Growth Hormone Releaser Attenuates β-Amyloid (1 – 42)-Induced Memory Impairment in Mice

Abstract

Abstract. Accumulating evidence indicates that growth hormone (GH) might be effective at preventing the development of Alzheimer's disease. However, exogenous GH treatment has exhibited side effects for clinical application; thus supplementation with amino acids to promote the release of GH could be a possible alternative treatment. In this study, mice that were fed with a diet of GH-releasing supplements had significantly attenuated memory impairments and hippocampal changes in the acetylcholinesterase activity and acetylcholine level induced by amyloid beta protein (Aβ) (1 -42). Our results suggest that the use of GH-releasing supplement exerts beneficial effects on the memory impairment induced by Aβ (1 -42).

Growth Hormone–Releaser Diet Attenuates β-Amyloid(1-42)–Induced Cognitive Impairment via Stimulation of the Insulin-Like Growth Factor (IGF)-1 Receptor in Mice

“…We have previously reported the positive effects of the GH-releaser diet on Aβ(1-42)-induced cognitive impairment in the water maze and passive avoidance tests in mice (3). In this study, learning and memory capacities were evaluated with a conditioned-fear learning test (5).…”

“…As oral administration of some amino acids (e.g., arginine, glutamine, glycine, and lysine) increases the release of endogenous GH (2), supplementation may be a useful pharmacological intervention. We have previously demonstrated that a "GH-releaser diet" significantly prevented β-amyloid (Aβ) (1-42)-induced learning impairment (3). In this study, we examined whether the IGF-1 receptor was involved in the GH-releaser diet-mediated pharmacological action of Aβ(1-42)-induced toxicity in mice.…”

Effect of intra-hippocampal injection of human recombinant growth hormone on synaptic plasticity in the nucleus basalis magnocellularis-lesioned aged rats

“…The evidence suggests that a functional link may exist between the cholinergic system and growth hormone (GH) secretion. For example, the secretion of GH from the pituitary is enhanced by acetylcholinesterase inhibitor (pyridostigmine) 7 and a primary mediator of growth hormone/insulin-like growth factor-1 (IGF-1) or GH-releasing hormone, which can stimulate secretion of acetylcholine from rat cortical slices and the hippocampus respectively 8,9 . It has recently been shown that age-related reductions in plasma GH, known as somatopause, is associated with increased incidence of cognitive impairment and AD, and can be compensated through GH treatment 10,11 .…”

“…It has recently been shown that age-related reductions in plasma GH, known as somatopause, is associated with increased incidence of cognitive impairment and AD, and can be compensated through GH treatment 10,11 . Various central effects of GH, such as cell genesis, neurogenesis 12 and angiogenesis 13 , suggest that GH administration may be effective in preventing the development or progression of AD 9,14,15 . Molecular mechanisms of improved cognitive functions after GH treatment are not known but may be due to the direct impact of the hormone on the brain.…”

Transmembrane Delivery and Biological Effect of Human Growth Hormone Via a Phage Displayed Peptide In Vivo and In Vitro

“…8 Growth hormone releaser, such as arginine, glutamine, glycine, and lysine, has been found to increase endogenous GH release, and to attenuate the b-amyloid peptide (Ab)-induced memory impairment in mice. 9 In addition, there is substantial evidence that an increased availability of hypothalamic acetylcholine can stimulate GH release, probably via suppression of somatostatin. Cholinesterase-inhibitors, such as rivastigmine and donepezil, in AD therapy have also been found to elicit GH secretion and enhance a GH response to GH-releasing hormone.…”