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Neurology 2003;61:206-211
© 2003 American Academy of Neurology

Aß1–42 promotes cholinergic sprouting in patients with AD and Lewy body variant of AD

E. Masliah, MD, M. Alford, BA, A. Adame, E. Rockenstein, BS, D. Galasko, MD, D. Salmon, PhD, L. A. Hansen, MD and L. J. Thal, MD

From the Departments of Neurosciences (Drs. Masliah, Galasko, Salmon, Hansen, and Thal, M. Alford, A. Adame, and E. Rockenstein) and Pathology (Drs. Masliah and Hansen), University of California, San Diego, La Jolla, CA.

Address correspondence and reprint requests to Dr. E. Masliah, Department of Neurosciences, University of California, San Diego, La Jolla, CA 92093-0624; e-mail: emasliah @ucsd.edu

Background: The neurodegenerative process in Alzheimer’s disease (AD) and in the Lewy body variant of AD (LBV) patients is characterized by cholinergic dysfunction and deposition of amyloid ß-peptide (Aß) 1–40 and 1–42; however, the differential effects of Aß species on the cholinergic system are not completely clear.

Objective: To better understand the relationship between levels of Aß1–40 and 1–42 on cholinergic deficits in AD and LBV patients.

Methods: Levels of choline acetyltransferase (ChAT) activity and ChAT immunoreactivity in the plaques in the frontal cortex of patients with AD and LBV were correlated with Aß1–42 and 1–40 levels determined by ELISA and with neuropathologic and neurologic markers.

Results: Although the overall levels of ChAT activity were reduced in AD and LBV cases, there was a direct correlation with Aß1–42 levels. Furthermore, patients with high Aß1–42 levels had more abundant cholinergic dystrophic neurites in the plaques than cases with lower Aß1–42.

Conclusion: Aß1–42 may also trigger cholinergic dysfunction by promoting aberrant neuritic sprouting.




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