27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
This analysis indicated that patients with type 2 diabetes under treatment with DPP-4 inhibitors presented with the lowest risk of dementia, followed by those treated with metformin and thiazolidinedione, while treatment with insulin was associated with the highest risk. 5 key findings →
Design: meta-analysis Participants: 530,355 Evidence: high
Full summary, score breakdown and related studies → Original source
Of note, dramatic progress has been made in recent years in diabetes research and clinical practice, which includes approval of antidiabetic agents with novel mechanisms of action along with publication of clinical trial results with these drugs, and novel diagnostic and therapeutic devices, such as continuous glucose monitoring (CGM) and sensor augmented pumps (SAP). 5 key findings →
Design: randomized controlled trial 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
The 2020 pipeline has innovations in clinical trials and treatment targets that provide hope for greater success in AD drug development programs. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer disease (AD) may develop after the onset of type 2 diabetes mellitus (T2DM), and the risk of AD may depend on the antidiabetic drug administered. 2 key findings →
Participants: 85 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer Disease (AD) is a neurodegenerative disease characterized by two neuropathological hallmarks: extracellular deposition of amyloid plaques and intracellular neurofibrillary tangles. 4 key findings →
Evidence: low
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Amyloid-β (Aβ) deposits are a relatively late consequence of Aβ aggregation in Alzheimer's disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Neurofibrillary tangles (NFTs) composed of hyperphosphorylated and misfolded tau protein are a pathological hallmark of Alzheimer's disease and other tauopathy conditions. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a major cause of morbidity worldwide and its prevalence is expected to rise. 1 key finding →
Evidence: high
Full summary, score breakdown and related studies → Original source
Alzheimer disease (AD) is a chronic neurodegenerative disorder with complex pathophysiology that affects over 50 million people worldwide. 4 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
In October 2019, a Swiss panel of experts met for the Dementia Summit in Brunnen, Switzerland, to discuss the latest scientific findings on basic and clinical research, as well as practical and political approaches to the challenges of dementia disorders in Switzerland. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Tau deposition in the brain is a pathological hallmark of many neurodegenerative disorders, including Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Polygala tenuifolia and its active components have multiplex neuroprotective potential associated with AD, such as anti-A β aggregation, anti-Tau protein, anti-inflammation, antioxidant, anti-neuronal apoptosis, enhancing central cholinergic system and promote neuronal proliferation. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common form of dementia worldwide, being characterized by the deposition of senile plaques, neurofibrillary tangles (enriched in the amyloid beta (Aβ) peptide and hyperphosphorylated tau (p-tau), respectively) and memory loss. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) and Parkinson's disease (PD) are neurodegenerative diseases (NDD) characterized by progressive degeneration of the central nervous system, and few medications are available to halt the progression of AD and PD. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a neurodegenerative disorder for which there is no cure. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Several flavonoids have been recognized as nutraceuticals, and myricetin is a good example. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The reduction of tau or hyperphosphorylated tau (p-tau) has been proposed as a therapeutic strategy for Alzheimer's disease (AD) and frontotemporal dementia (FTD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Following acute myocardial infarction, re-establishment of coronary perfusion aggravates further injuries in the heart and remote organs including the brain as a consequence of ischemia/reperfusion (I/R) injury. 1 key finding →
Participants: 30 Evidence: low
Full summary, score breakdown and related studies → Original source
Neuronal insulin resistance is a significant feature of Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alogliptin treatment alleviated LPS-induced cognitive impairment as assessed by Morris water maze and novel object recognition tests. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our results demonstrate that DA5‐CH has neuroprotective effects in the STZ‐induced animal model and that DA5‐CH has potential to treat neurodegenerative disorders such as AD. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Vildagliptin (Vilda), a dipeptidyl peptidase-4 (DPP-4) inhibitor, has been highlighted as a promising therapeutic agent for neurodegenerative diseases as Alzheimer's and Parkinson's diseases. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Glucagon-like peptide-1 (GLP-1) receptor agonists are a class of antidiabetic drugs that improve the glycaemia via several molecular pathways. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The burden of Alzheimer disease (AD) on the US healthcare system is substantial and increasing. 4 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
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 →