doi:10.1038/nindia.2014.13 Published online 27 January 2014
Researchers have identified possible involvement of copper metabolism proteins in sporadic Alzheimer's disease (AD) and Parkinson's disease (PD)1 .
The pathoetiology of these neurodegenerative diseases, constituting a major worldwide health problem in the elderly, have not yet been clearly explained. Copper is an indispensable trace element for human nutrition, especially for the development and functioning of the central nervous system. Conspicuously, excess copper as well as its deficiency has been implicated in the pathophysiology such neurodegenerative diseases.
Aberrations in copper homeostatic mechanisms together with aging causes an acceleration in the copper toxicity mediated oxidative stress, which is harmful to the central nervous system functioning. Notably, amyloid precursor protein (APP) and α-synuclein proteins implicated in AD and PD, respectively are copper binding proteins.
To identify the role of copper metabolism proteins in AD and PD, the researchers first constructed the 'copper interactome' with the help of network biology using ceruloplasmin and a set of proteins directly involved in human copper metabolism. They then merged the 'copper interactome' with three proteins involved in AD and two causing PD in humans. The researchers found that copper metabolism proteins, superoxide dismutase 1 and ceruloplasmin may represent direct and indirect linkage with AD and PD, respectively.
The study raises the prospect of finding connections between the 'copper status' and the AD and PD by means of the 'copper interactome', says lead researcher Rajendra Prasad. Co-researcher Amit Pal says it provides new insights on the role of metals, especially copper, in AD and PD and recognises novel therapy targets for multifactorial neurodegenerative diseases.
The authors of this work are from: Postgraduate Institute of Medical Education and Research, Chandigarh and Panjab University, Chandigarh, India.