Linked Life Data

11830760

Source:http://linkedlifedata.com/resource/pubmed/id/11830760

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2002-2-6
pubmed:abstractText
The neuropeptide galanin (GAL) is widely distributed in the mammalian CNS. Several lines of evidence suggest that GAL may play a critical role in cognitive processes such as memory and attention through an inhibitory modulation of cholinergic basal forebrain activity. Furthermore, GAL fibers hyperinnervate remaining cholinergic basal forebrain neurons in Alzheimer's disease (AD). This suggests that GAL activity impacts cholinergic dysfunction in advanced AD. Pharmacological and in vitro autoradiographic studies indicate the presence of heterogeneous populations of GAL receptor (GALR) sites in the basal forebrain which bind GAL with both high and low affinity. Interestingly, we have recently observed that GALR binding sites increase in the anterior basal forebrain in late-stage AD. Three G protein-coupled GALRs have been identified to date that signal through a diverse array of effector pathways in vitro, including adenylyl cyclase inhibition and phospholipase C activation. The repertoire and distribution of GALR expression in the basal forebrain remains unknown, as does the nature of GAL and GALR plasticity in the AD basal forebrain. Recently, GAL knockout and overexpressing transgenic mice have been generated to facilitate our understanding of GAL activity in basal forebrain function. GAL knockout mice result in fewer cholinergic basal forebrain neurons and memory deficits. On the other hand, mice overexpressing GAL display hyperinnervation of basal forebrain and memory deficits. These data highlight the need to explore further the putative mechanisms by which GAL signaling might be beneficial or deleterious for cholinergic cell survival and activity within basal forebrain. This information will be critical to understanding whether pharmacological manipulation of GALRs would be effective for the amelioration of cognitive deficits in AD.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1080-563X
pubmed:author
pubmed:issnType
Print
pubmed:volume
7
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
445-70
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:11830760-Alzheimer Disease, pubmed-meshheading:11830760-Amino Acid Sequence, pubmed-meshheading:11830760-Animals, pubmed-meshheading:11830760-Brain, pubmed-meshheading:11830760-Cholinergic Fibers, pubmed-meshheading:11830760-Cognition Disorders, pubmed-meshheading:11830760-GTP-Binding Proteins, pubmed-meshheading:11830760-Galanin, pubmed-meshheading:11830760-Humans, pubmed-meshheading:11830760-Ligands, pubmed-meshheading:11830760-Mice, pubmed-meshheading:11830760-Mice, Knockout, pubmed-meshheading:11830760-Mice, Transgenic, pubmed-meshheading:11830760-Molecular Sequence Data, pubmed-meshheading:11830760-Neuronal Plasticity, pubmed-meshheading:11830760-Receptors, Galanin, pubmed-meshheading:11830760-Receptors, Neuropeptide, pubmed-meshheading:11830760-Signal Transduction
pubmed:year
2001
pubmed:articleTitle
Galanin: neurobiologic mechanisms and therapeutic potential for Alzheimer's disease.
pubmed:affiliation
Department of Neurological Sciences, Rush-Presbyterian-St. Luke's Medical Center, 2242 West Harrison Street, Chicago, IL 60612, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review