Journal
CELLULAR AND MOLECULAR LIFE SCIENCES
Volume 65, Issue 12, Pages 1842-1853Publisher
SPRINGER BASEL AG
DOI: 10.1007/s00018-008-8159-2
Keywords
galanin; Alzheimer's disease; cholinergic basal forebrain; hippocampus; plasticity
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Funding
- NIA NIH HHS [R21 AG030500, R01 AG043375, P01 AG009466, R01 AG010668-15, AG10688, AG09466, AG14449, AG10161, R21 AG030500-01A2, R01 AG010668, P01 AG014449, AG26032, P01 AG009466-100007] Funding Source: Medline
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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.
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