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A New Strategy for Neuroprotection in Parkinsonís Disease
- Sep 16 2010
The motor symptoms of Parkinson’s disease (PD) develop when nerve cells in the brain die – cells that normally produce the chemical messenger dopamine. A new review finds that only about 30 percent of a person’s dopamine neurons have died by the time that individual is diagnosed with the disease. These new findings contrast with the widely-cited number from previous studies, that 50 percent or more of these cells have been lost at this time. The report appeared in the June 2010 issue of Annals of Neurology.
Nerve cells have a typical shape: a round-ish cell body with thread-like protrusions called dendrites, and a long tail known as the axon. The axon is important because it connects one nerve cell to the next, allowing them to communicate. Much research has focused on how nerve cell bodies can be injured and then self-destruct, a process called programmed cell death. Strategies for preventing the death of dopamine neurons, and thus the development of PD, have been aimed at protecting nerve cell bodies from damage.
In a new analysis of current research, Robert E. Burke, M.D., and his colleagues at Columbia University Medical Center, with funding from a PDF center grant, propose that cell death is instead the last step in a process that begins with the degeneration of axons — the nerve cell’s long tail. They argue that it is not cell death the leads to the onset of PD. Instead, researchers say that it is the poorly functioning axons that disrupt dopamine transmission and lead to PD symptoms before cells die.
The authors believe there is evidence for this new perspective in several lines of research. Analyzing previously-reported data, they emphasize that:
- Only about 30 percent of dopamine neurons had died at the time of diagnosis due to PD.
- However, dopamine levels had decreased more dramatically than could be explained by cell death alone. One explanation for this is damage to axons.
- The Columbia scientists and others also have discovered molecular mechanisms leading to axon degeneration, which differ from those that lead to programmed cell death.
What Does it Mean?
Because of previous research which found that fifty percent or more of the nerve cells in the substantia nigra have died by the time PD was diagnosed, research has recently focused on methods of making earlier diagnosis of PD (e.g., biological markers).
The hypothesis of Dr. Burke and his colleagues, which says that people newly diagnosed with PD may have more dopamine neurons than previously thought, provides grounds for optimism that therapies aimed at protecting these cells can be effective for PD. They recommend a new emphasis on neurorestoration therapies - therapies which would protect neurons by improving the health of axons. Restoring the health of axons might alleviate motor symptoms, prevent cell death, and, the authors say, possibly slow PD progression.
The scientists caution that the field of understanding mechanisms of axon regeneration and the potential for axon regrowth is in its early stages.
To learn more about the role of the neuron, read "What is PD?" on PDF's website.
Reference:Cheng HC, Ulane CM, Burke RE. Clinical progression in Parkinson disease and the neurobiology of axons. Ann Neurol. 2010 Jun;67(6):715-25.
Source Date: Sep 16 2010