Tau pathology is essential in the pathogenesis of Alzheimer's disease (AD) and related tauopathies. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Tau pathology is essential in the pathogenesis of Alzheimer's disease (AD) and related tauopathies. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Semaglutide, one of the most potent glucagon-like peptide (GLP)-1 analogs, has widely been used to treat type II diabetes mellitus and obesity. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The glucagon-like peptide-1 (GLP-1) is a pleiotropic hormone very well known for its incretin effect in the glucose-dependent stimulation of insulin secretion. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Prevention of cardiovascular events and regression of atherosclerotic changes are the primary aims of preventive cardiovascular medicine. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The effects of LRGT on animal models show significant benefits in AD pathology and cognitive impairment. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The therapeutic benefits of the incretin hormone, glucagon-like peptide 1 (GLP1), for people with type 2 diabetes and/or obesity, are now firmly established. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Diabetes mellitus can result in severe complications, such as neurodegenerative diseases including cognitive impairment and dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Aging is a crucial risk factor for common neurodegenerative diseases, such as Alzheimer's disease (AD) and Parkinson's disease (PD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Type 2 diabetes mellitus (T2DM) and Alzheimer's disease (AD) commonly co-occur. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
GLP-1 is derived from intestinal L cells, which takes effect through binding to GLP-1R and is inactivated by the enzyme dipeptidyl peptidase-4 (DPP-4). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Stimulation of glucagon-like peptide-1 (GLP-1) receptors increases the insulin release in the pancreas during high glucose levels, and also stimulates a feeling of satiety. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
To help ensure an expanded healthy lifespan for as many people as possible worldwide, there is a need to prevent or manage a number of prevalent chronic diseases directly and indirectly closely related to aging, including diabetes and obesity. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Glaucoma is a common ocular neurodegenerative disease characterized by the progressive loss of retinal ganglion cells and their axons. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Increasing evidence shows a close relationship between Alzheimer's disease (AD) and type 2 diabetes mellitus (T2DM). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The glucagon-like peptide-1 (GLP-1) is a pleiotropic hormone well known for its incretin effect in the glucose-dependent stimulation of insulin secretion. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Both act by binding with fibrillary conformations of Aβ plaques in the brain. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) treatment includes both non-pharmacological and pharmacological approaches. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Prevalence of dementia continues to increase with limited pharmacotherapy options available. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Acetylcholinesterase (AchE), hydrolase enzyme, regulates the hydrolysis of acetylcholine neurotransmitter in the neurons. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dementia is a debilitating neurological condition that is characterized by persistent cognitive decline. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common form of dementia, with a high impact worldwide, accounting for more than 46 million cases. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The past 30 years have seen multiple attempts at demonstrating the safety and efficacy of drugs for Alzheimer's disease (AD), predominantly to improve symptoms. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The cholinesterase inhibitor donepezil is used to improve Aβ pathology and cognitive function in patients with Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's Disease (AD) is characterized as a progressive neurodegenerative disease most commonly associated with memory deficits and cognitive decline. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
All cholinesterase inhibitors reduced cognitive deficits with the following optimal daily doses: galantamine 1.25 mg kg(-1), rivastigmine 0.5 mg kg(-1) and donepezil 0.3 mg kg(-1). 5 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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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.
1,034 records (3.6% 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 →