ArticlePloS one2014
The anti-diabetic drug metformin reduces BACE1 protein level by interfering with the MID1 complex.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 86 citations in OpenAlex.
- Aberrant expression of the MID1 protein in neurons of Huntington's disease brain.Frontiers in genetics · 2026Article
- Novel targets and therapies of metformin in dementia: old drug, new insights.Frontiers in pharmacology · 2024Review
- Repositioning of Anti-Diabetic Drugs against Dementia: Insight from Molecular Perspectives to Clinical Trials.International journal of molecular sciences · 2023Review
- BACE1: More than just a β-secretase.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2022Review
- Recent Advances Towards Diagnosis and Therapeutic Fingerprinting for Alzheimer's Disease.Journal of molecular neuroscience : MN · 2022Review
- The association of antidiabetic medications and Mini-Mental State Examination scores in patients with diabetes and dementia.Alzheimer's research & therapy · 2021Article
- The interplay among oxidative stress, brain insulin resistance and AMPK dysfunction contribute to neurodegeneration in type 2 diabetes and Alzheimer disease.Free radical biology & medicine · 2021Review
- Metformin activates chaperone-mediated autophagy and improves disease pathologies in an Alzheimer disease mouse model.Protein & cell · 2021 · on this mapArticle
- Metformin a Potential Pharmacological Strategy in Late Onset Alzheimer's Disease Treatment.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Metformin attenuates plaque-associated tau pathology and reduces amyloid-β burden in APP/PS1 mice.Alzheimer's research & therapy · 2021Article
- The MID1 Protein: A Promising Therapeutic Target in Huntington's Disease.Frontiers in genetics · 2021Article
- Review
- Brain Protein Synthesis Rates in the UM-HET3 Mouse Following Treatment With Rapamycin or Rapamycin With Metformin.The journals of gerontology. Series A, Biological sciences and medical sciences · 2020Article
- High-glucose-induced apoptosis, ROS production and pro-inflammatory response in cardiomyocytes is attenuated by metformin treatment via PP2A activation.Journal of biosciences · 2020Article
- The Bewildering Effect of AMPK Activators in Alzheimer's Disease: Review of the Current Evidence.BioMed research international · 2020Review
- Network-centric medicine for peripheral nerve injury: Treating the whole to boost endogenous mechanisms of neuroprotection and regeneration.Neural regeneration research · 2019Article
- Metformin Inhibit Lung Cancer Cell Growth and Invasion in Vitro as Well as Tumor Formation in Vivo Partially by Activating PP2A.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Inhibition of the MID1 protein complex: a novel approach targeting APP protein synthesis.Cell death discovery · 2018Article
- Metformin and its sulphonamide derivative simultaneously potentiateanti-cholinesterase activity of donepezil and inhibit beta-amyloid aggregation.Journal of enzyme inhibition and medicinal chemistry · 2018Article
- Endoplasmic Reticulum Stress Induces Myostatin High Molecular Weight Aggregates and Impairs Mature Myostatin Secretion.Molecular neurobiology · 2018Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD), the most common form of dementia in the elderly, is characterized by two neuropathological hallmarks: senile plaques, which are composed of Aβ peptides, and neurofibrillary tangles, which are composed of hyperphosphorylated TAU protein. Diabetic patients with dysregulated insulin signalling are at increased risk of developing AD. Further, several animal models of diabetes show increased Aβ expression and hyperphosphorylated tau. As we have shown recently, the anti-diabetic drug metformin is capable of dephosphorylating tau at AD-relevant phospho-sites. Here, we investigated the effect of metformin on the main amyloidogenic enzyme BACE1 and, thus, on the production of Aβ peptides, the second pathological hallmark of AD. We find similar results in cultures of primary neurons, a human cell line model of AD and in vivo in mice. We show that treatment with metformin decreases BACE1 protein expression by interfering with an mRNA-protein complex that contains the ubiquitin ligase MID1, thereby reducing BACE1 activity. Together with our previous findings these results indicate that metformin may target both pathological hallmarks of AD and may be of therapeutic value for treating and/or preventing AD.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.