Molecular Cloning of Human Growth Inhibitory Factor CDNA and Its Down-Regulation in Alzheimer’s Disease
Alzheimer’s disease (AD) is the most common dementing illness in man (Mann et al., 1988). AD is characterized by the presence of numerous senile plaques and neurofibrillary tangles throughout the cerebral cortex (Hirano and Zimmerman 1962; Kidd 1964; Schoenberg et al., 1987; Yamaguchi et al., 1988; Wisniewski et al., 1989). The major protein in senile plaques has been identified as a 39 ~ 42-amino-acid polypeptide referred to as the β/A4 protein (Masters et al., 1985; Selkoe et al., 1986). The major component of neurofibrillary tangles has also been identified as tau, a microtubule-associated phosphoprotein (Kondo et al., 1988; Wischik et al., 1988). The molecular mechanisms which lead to neuronal loss, and the accumulation of senile plaques followed by neurofibrillary tangles in AD, however, remain unexplained.
KeywordsNeurofibrillary Tangle Growth Inhibitory Activity Growth Inhibitory Factor Neurotrophic Activity Immunohistochemical Observation
Unable to display preview. Download preview PDF.