Neuroprotection in Parkinson's disease

Abstract

A major focus in Parkinson's disease (PD) research is to produce drugs or other interventions that can slow or stop clinical progression. This should include an effect on both motor and non-motor symptoms and so target dopaminergic and non-dopaminergic pathways. It is logical to assume that the best chance of developing such therapies will be based on forming a better understanding of the aetiology and pathogenesis of PD and to identify critical molecular targets. There have been great advances in finding different genetic causes and risk factors for PD, but less so in the discovery of environmental contributions. The separate genetic causes still share common pathways to cell dysfunction and death, and these interconnect at several levels. Despite the major advances in genetics and PD pathogenesis, we still do not have good models of PD that can be used with confidence to accurately predict the effect of drugs on disease progression. Clinical trial design and study population selection are also areas that represent significant challenges to testing any putative neuro-protective agent. Several drugs have attracted attention as potential neuroprotective agents in PD. There are numerous studies demonstrating beneficial effects in the laboratory, but clinical efficacy for neuroprotection remains unproven.