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Reduction of Choline Acetyltransferase Activity in Primary Visual Cortex in Mild to Moderate Alzheimer's Disease
Milos D. Ikonomovic, MD;
Elliott J. Mufson, PhD;
Joanne Wuu, ScM;
David A. Bennett, MD;
Steven T. DeKosky, MD
Arch Neurol. 2005;62:425-430.
Background Cholinergic deficits in the primary visual cortex (PVC) may underlie some of the abnormalities in visual processing and global cognitive performance in Alzheimer’s disease (AD).
Objective To correlate measures of general cognition (Mini-Mental State Examination and Global Cognitive Score) and visuospatial function with choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) activities, and nerve growth factor protein levels in the PVC.
Design The ChAT and AChE enzyme assays and a nerve growth factor protein enzyme-linked immunoabsorbent assay were performed on PVC tissue samples from subjects clinically diagnosed as having mild cognitive impairment (MCI), AD, or no cognitive impairment (NCI).
Setting and Patients Nuns, priests and brothers enrolled in the Religious Order Study, with annual premortem records of neuropsychological testing.
Results Significant differences in ChAT activity, but not in AChE activity or nerve growth factor protein levels, were found among diagnostic groups (P = .049). The ChAT activity was lower in AD than in MCI or NCI (P<.01); MCI was not different from NCI. The PVC ChAT activity correlated with measures of overall cognitive function (Mini-Mental State Examination and Global Cognitive Score), but less so with a composite measure of visuospatial function.
Conclusions The reduction in ChAT activity in the PVC of mild to moderate AD, but not in MCI, might serve to distinguish between clinical and preclinical forms of the disease. It appears that this change relates to generalized cognitive abnormalities but not specifically to visuospatial function.
Author Affiliations: Departments of Neurology and Psychiatry and the Alzheimer’s Disease Research Center, University of Pittsburgh, Pittsburgh, Pa (Drs Ikonomovic and DeKosky); and the Department of Neurological Sciences (Drs Mufson and Bennett and Ms Wuu), Rush University Medical Center and Rush Alzheimer’s Disease Center (Dr Bennett), Chicago, Ill.
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