Another weak spot has been found in Alzheimer's disease
A new target for the treatment of Alzheimer's disease
LifeSciencesToday based on ScienceDaily: New therapeutic target for Alzheimer's disease identifiedA group of scientists from the Louisiana State University Health Sciences Center, New Orleans, led by Associate Professor of Neurology Chu Chen, PhD, believes that the enzyme monoacylglycerol lipase (MAGL) may become a new therapeutic target of drugs for the treatment or prevention of Alzheimer's disease.
Article by Rongqing Chen et al. Monoacylglycerol Lipase Is a Therapeutic Target for Alzheimer's Disease published in the Online Now section of the journal Cell Reports.
Scientists have found that inhibition of the enzyme MAGL, well known for its role in the decomposition of brain-synthesized cannabinoids, suppresses the formation and accumulation of beta-amyloid plaques, which are a characteristic feature of Alzheimer's disease, neuroinflammation and neurodegeneration, which leads to increased brain plasticity and learning ability, as well as improved memory.
"Our results suggest that MAGL contributes to the etiology and development of Alzheimer's disease and that blocking it is a promising therapeutic target," notes Dr. Chu Chen.
By blocking the MAGL enzyme in mice with a highly selective and powerful inhibitor, the scientists found that inactivation of MAGL for eight weeks is enough to reduce the formation and deposition of beta-amyloid plaques and suppress the function of one of the genes (the enzyme BACE1 – beta-site amyloid precursor protein cleaving enzyme 1) involved in the process of beta-amyloid into a substance toxic to brain cells. In addition, the inhibition of MAGL decreased the rates of neuroinflammation and neurodegeneration. The scientists concluded that inactivation of MAGL in mice not only preserves the structural and functional integrity of synapses associated with the cognitive functions of hippocampal neurons, but also increases the ability to learn and improves memory, which was confirmed by behavioral tests.
In mice with the Alzheimer's disease model, MAGL inhibition suppresses the formation and accumulation of beta-amyloid plaques and the expression of the enzyme BACE1, reduces neuroinflammation and neurodegeneration, preserves the structural and functional integrity of synapses in the hippocampus, increases brain plasticity, learning ability, and improves memory. (Photo: cell.com/cell-reports )
Alzheimer's disease is a neurodegenerative disease characterized by the accumulation and deposition of amyloid plaques and neurofibrillary tangles, neuroinflammation, synaptic dysfunction, progressive deterioration of cognitive abilities and memory loss caused by mass death of nerve cells. This disease is the most common cause of dementia in the elderly, that is, 5.4 million people in the United States and 36 million worldwide. Unfortunately, the few drugs that are currently approved by the Food and Drug Administration (Food and Drug Administration) have only a minor and short-term effect on clinical symptoms. None of them demonstrated a noticeable effect on the progression of the disease or its prevention.
"There is a great need for new methods of prevention and treatment of this serious disease," Dr. Chen emphasizes. Although the molecular mechanisms underlying the positive effects of MAGL inhibition have yet to be established, he and his colleagues believe that this enzyme, which regulates endocannabinoid and prostaglandin signaling, contributes to the pathogenesis and neuropathology of Alzheimer's disease and, therefore, is a promising therapeutic target for the prevention and treatment of this disease.
The study involved scientists from the Massachusetts Institute of Technology (Massachusetts Institute of Technology).
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