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Prevention of Alzheimer disease (AD) is a medical challenge owing to its complex pathogenesis, which involves amyloid-β (Aβ) and tau aggregation, neuroinflammation and progressive neurodegeneration. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Experimental drugs lowering brain tau are heralded as improvements in the treatment of Alzheimer's disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tauopathies represent a class of neurodegenerative diseases (NDs), including Alzheimer's disease (AD), progressive supranuclear palsy (PSP), Pick's disease (PiD), and corticobasal degeneration (CBD), defined by intracellular accumulation of misfolded and hyperphosphorylated tau protein. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Nanobodies (single-domain antibodies, VHHs) have emerged as versatile tools for evaluating and treating Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Abnormal accumulation of tau proteins in the brain is a hallmark of neurodegenerative diseases such as Alzheimer's disease and is closely linked with neuronal cell death. 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 →