Tau protein is involved in maintaining neuronal structure. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
28,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
Tau protein is involved in maintaining neuronal structure. 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
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
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
Metformin is one of the most widely prescribed hypoglycemic drugs and has the potential to treat many diseases. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Clinical trials of new drugs for Alzheimer's disease (AD) have ended with disappointing results, with tremendous resources and time. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) presents a complex pathology entangling numerous pathological factors, including amyloid-β (Aβ), metal ions, and reactive oxygen species (ROS). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Drug repurposing aims to find new uses for already existing and approved drugs. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In silico reuse of old drugs (also known as drug repositioning) to treat common and rare diseases is increasingly becoming an attractive proposition because it involves the use of de-risked drugs, with potentially lower overall development costs and shorter development timelines. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dementia with Lewy bodies (DLB) is characterized by the toxic accumulation of α-synuclein protein inside neural cells; this results in neurodegeneration which is clinically accompanied by behavioral and psychological changes. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurofibrillary tangles, which consist of highly phosphorylated tau protein, and senile plaques (SPs) are pathological hallmarks of Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In this issue of Neuron, Wang et al. employ an impressive multi-omics approach, including gene co-expression network analyses and drug repositioning, to normalize disease-disrupted gene modules and identify a therapeutically relevant driver of Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microcystin-leucine-arginine (MC-LR) is a toxin secreted by freshwater cyanobacteria that is considered a potential environmental risk factor for Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Experimental data reveal that lithium is capable of attenuating Alzheimer's disease pathology and stimulating adult hippocampal neurogenesis. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Insulin deficiency or resistance can promote dementia and hallmarks of Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In this study, a drug repositioning algorithm based on a deep autoencoder and adaptive fusion was proposed to mitigate the problems of decreased precision and low-efficiency multisource data fusion caused by data sparseness. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
According to the FDA, aducanumab (Aduhelm), the recently approved anti-Alzheimer drug, reduces the level of cerebral amyloid plaques-a hallmark finding in patients with Alzheimer's disease-and this will result in a reduction in clinical decline. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
We found that both Adu and SUS reduced the total plaque area in the hippocampus to a similar degree, with no additive effect in the combination treatment (SUS+Adu). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tau immunotherapies have advanced from proof-of-concept studies to over a dozen clinical trials for Alzheimer's disease (AD) and other tauopathies. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tau has become an attractive alternative target for passive immunotherapy efforts for Alzheimer's disease (AD). 1 key finding →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Type 2 diabetes mellitus and the associated desensitisation of insulin signalling has been identified as a risk factor for progressive neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease and others. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The glucagon-like peptide-1 (GLP-1) was shown to have neuroprotective effects in Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive neurodegenerative disease, also regarded as "type 3 diabetes" for the last few years because of the brain insulin resistance (IR) and dysregulation of insulin signaling in the brain, which can further promote pathological progression of AD. 1 key finding →
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 28,980 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 28,980 records, built mostly from automated pulls of Europe PMC (62.8% of the library) and OpenAlex (17.6%), 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.
1,038 records (3.6% of the library) are not peer-reviewed — 966 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 →