Parkinson's disease (PD) is the second most common neurodegenerative d
isorder worldwide and is characterised by cardinal clinical features a
nd specific pathological findings. It is possible to detect PD early o
n in the course of the disease, and certain laboratory studies may ide
ntify preclinical stages. Based on this information, and the hypothesi
s that there is a long preclinical period, there appears to be a windo
w of opportunity to influence the natural course of the disease. Postu
lates regarding pathogenesis, such as oxidative stress and excitotoxic
ity, have led to the discovery of abnormal mitochondrial function in P
D and a search for biochemical markers. Functional imaging studies hav
e detected subclinical nigral dopaminergic dysfunction in individuals
at risk of developing PD. Current symptomatic therapies are aimed at e
nhancing dopaminergic transmission. However, some commonly used PD med
ications may have alternative actions with both symptomatic and neurop
rotective consequences. Bromocriptine has been postulated to have anti
oxidant effects and amantadine to have N-methyl-D-aspartate (NMDA) rec
eptor antagonistic properties. Both have been reported to be associate
d with improved survival in PD. Additionally, monoamine oxidase type B
inhibitors may provide neuroprotection. Recent new medications are al
so under study with regard to neuroprotection. Despite these advances,
until there is a better understanding of the aetiology and pathogenes
is of PD, there will be no definitive long-term benefit of early diagn
osis and treatment of PD.