Transforming growth factor beta2 level is elevated in neurons of Alzheimer's disease brains.
Our earlier studies in vitro indicated that expression of TGFbeta2 was induced by toxic amyloid betas (Abetas) in both glial and neuronal cells and increased levels of TGFbeta2 triggered a neuronal cell death pathway related to Alzheimer's disease (AD) by binding to the extracellular domain of amyloid beta precursor protein (APP). In this study we have demonstrated by immunohistochemical analysis that the levels of TGFbeta2 are elevated in cells mainly consisting of neurons of both the hippocampi and cerebral cortices of human AD brains. This result indicates that upregulation of the TGFbeta2 level is a common pathological feature of AD brains and suggests that it may be closely linked to the development of neuronal death related to AD.
Noguchi
Atsushi
A
Department of Cell Biology and Neuroscience, KEIO University School of Medicine, Shinjuku-ku, Tokyo, Japan.
Nawa
Mikiro
M
Aiso
Sadakazu
S
Okamoto
Koichi
K
Matsuoka
Masaaki
M
D000368:Aged; D000369:Aged, 80 and over; D000544:Alzheimer Disease / Q000378:metabolism*; D000818:Animals; D000918:Antibody Specificity; D019556:COS Cells; D016923:Cell Death; D002540:Cerebral Cortex / Q000166:cytology / Q000378:metabolism*; D002522:Chlorocebus aethiops; D005260:Female; D006624:Hippocampus / Q000166:cytology / Q000378:metabolism*; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D009474:Neurons / Q000378:metabolism*; D053781:Transforming Growth Factor beta2 / Q000096:biosynthesis*; D015854:Up-Regulation
D053781:Transforming Growth Factor beta2