Application of shRNA of targeted knockdown SIRT2 gene and precursor of nicotinamide adenine dinucleotide in preparation of medicine for treating neurodegenerative diseases

Abstract

The invention provides an application of shRNA (short hairpin Ribonucleic Acid) of targeted knockdown SIRT2 gene and a precursor of nicotinamide adenine dinucleotide in preparation of a medicine for treating neurodegenerative diseases, and the precursor of nicotinamide adenine dinucleotide can promote SIRT2 to enter a cell nucleus of an oligodendroglia precursor cell. Therefore, the differentiation of precursor cells of the oligodendroglia cells into mature oligodendroglia cells is promoted, myelin sheaths are repaired, the treatment of the demyelination diseases is further realized, and the effect of treating the demyelination diseases is fundamentally achieved. The medicine is good in taking safety, low in cost and high in patient compliance.

Description

technical field [0001] The disclosure relates to the technical field of genetic engineering, and in particular to the application of shRNA targeted to knock down SIRT2 gene and the precursor of nicotinamide adenine dinucleotide in the preparation of drugs for treating neurodegenerative diseases. Background technique [0002] Demyelination is one of the early events of nervous system aging and neurodegenerative diseases such as Alzheimer's disease and Huntington's disease, and is the characteristic pathological basis of nervous system demyelinating diseases such as multiple sclerosis. Ten to twenty years after the onset of central nervous system demyelinating diseases, many patients develop a gradual clinical course, which eventually leads to impaired mobility and cognitive abilities, seriously affecting the quality of life of patients and even leading to death. [0003] For demyelinating diseases of the central nervous system, there is no drug that can effectively promote my...

AI Technical Summary

Problems solved by technology

[0003] For demyelinating diseases of the central nervous system, there is no drug that can effectively promote myelin repair in clinical practice. At present, the main treatment method is to give immunomodulators. Although immunomodulators can slow down the disease process, they have no effect on the repair of myelin and cannot Completely prevent the development of the disease, treat the symptoms but not the root cause; in addition, immunomodulators are expensive, which increases the financial difficulties of patients and reduces patient compliance

Images