Abstract
There is increasing evidence that an aberrant sprouting response may contribute to some of the neuronal alterations observed in Alzheimer's disease (AD). In this study, we demonstrate that in the rat CNS, sprouting results in the reinduction of the embryonic form of the mRNA for α-tubulin. The fetal form of α-tubulin mRNA was also elevated in the hippocampus obtained from five AD patients, as compared to five elderly controls. These results suggest that the reexpression of embryonic forms of cytoskeletal proteins, in association with an aberrant sprouting response, may contribute to the neuropathological alterations in AD.
Original language | English |
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Pages (from-to) | 54-61 |
Number of pages | 8 |
Journal | Neuroscience Letters |
Volume | 109 |
Issue number | 1-2 |
DOIs | |
State | Published - Feb 5 1990 |
Bibliographical note
Funding Information:We thank Suzanne Cooper and Lenna Mah for excellent technical assistance and Ann Clark, Jennifer Kahle, Rich Murphy, and Ann Atchison for critical reviews of the manuscript. This work was supported by a NIA LEAD award and by a Medical Research Council (Canada) grant. F.D.M. is an Alberta Heritage Foundation Medical Research Scholar and this study was completed during the tenure of J.W.G. as a National Down Syndrome Society Science Scholar.
Keywords
- Alzheimer's disease
- Development
- In situ hybridization
- Messenger RNA
- Sprouting
- Tubulin
ASJC Scopus subject areas
- Neuroscience (all)