Conclusions And Perspectives

The above findings, clearly demonstrated that NO and RNS play a main role in the development of neurodegenerative disorders. The mechanism(s) by which nitrosative stress is involved in the pathogenesis of neurodegenerative diseases is manifold. In fact, NO itself has been shown to regulate selected proteins, such as parkin, MMP-9 and GAPDH, via an S-nitrosylation reaction thus triggering the onset and progression of PD and other neurodegenerative disorders. On the other hand, NO can react with ROS, in particular superoxide, derived from mitochondrial impairment and form peroxynitrite which, in turn, nitrosate proteins and form 3-NT-modified proteins which cause an impairment in cellular metabolic pathways and therefore cell death. From these data, it is possible to hypothesize that drugs which are able to counteract iNOS induction and therefore, excess NO formation, can be very useful to limit the deleterious consequences of oxidative and nitrosative stress associated with neurodegenerative disorders.

Furthermore, the compelling evidence of the vitagene network as a defense system operating in the brain during times of oxidative and nitrosative stress opens new perspectives in the treatment of ND. The evidence that phenolic compounds, such as curcumin and ferulic acid, can induce HO-1 and reduce AD, strongly indicates the therapeutic potential of nutritional compounds against ND. Conceivably, the pharmacological or nutritional manipulation of endogenous cellular defense mechanisms represents an innovative approach to therapeutic intervention in diseases causing tissue damage, such as neurodegeneration, and suggests potential novel therapeutic strategies relying upon the simultaneous activation of cytoprotective genes of the cell life program and down-regulation of pro-inflammatory and pro-oxidative genes involved in programmed cell death. A strong evidence that a crosstalk between stress responsive genes is critical for cell stress tolerance is presented here, highlighting compelling reason for a renewed effort to understand the central role of this most extraordinary defense system in biology and medicine. All of the above evidence support also the notion that stimulation of various maintenance and repair pathways through exogenous intervention, such as mild stress or compounds targeting the heat shock signal pathway, such as acetylcarnitine may have biological significance as a novel approach to delay the onset of various age-associated alterations in cells, tissues and organisms. Hence, by maintaining or recovering the activity of vitagenes it can be possible to delay the aging process and decrease the occurrence of age-related diseases with resulting prolongation of a healthy life span.

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