The apoptosis to which the nerve cell death in central diseases, such as brain ischemia disease, Alzheimer's disease, and Parkinson's disease, advances by prolonged stress exposure except for an acute term is considered to be the cause of development of symptoms. If a nerve cells become senile, folding of the protein in an endoplasmic reticulum will become unusual, and, as a result, old junk proteins will be accumulated. It has been shown clearly by the latest research that this is the main causes of the long-term stress of a nerve cell. β-Amyloid peptide acts as nerve toxicity especially about Alzheimer's disease. The production of this peptide originates in misfolding of the amyloid precursor protein (APP) being caused by endoplasmic reticulum stress. Therefore, it is expected by the promotion of discovery of the molecular chaperone which performs a protein folding, especially the factor called GRP78 that these central disease can recover. Therefore, it is expected by the promotion o
f discovery of the molecular chaperone which performs a proteinic folding, especially the factor called GRP78 that these central disease can recover. As a result of screening for the regulators of GRP78 expression, the new substance designated as versipelostatin was discovered as an inhibitor of molecular chaperone expression from the microbial secondary metabolites. Although development was furthered as a present anti-neoplasm agent in order that this substance might indicate a reverse action to be a central disease curative medicine, as a result of examining the effect over a nerve cell, it became clear that the same nerve cell death as the model of Alzheimer's disease was guided, and it became clear that this substance is a useful tool proving the onset of Alzheimer's disease and the relation of endoplasmic reticulum stress. The cause of stress is indued by the oxygen radical besides the above-mentioned endoplasmic reticulum stress over a long period of time. The typical thing is observed by the cell death of the substantia nigra which is the pathology view of Parkinson's disease. Then, as a result of screening for the substance which protects PC12 cell from the L-DOPA toxicity in which Parkinson's disease carries out and its promotion, the new substance halxazone was discovered. Although this substance showed cell protective activity by low concentration with an anti-oxidative activities, L-DOPA toxicity was not ameliorated by other antioxidants such as vitamin E. To reveal the action mechanism of halxazone against L-DOPA toxicity, the effects of antioxidants were examined using ESR. Only halxazone specifically scavenged the radical production from catechol oxidation.
The still more detailed mechanism about the present book substance is due to be examined. Less