Journal
NEURODEGENERATIVE DISEASES
Volume 8, Issue 5, Pages 300-309Publisher
KARGER
DOI: 10.1159/000323468
Keywords
Neuropeptide Y; Beta-amyloid; Neuroblastoma; Neurotrophins
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Funding
- nEUROsyn Italian Ministry of Health [RC2008]
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Background: In the central nervous system, several neuropeptides are believed to be involved in the pathophysiology of Alzheimer's disease (AD). Among them, neuropeptide Y (NPY) is a small peptide widely distributed throughout the brain, where it serves as a neurotransmitter and/or a modulator of several neuroendocrine functions. More recently, NPY has generated interest because of its role in neuroprotection against excitotoxicity and modulation of neurogenesis. Interestingly, these effects are also influenced by neurotrophins, critical molecules for the function and survival of neurons that degenerate in AD. Objective: Our purpose was to investigate whether NPY might be a neuroprotective agent in AD and whether neurotrophins are involved in NPY-induced neuroprotection. Methods: To test this hypothesis, we exposed the SH-SY5Y neuroblastoma cell line to toxic concentrations of beta-amyloid (A beta) peptide fragment 25-35 (A beta(25-35)) and measured cell survival and neurotrophin expression before and after a preincubation with NPY in the growth medium. Results: Our results demonstrated that preincubation with NPY prevented cell loss due to the toxic effect of A beta(25-35). Moreover, while intracellular production of nerve growth factor and brain-derived neurotrophic factor were reduced by A beta, NPY restored or even increased neurotrophin protein and mRNA in SH-SY5Y cells. Conclusion: In conclusion, this study demonstrates that NPY increases the survival of SH-SY5Y neuroblastoma cells and counteracts the toxic effect of A beta. In addition, NPY restores the neurotrophin levels in these cells. Although preliminary, these observations might be useful to understand the pathology of Alzheimer's and/or develop new therapeutic strategies. Copyright (C) 2011 S. Karger AG, Basel
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