Current advances in Parkinson's disease

doi:10.1016/S0166-2236(00)01850-6

Trends in Neurosciences

Volume 24, Issue 7, 1 July 2001, Pages 367-369

https://doi.org/10.1016/S0166-2236(00)01850-6 Get rights and content

Abstract

Current Advances in Parkinson's Disease: Challenges and Developments. Held at York, UK. 11–12, March, 2001.

Section snippets

Aetiology

In his round up of recent advances in the genetic understanding of PD, the chairman,Tony Schapira (Royal Free and University College Medical School, London, UK) concluded that the most common cause of the disease is probably a genetic susceptibility to certain environmental agents. Those with younger onset PD are much more likely to have a significant genetic component, but this factor does not reduce the occurrence of a genetic susceptibility to environmental factors in later onset PD.

Recently

Pathogenesis

In addition Schapira presented information on the biochemical abnormalities that result in neuronal dysfunction and death: mitochondrial dysfunction, free radical damage, inflammation and cytotoxicity, and even apoptosis. Laboratory evidence suggests that if all such biochemical disorders conspire to cause a cell to dysfunction before killing it, this would leave many cells dysfunctional but not dead, such cells are the targets of drugs that have a neuroprotective action.

Imaging

One of the biggest problems with PD is in its diagnosis, this has mostly been clinical without recourse to the laboratory and only confirmed at post-mortem. However, David Brooks (Hammersmith Hospital, London, UK) presented evidence of recent advances in imaging techniques using SPECT (single photon emission-completed tomography) and PET (position emission tomography) scanning that could make accurate in vivo diagnosis a real possibility.

Surgery

Surgical therapy for PD is rapidly expanding. The relatively recent discovery of the limitations of l-dopa, and the understanding that its long-term use is associated with disabling motor complications, has invoked a renewed interest in surgical procedures. However, Warren Olanow (Mount Sinai Medical Center, New York, USA) pointed out that surgery is still only recommended when other treatments have no benefit, although it is most effective when performed during the earlier stages of the

l-dopa

The mainstay of treatment for the symptoms of PD remains drug therapy and l-dopa has been used in this context for over 30 years. However, there is still a great deal of controversy over its place in treatment, how it works, and what exactly causes the disabling dyskinesias and motor complications associated with its long-term use. William Koller (Miami University, USA), in assessing the strengths and weaknesses of this ‘gold standard’ drug Koller noted that all PD patients will sooner or later

Beyond l-dopa

The short half-life of l-dopa (1.5 hours) is implicated in the increased risk of developing disabling dyskinesias. In contrast to l-dopa, which is taken up by CNS cells and converted to dopamine, dopamine agonists directly stimulate dopamine receptors. In addition, dopamine agonists have a much longer half-life (ropinirole 6–8 hrs, pramipexole 8–12 hrs and pergolide 7–16 and cabergoline 63–68 hrs), they can be used as mono or adjunct therapy, they might delay or reduce motor fluctuations and

Emerging use of dopamine agonists

Jean Hubble (Madden National Parkinson Foundation Center of Excellence, Columbus, USA) concurred that the greatest challenges in the treatment of PD are ‘how to treat those with no definable disability?’, and ‘what to use as a first-line treatment as the disease progresses and an intervention is needed?’, and conclude that dopamine agonists currently appear to be the most useful. Hubble illustrated, using data on pramipexole and ropinirole, that dopamine agonists are rarely, if ever, associated

Non-dopaminergic complications

The non-dopaminergic complications in PD reflect a widespread degeneration in brainstem nuclei and might be extremely difficult to locate and treat. Depression is a major complication that does not respond to dopaminergic therapy in a satisfactory way. In his investigation of such complications, David Burn (Newcastle General Hospital, UK) said that difficulties in ascertaining depression, plus differences in samples and subgroups, meant that estimates of the prevalence of depression in PD

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