Galanin in Alzheimer Disease
- Scott E. Counts1,
- Sylvia E. Perez1,
- Stephen D. Ginsberg2,
- Sonsoles de Lacalle3 and
- Elliott J. Mufson1
- 1Department of Neurological Sciences, Rush-Presbyterian-St. Luke’s Medical Center, 2242 West Harrison Street, Chicago, IL 60612,
- 2Center for Dementia Research, Nathan Kline Institute, Departments of Psychiatry and Physiology & Neuroscience, New York University School of Medicine, 140 Old Orangeburg Road, Orangeburg, NY 10962
- 3Department of Biological Sciences, California State University, Los Angeles, 5151 State University Drive, Los Angeles, CA 90032
Abstract
Galanin (GAL) and GAL receptors (GALR) are overexpressed in limbic brain regions associated with cognition in Alzheimer disease (AD). The functional consequences of this overexpression are unclear. Because GAL inhibits cholinergic transmission and restricts long-term potentiation in the hippocampus, GAL overexpression may exacerbate clinical features of AD. In contrast, GAL expression increases in response to neuronal injury, and galaninergic hyperinnervation prevents the decreased production of protein phosphatase 1 subtype mRNAs in cholinergic basal forebrain neurons in AD. Thus, GAL may also be neuroprotective for AD. Further elucidation of GAL activity in selectively vulnerable brain regions will help gauge the therapeutic potential of GALR ligands for the treatment of AD.
- © American Society for Pharmacology and Experimental Theraputics 2003
