No treatment has been shown to be neuroprotective. —Suchowersky et al., AAN Practice Parameter, re: Parkinson disease1 Strategies for slowing the progression of Parkinson disease (PD) have been a focus of scientific research for many years. An understanding of the pathogenic mechanisms is obviously crucial to this endeavor. In the last decade, certain evidence has pointed to programmed cell death, apoptosis, as the final common pathway in PD neurodegeneration,2,3 albeit with some controversy.4,5 In this issue of Neurology ®, the Parkinson Study Group (PSG) reports the results of a multicenter clinical trial investigating CEP-1347, which is an upstream inhibitor of the specific apoptotic pathway thought to be active in PD pathogenesis.6 It was predicted that it would slow the progression of PD. Evidence suggests that if classic apoptosis is operative in PD, this might proceed through the JNK (c-Jun NH2-terminal Kinase) signaling pathway.7–9 The enzyme, JNK, phosphorylates c-jun and other transcription factors, activating this apoptotic cascade. On a general note, this cascade is known …
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J. Eric Ahlskog (2007) studied this question.
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