Document Type
Article
Date of Original Version
2014
Department
Biomedical and Pharmaceutical Sciences
Abstract
The sporadic nature in over 90% of Alzheimer's disease (AD) cases, the differential susceptibility and course of illness, and latent onset of the disease suggest involvement of an environmental component in the etiology of late onset AD (LOAD). Recent reports from our lab have demonstrated that molecular alterations favor abundant tau phosphorylation and immunoreactivity in the frontal cortex of aged primates with infantile lead (Pb) exposure (Bihaqi and Zawia, 2013). Here we report that developmental Pb exposure results in elevation of protein and mRNA levels of tau in aged mice. Western blot analysis revealed aberrant site-specific tau hyperphosphorylation accompanied by elevated cyclin dependent kinase 5 (CDK5) levels in aged mice with prior Pb exposure. Mice with developmental Pb exposure also displayed altered protein ratio of p35/p25 with more Serine/Threonine phosphatase activity at old age. These changes favored increase in tau phosphorylation, thus providing evidence that neurodegenerative diseases may be in part due to environmental influences that occur during development.
Citation/Publisher Attribution
Bihaqi, S. W., Bahmani, A., Adem, A., & Zawia, N. H. (2014). Infantile postnatal exposure to lead (Pb) enhances tau expression in the cerebral cortex of aged mice: Relevance to AD. NeuroToxicology, 44, 114-120. doi: 10.1016/j.neuro.2014.06.008
Available at: https://doi.org/10.1016/j.neuro.2014.06.008
Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License.
Comment
Syed Waseem Bihaqi and Asadeh Bahmani are in the Department of Biomedical and Pharmaceutical Sciences.
Abdu Adem is a part of the Interdisciplinary Neuroscience Program.
Nasser H. Zawia is in both the department and program.
Author Manuscript
This is a pre-publication author manuscript of the final, published article.