ABSTRACT
@#Alzheimer's disease (AD) is a common progressive degenerative disease of the central nervous system. It's also a main cause for dementia in presenium and senectitude. In the past few years, the discoveries in vitro expansion of neural stem cells (NSCs) indicate a new way for recovery and replacement of damaged neurons as well as reconstruction of the neural circuit, and offer a useful future therapy for AD. There are two main promising approaches in NSCs replacement therapy. They are endogenetic approach, inducing proliferation and differentiation of endogenetic NSCs, improving self-repair of central nervous system, and exogenous approach, ransplantation of exogenous tissue and promoting proliferation of endogenous NSCs. However, it may not become truth before the mechanism of NSCs' proliferation, migration, differentiation and it's integration with the host tissues to be elucidated.
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<p><b>OBJECTIVE</b>To identify the mutation of Cu/Zn superoxide dismutase(SOD1) gene in an amyotrophic lateral sclerosis (ALS) family with unique phenotype.</p><p><b>METHODS</b>Five exons of SOD1 gene were amplified by PCR. The differences of these products were analyzed by PCR-single strand conformation polymorphism and visualized by silver staining.</p><p><b>RESULTS</b>Abnormal bands were found in exons 2 and 5 of SOD1 gene in several familial members. DNA sequence analysis verified that a base pair insertion occurred in the codon area of exon 2 and in the intron area of exon 5. And the insertion mutation of exon 2 led to a frameshift mutation and premature stop. It is a new type of SOD1 mutation which may be associated with familial amyotrophic lateral sclerosis.</p><p><b>CONCLUSION</b>Insertion mutation of exon 2 may be responsible for the disease of an ALS family in Chongqing.</p>
Subject(s)
Adult , Humans , Amyotrophic Lateral Sclerosis , Genetics , Mutation , Polymorphism, Single-Stranded Conformational , Superoxide Dismutase , Genetics , Superoxide Dismutase-1ABSTRACT
Objective To study the pattern of activities of microglia, the patholgical changes of chronically hypoperfused brain of rats and the interrelationship between them. Methods Model of chronically hypoperfused brain was established in rat by the ligation of both common carotid arteries, and the histopathological changes of brain were observed with light microscope. The activity of microglia of the brain were also observed with immunohistochemistry method and the number of microglia was measured with image analyzer. Results Extensive activation of microglia was observed after chronic cerebral hypoperfusion and the activation was increased with the elapse of time of hypoperfusion. There were obvious pathological change in the brain after the chronic cerebral hypoperfusion, such as myelinic degeneration and formation of glial nodule in white matter. After treated with cyclosporin A, the number of microglia was obviously reduced, but the pathological change was evidently decreased. Conclusion The activation of microglia resulted from chronic cerebral hypoperfusion is relates to the pathological changes of the brain. However, cyclosporin A can decrease the pathological change and inhibit the activation of microglia.
ABSTRACT
Objective To study the pattern of activities of microglia, the patholgical changes of chronically hypoperfused brain of rats and the interrelationship between them. Methods Model of chronically hypoperfused brain was established in rat by the ligation of both common carotid arteries, and the histopathological changes of brain were observed with light microscope. The activity of microglia of the brain were also observed with immunohistochemistry method and the number of microglia was measured with image analyzer. Results Extensive activation of microglia was observed after chronic cerebral hypoperfusion and the activation was increased with the elapse of time of hypoperfusion. There were obvious pathological change in the brain after the chronic cerebral hypoperfusion, such as myelinic degeneration and formation of glial nodule in white matter. After treated with cyclosporin A, the number of microglia was obviously reduced, but the pathological change was evidently decreased. Conclusion The activation of microglia resulted from chronic cerebral hypoperfusion is relates to the pathological changes of the brain. However, cyclosporin A can decrease the pathological change and inhibit the activation of microglia.