Abstract
Current therapeutic strategies available to Parkinson’s disease (PD) patients are directed toward symptom management. As the disease progresses, these strategies inevitably fall short as neurodegeneration continues. Evidence from epidemiological studies strongly supports that long-term tobacco users are less likely to be diagnosed with PD. Further, animal model studies support that nicotine, the psychoactive and addictive component of tobacco, is neuroprotective. However, clinical trials have failed to replicate nicotine-mediated neuroprotection, perhaps because nicotine needs to be administered much earlier in the disease process, possibly even before disease onset, which many scientists and clinicians believe is years or even decades before symptoms occur. This creates a major obstacle in therapeutic development since the vast majority of patients acquire PD from unknown causes and because patients are typically diagnosed after motor symptom onset, when degeneration is advanced. Nonetheless, mechanisms by which nicotine may offer neuroprotection in animal models are emerging, and these include processes mediated by and those that are independent of nicotinic acetylcholine receptors (nAChRs).
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Buhlman, L.M., Hu, J. (2016). Early Nicotine Exposure Is Protective in Familial and Idiopathic Models of Parkinson’s Disease. In: Buhlman, L. (eds) Mitochondrial Mechanisms of Degeneration and Repair in Parkinson's Disease. Springer, Cham. https://doi.org/10.1007/978-3-319-42139-1_11
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