Dr. Cui Guohong and Dr. He Qing from the Department of Neurology, the Ninth People’s Hospital, Shanghai Jiaotong University School of Medicine have made new progress in the research of Alzheimer’s disease and Parkinson’s disease, respectively. The relevant results were recently published in Molecular Neurobiology "on.
Alzheimer's disease (AD) is the third leading killer of the elderly after cardiovascular diseases and tumors, but its etiology and mechanism are still unknown in modern medicine, and it is excellent in related treatments. There is no specificity. Cui Guohong’s rat model experiments show that NSC transplantation can differentiate into neurons and improve the learning and memory ability of AD rats to a certain extent. However, the pathological microenvironment of AD (such as Aβ deposition and immune inflammatory response) does not promote the survival, differentiation and functional integration of NSC and the host, which has a profound impact on the therapeutic effect of stem cell transplantation. Studies have shown that biomaterials can provide a good microenvironment for the growth of transplanted stem cells. This promotes the survival and differentiation of transplanted stem cells. Cui Guohong plays an important role in the design and synthesis of its own peptides, which can promote the survival and differentiation of NSC in vivo and in vitro, and improve the effectiveness of stem cell transplantation in the treatment of AD.
Parkinson's disease (PD) is another common degenerative neurological disease in the elderly. Heqing used the adenovirus vector AAV1/2 to successfully prepare a rat PD model by transporting the A53T point mutant α-n-alkane in three dimensions and injecting it into the rat substantia nigra. Rats exhibit reduced spontaneous activity and black dopaminergic neurons. Loss, the release of striatal dopamine and other mediators is reduced, and the abnormal accumulation of α-n-butenedioic acid. This model provides an excellent model tool for studying the pathological mechanism and intervention methods of α-n-butene-mediated PD. At the same time, Heqing found that trehalose enhances brain autophagy, thereby promoting the degradation of black α-sinucrane in rats, which can alleviate the above symptoms of PD rats. Trehalose can also inhibit dopaminergic nerves caused by inflammation.