Research on the pathogenesis of Alzheimers disease.docVIP

 PAGE \* MERGEFORMAT 14 Research on the pathogenesis of Alzheimer’s disease [Keywords:] Alzheimer’s disease; precursor protein; carrier protein E Class Alzheimer’s disease (Alzheimer’s disease, AD) occurred in early old age or older with chronic progressive neurodegenerative disease characterized by pathological neurofibrillary tangles inside nerve cells, extracellular deposition of amyloid protein in senile plaques caused by and neuronal loss. German scholar Alois Alzheimer [1] in 1907 observed a mental illness in patients with special clinical manifestations and pathological changes, and he carried out the first time. As human life expectancy increases, many countries have been or are about to enter an aged society with age-related diseases have become a social concern and related interdisciplinary research hot spots. 1 and AD-related genes 1.1 precursor protein gene precursor protein (Amyloid precursor protein, APP) gene located in the long arm of chromosome 21, from the composition of the 19 exons. APP gene transcription by different splicing patterns can generate several kinds of APP subtypes. Senile plaques β  core mainly composed of amyloid protein (amyloid protein beta, β  AP), that contain 39 ~ 43 amino acid hydrophobic peptide, the relative molecular mass of 4.0ku, three-dimensional structure was β -fold, with a strong self-polymerization of , easy to form extremely difficult to dissolve the precipitation. The study found, β  AP can be induced in rats and human microglia cells to secrete inflammatory cytokines and chemical factors, promote cell injury effects of free radicals and increased inflammatory cytokines induced reactions. β  AP on nerve cells have the dual role of nutrition and toxicity, that at low concentration of undifferentiated immature neurons neurotrophic effects, while in high concentration not only has differentiated mature neurons neurotoxicity, but also can increase the toxicity of many substances, such as excitator