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NEUROLOGY 1987;37:905
© 1987 American Academy of Neurology

Reductions in corticotropin releasing factor-like immunoreactivity in cerebral cortex in Alzheimer's disease, Parkinson's disease, and progressive supranuclear palsy

P. J. Whitehouse, MD, PhD, W. W. Vale, PhD, R. M. Zweig, MD, H. S. Singer, MD, R. Mayeux, MD, M. J. Kuhar, PhD, D. L. Price, MD and E. B. De Souza, PhD

Departments of Neurology (Drs. Whitehouse, Singer, and Price), Neuroscience (Drs. Whitehouse and Price), Pathology (Drs. Zweig and Price), Pediatrics (Dr. Singer), and the Neuropathology Laboratory (Drs. Whitehouse, Zweig, and Price), The Johns Hopkins University School of Medicine, Baltimore; the Neuroscience Branch (Drs. Kuhar and De Souza), Addiction Research Center, National Institute on Drug Abuse, Baltimore, MD; the Clayton Foundation Laboratories for Peptide Biology (Dr. Vale), The Salk Institute, La Jolla, CA and the Department of Neurology (Dr. Mayeux), Columbia University, New York, NY.

Dementias occurring in Alzheimer's disease, Parkinson's disease, and progressive supranuclear palsy are associated with dysfunction and death of neurons in a variety of cell populations, including cholinergic, monoaminergic, and peptidergic systems. In the present investigation of these three disorders, we demonstrated decreased levels of corticotropin releasing factor (CRF)-like immunoreactivity in the frontal, temporal, and occipital poles of the neocortex. Moreover, reductions in peptidergic immunoreactivity correlated with reductions in the activity of choline acetyltransferase, the enzyme that catalyzes the formation of acetylcholine. The reduction in cortical CRF levels may be due to abnormalities of intrinsic cortical neurons or to dysfunction in neurons that contain CRF and innervate cortex.

Address correspondence and reprint requests to Dr. Whitehouse, Department of Neurology, University Hospitals of Cleveland, 2074 Abington Road, Cleveland, OH 44106.

Supported by grants from the US Public Health Service (NIH NS 07179, NS 20471, AG 03359, AG 05146, and NS 15080) and the Parkinson's Disease Foundation, funds from the Robert L. and Clara G. Patterson Trust and the Claster Family, and fellowships from The Commonwealth Fund, The McKnight Foundation, and the Alfred P. Sloan Foundation. Research was conducted in part by the Clayton Foundation for Research, California Division. Wylie W. Vale is a Senior Clayton Foundation Investigator.

Received June 18, 1986. Accepted for publication in final form October 7, 1986.

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