Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0751295 (memory loss)
 3,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Amyloid beta protein (Abeta) is thought to be responsible for the loss of memory in Alzheimer's disease (AD). A significant decrease in [Arg(8)]-vasopressin (AVP) in the AD brain has been found. However, it is unclear whether the decrease in AVP is involved in Abeta-induced impairment of memory and whether AVP can protect against Abeta-induced neurotoxicity. The present study examines the effects of intracerebroventricular (i.c.v.) injection of AVP on hippocampal long-term potentiation (LTP), a synaptic model of memory, and investigates the potential protective function of AVP in Abeta-induced LTP impairment. The results showed that (1) i.c.v. injection of different concentrations of AVP or Abeta(25-35) did not affect the baseline field excitatory postsynaptic potentials (fEPSPs); (2) AVP administration alone induced a significant increase in HFS-induced LTP, while Abeta(25-35) significantly suppressed HFS-induced LTP; (3) Abeta(25-35)-induced LTP suppression was significantly prevented by the pretreatment with AVP; (4) paired-pulse facilitation did not change after separate application or co-application of AVP and Abeta(25-35). These results indicate that AVP can potentiate hippocampal synaptic plasticity and dose-dependently prevent Abeta(25-35)-induced LTP impairment. Thus, the present study provides further insight into the mechanisms by which Abeta impairs synaptic plasticity and suggests an important approach in the treatment of AD.
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PMID:Arginine vasopressin prevents amyloid beta protein-induced impairment of long-term potentiation in rat hippocampus in vivo. 1905 64

Amyloid beta protein (Abeta) is thought to be responsible for loss of memory in Alzheimer's disease (AD). A significant decrease in [Arg(8)]-vasopressin (AVP) has been found in the AD brain and in plasma; however, it is unclear whether this decrease in AVP is involved in Abeta-induced impairment of spatial cognition and whether AVP can protect against Abeta-induced deficits in cognitive function. The present study examined the effects of intracerebroventricular (i.c.v.) injection of AVP on spatial learning and memory in the Morris water maze test and investigated the potential protective function of AVP against Abeta-induced impairment in spatial cognition. The results were as follows: (1) i.c.v. injection of 25 nmol Abeta(25-35) resulted in a significant decline in spatial learning and memory; (2) 1 nmol and 10 nmol, but not 0.1 nmol, AVP injections markedly improved learning and memory; (3) pretreatment with 1 nmol or 10 nmol, but not 0.1 nmol, AVP effectively reversed the impairment in spatial learning and memory induced by Abeta(25-35); and (4) none of the drugs, including Abeta(25-35) and different concentrations of AVP, affected the vision or swimming speed of the rats. These results indicate that Abeta(25-35) could significantly impair spatial learning and memory in rats, and pretreatment with AVP centrally can enhance spatial learning and effectively prevent the behavioral impairment induced by neurotoxic Abeta(25-35). Thus, the present study provides further insight into the mechanisms by which Abeta impairs spatial learning and memory, suggesting that up-regulation of central AVP might be beneficial in the prevention and treatment of AD.
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PMID:Arginine vasopressin prevents against Abeta(25-35)-induced impairment of spatial learning and memory in rats. 2013 85