Alzheimer’s disease: regulating copper in the brain stops memory loss among mice
Alzheimer’s disease is characterized by the presence of amyloid plaques* in the patient’s brain. These plaques sequester copper, and contain approximately five times as much as a healthy brain. Two CNRS scientists from the Coordination Chemistry Laboratory recently developed, with their colleagues from the Guangdong University of Technology and Shenzhen University (China), a molecule that regulates the circulation of copper in the brain. This patented molecule** extracts the copper trapped in amyloid plaques, and reintroduces it in the brain’s normal enzymatic circuit (which needs copper to function). Administered orally to “Alzheimer” mice,*** this molecule inhibits memory loss among sick mice. These results, which were published in ACS Chemical Neuroscience, open a new therapeutic avenue that could prove effective in early stages of Alzheimer’s disease among humans. The scientists are now seeking a pharmaceutical partner to develop preclinical trials for this drug candidate.
*- An amyloid plaque is an extracellular aggregate of protein fragments. These plaques are present in various neurodegenerative diseases.
**- Chinese patent no. 201610369550.X, 27 May 2016. PCT No. PCT/CN2017/085886, published on 30 November 2017. WO 2017/202360 A1. CNRS File no. O/Ref 08792-01. US Patent 10,807,957 B2, 20 October 2020.
***- The research team obtained positive results for three types of mouse models for Alzheimer’s: transgenic mice on the one hand, and two new models of non-transgenic mice on the other. These non-transgenic models are the closest to the reality of Alzheimer’s disease, which in the vast majority of cases is not genetic in origin.
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