Galanin in Alzheimer's disease: Neuroinhibitory or neuroprotective?
Document Type
Article
Abstract
Galanin (GAL) and GAL receptors (GALRs) are overexpressed in degenerating brain regions associated with cognitive decline in Alzheimer's disease (AD). The functional consequences of GAL plasticity in AD are unclear. GAL inhibits cholinergic transmission in the hippocampus and impairs spatial memory in rodent models, suggesting GAL overexpression exacerbates cognitive impairment in AD. By contrast, gene expression profiling of individual cholinergic basal forebrain (CBF) neurons aspirated from AD tissue revealed that GAL hyperinnervation positively regulatesmRNAs that promote CBF neuronal function and survival. GAL also exerts neuroprotective effects in rodent models of neurotoxicity. These data support the growing concept that GAL overexpression preserves CBF neuron function which in turn may slow the onset of AD symptoms. Further elucidation of GAL activity in selectively vulnerable brain regions will help gauge the therapeutic potential of GALR ligands for the treatment of AD. (Part of a Multi-author Review). © 2008 Birkhaueser.
Keywords
Alzheimer's disease, Cholinergic basal forebrain, Galanin, Hippocampus, Plasticity
Publication Date
6-1-2008
Publication Title
Cellular and Molecular Life Sciences
ISSN
1420682X
E-ISSN
15691632
Volume
65
Issue
12
First Page
1842
Last Page
1853
PubMed ID
18500641
Digital Object Identifier (DOI)
10.1007/s00018-008-8159-2
Recommended Citation
Counts, S. E.; Perez, S. E.; and Mufson, E. J., "Galanin in Alzheimer's disease: Neuroinhibitory or neuroprotective?" (2008). Translational Neuroscience. 1627.
https://scholar.barrowneuro.org/neurobiology/1627