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NEUROLOGY 1987;37:1057
© 1987 American Academy of Neurology

Alzheimer's disease

Low levels of peptide a-amidation activity in brain and CSF

G. S. Wand, MD, C. May, MD, V. May, PhD, P. J. Whitehouse, MD, PhD, S. I. Rapoport, MD and B. A. Eipper, PhD

Departments of Medicine (Dr. Wand) and Neuroscience (Drs. V. May, Whitehouse, and Eipper), and the Neuropathology Laboratory, Department of Neurology (Dr. Whitehouse), The Johns Hopkins University School of Medicine, Baltimore; and the Laboratory of Neurosciences (Drs. c. May and Rapoport), National Institute on Aging, Bethesda, MD.

Carboxyl terminal a-amidation confers biologic activity to many neuropeptides. Levels of a-amidating activity, peptidyl-glycine {alpha}-amidating monooxygenase (PAM), were reduced in the CSF of patients with dementia of the Alzheimer type (DAT) compared with healthy, age-matched controls. Repeat lumbar puncture data revealed a decline in CSF PAM activity of approximately 16% per year in DAT patients. Of the cerebral cortical regions examined, only the temporal pole showed reduced PAM activity in patients with Alzheimer's disease (AD) compared with controls. These studies may indicate selective dysfunction of neurons which normally synthesize biologically active, a-amidated peptides in the CNS of AD patients.

Address correspondence and reprint requests to Dr. Wand, Department of Neuroscience, The Johns Hopkins School of Medicine, 725 N. Wolfe Street WBSB 907, Baltimore, MD 21205.

Presented in part at the thirty-seventh annual meeting of the American Academy of Neurology, Dallas, TX, April 1985.

Supported by Grants AM-32949 and AM-01298 from the National Institutes of Health and Grants DA-00098 and DA-00266 from the National Institute of Drug Abuse.

Received July 3, 1986. Accepted for publication in final form September 19, 1986.






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