Scientists from the Institute of Cytology of the Russian Academy of Sciences (INC) and the Ural Federal University have selected a compound that enhances the activity of the synthesis of chaperone proteins, which prevents the development of Alzheimer’s disease in aging nerve cells. This was reported to socialbites.ca at the Institute of Scientific Centers of the Russian Academy of Sciences.
Today, the amyloid hypothesis of the development of Alzheimer’s disease is popular in the scientific community. According to this concept, the cause of the disease is the appearance of beta-amyloid peptide in the brain tissues with age, on the basis of the formation of plaques that are toxic to nerve cells. As a result, neurons die and the person suffers from dementia.
“Alzheimer’s disease progresses with age, and this is mainly due to a decrease in the amount of heat shock proteins (chaperones) whose myriad functions are to protect cells from beta-amyloid. “We synthesized a new, breakthrough compound IA-50, which causes the accumulation of chaperones in aging nerve cells,” says Vladimir Lazarev, senior researcher at the Laboratory of Cell Defense Mechanisms of the Institute of Scientific Centers of the Russian Academy of Sciences.
IA-50 belongs to the group of indolylazines, representatives of this class of compounds activate the synthesis and accumulation of chaperones in nerve cells. Compound IA-50 was chosen based on computer simulation data as it can easily penetrate the membranes of senescent neurons.
“The results of the experiments showed that the use of IA-50 activates the synthesis of chaperones and contributes to their accumulation in brain tissues, as well as inhibits the development of memory impairment and the formation of beta-amyloid plaques. The data generally clarifies our ideas about potential neuroprotectors that could form the basis for the development of drugs for the effective treatment of neurodegenerative diseases such as Alzheimer’s disease in the future.”
The experiments were carried out on several cell models: on aging and “young” human neurons, as well as on transgenic mice with cognitive impairments caused by the development of Alzheimer’s disease.
Source: Gazeta
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