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Abstract
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 β-peptide (Aβ) 1–40 and 1–42; however, the differential effects of Aβ species on the cholinergic system are not completely clear.
Objective: To better understand the relationship between levels of Aβ1–40 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 Aβ1–42 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 Aβ1–42 levels. Furthermore, patients with high Aβ1–42 levels had more abundant cholinergic dystrophic neurites in the plaques than cases with lower Aβ1–42.
Conclusion: Aβ1–42 may also trigger cholinergic dysfunction by promoting aberrant neuritic sprouting.
- Received June 11, 2002.
- Accepted March 28, 2003.
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