Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/110106
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Type: Journal article
Title: Neuronal response in Alzheimer's and Parkinson's disease: the effect of toxic proteins on intracellular pathways
Author: Majd, S.
Power, J.
Grantham, H.
Citation: BMC Neuroscience, 2015; 16(1):69-1-69-13
Publisher: BioMed Central Ltd.
Issue Date: 2015
ISSN: 1471-2202
1471-2202
Statement of
Responsibility: 
Shohreh Majd, John H. Power and Hugh J.M. Grantham
Abstract: Accumulation of protein aggregates is the leading cause of cellular dysfunction in neurodegenerative disorders. Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease, Prion disease and motor disorders such as amyotrophic lateral sclerosis, present with a similar pattern of progressive neuronal death, nervous system deterioration and cognitive impairment. The common characteristic is an unusual misfolding of proteins which is believed to cause protein deposition and trigger degenerative signals in the neurons. A similar clinical presentation seen in many neurodegenerative disorders suggests the possibility of shared neuronal responses in different disorders. Despite the difference in core elements of deposits in each neurodegenerative disorder, the cascade of neuronal reactions such as activation of glycogen synthase kinase-3 beta, mitogen-activated protein kinases, cell cycle re-entry and oxidative stress leading to a progressive neurodegeneration are surprisingly similar. This review focuses on protein toxicity in two neurodegenerative diseases, AD and PD. We reviewed the activated mechanisms of neurotoxicity in response to misfolded beta-amyloid and α-synuclein, two major toxic proteins in AD and PD, leading to neuronal apoptosis. The interaction between the proteins in producing an overlapping pathological pattern will be also discussed.
Keywords: Alzheimer’s disease; Parkinson’s disease; beta-amyloid; alpha-synuclein; intracellular signalling; neurotoxicity; neurodegeneration
Rights: © 2015 Majd et al. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
RMID: 0030042276
DOI: 10.1186/s12868-015-0211-1
Appears in Collections:Medicine publications

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