ABSTRACT
After many years of intense research, little still is known about the etiology of Parkinson’s disease (PD). The discovery of several monogenic forms of PD has substantially increased our knowledge of the mechanisms by which neurons die in PD.1-3 Abnormal protein processing, oxidative stress, and mitochondrial dysfunction seem to be the leading factors involved in the pathogenesis of PD.4-7 However, we should recognize that the genetic forms of PD identied so far only account for a minority of PD cases. The cause(s) of sporadic PD, which accounts for more than 80% of all PD subjects, still remains a mystery.8 We do not even know whether sporadic PD is primarily a genetic or an environmental disorder. This is a fundamental question, with profound implications for the future development of effective neuroprotective strategies. Although twins studies and some epidemiological observations support the view that sporadic PD may be triggered by the exposure to some, not yet identied, environmental factors,9,10 there is also evidence in favor of genetic causation.11 The role played by aging also should not be forgotten. Every single epidemiological study conducted so far has shown that aging is a major risk factor for PD.8 The risk of PD increases dramatically with age, affecting up to 4% of the population by the age of 90 years. This chapter will cover some of the most recent work on the etiology and pathogenesis of PD and will also touch on issues related to neuroprotection and management of PD.
