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Experimental gene therapy for Alzheimers Disease Research.doc

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Experimental gene therapy for Alzheimers Disease Research

 PAGE \* MERGEFORMAT 20 Experimental gene therapy for Alzheimer’s Disease Research Of: Kongwei Na Yi Min Zhang Lixia 1 Suan Ying Sun 2 Chai Xiqing [Keywords:] Alzheimer’s disease; amyloid protein; gene therapy Alzheimer’s disease (AD) The main symptoms are progressive memory and cognitive decline. At present, drug treatment is still the primary means of treatment of AD, but now mostly developed by the pharmaceutical chemical compound classes, not specific sites of drug action specificity is weak. On the contrary, the use of gene therapy is not only accurate positioning, the role of long duration, and no side-effects of non-target organ is an ideal method of treatment. In addition, although the study confirmed that cause of AD is a multi-mediated mediated disease, but the brain of amyloid (A) metabolism caused by the deposition of A fragments induced aggregation cascade is a major cause of AD. A steady-state level depends on the generation, clearance and inter-flow balance, therefore, if by means of gene therapy to reduce or increase A generation mediated A degradation, A to promote receptor-mediated brain drain, brain A inhibition of flow, can be effective treatment for AD. 1 gene therapy reduces A generation A hydrolysis by the secretion of amyloid precursor protein (APP) production. Body there @, , three kinds of enzymes involved in the secretion of APP degradation. @ Secretase cleavage site of APP protein in the middle of A molecules to avoid a complete sequence generation, and the decomposition of soluble amyloid precursor protein @ (soluble amyloid precursor protein @, sAPP @) on nerve cells has neurotrophic and neuroprotective effects, is the normal way the body metabolism of APP’s principal; secretase to APP cleavage into free sAPP and still with the membrane CTF99, CTF99 and then hydrolyzed by -secretase to generate P3 and containing 39 to 42 amino acid residues of A, A (particularly A40 and A42) aggregate to form amyloid plaques blo

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