Environmental factors in XXXX .

@entity5212 @entity286 @entity137 @entity304 @entity935 @entity191 @entity8584 @entity528
Evidence discussed in this review article lends strong support in favor of an etiologic role of environmentalfactors in @entity191 . First, thanks to the discovery of @entity5212 ( @entity5212 ), it is now clear that, by targeting the nigrostriatal system, neurotoxicants can reproduce the neurochemical and pathological features of idiopathic @entity304 . The sequence of toxic events triggered by @entity5212 has also provided us with intriguing clues concerning mechanisms of toxicant selectivity and nigrostriatal vulnerability. Relevant examples are (i) the role of the plasma membrane @entity935 transporter in facilitating the access of potentially toxic species into dopaminergic neurons; (ii) the vulnerability of the nigrostriatal system to failure of mitochondrial energy metabolism; and (iii) the contribution of inflammatory processes to tissue lesioning. Epidemiological and experimental data suggest the potential involvement of specific agents as neurotoxicants (e.g. pesticides) or neuroprotective compounds (e.g. @entity286 products) in the pathogenesis of @entity528 , further supporting a relationship between the environment and @entity191 . A likely scenario that emerges from our current knowledge is that neurodegeneration results from multiple events and interactive mechanisms. These may include (i) the synergistic action of endogenous and exogenous toxins (e.g. the ability of the pesticide @entity8584 to promote the @entity137 of other compounds); (ii) the interactions of toxic agents with endogenous elements (e.g. the protein alpha-synuclein); (iii) the tissue response to an @entity137 ; and, last but not least, (iv) the effects of environmental factors on the background of genetic predisposition and aging.
