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ShareDec. 26, 2008 — Parkinson disease is a neurodegenerative disorder that impairs movement, balance, speech, and other functions. It is characterized by the loss of nerves in the brain that produce a substance known as dopamine. Although the loss of dopamine-containing nerves is accompanied by accumulation of immune cells known as T cells, these accumulating T cells were not thought to have a role in the development of disease.
However, Stéphane Hunot, Etienne C. Hirsch, and colleagues, at INSERM UMR 679, France, have now shown that CD4+ T cells make a significant contribution to the development of disease in a mouse model of Parkinson disease.
In the study, a substantial number of CD4+ T cells and CD8+ T cells were observed to have accumulated in postmortem brain tissue from individuals with Parkinson disease and mice with a Parkinson-like disease. Importantly, mice lacking all T cells developed substantially less severe disease in the mouse model of Parkinson disease. Further analysis indicated that protection was specifically associated with a lack of CD4+ T cells expressing the protein FasL.
The authors therefore suggest that targeting the immune system might provide a new therapeutic approach to treating Parkinson disease. However, in an accompanying commentary, Stanley Appel, at Methodist Neurological Institute, Houston, warns that although these data provide rationale for immune-based strategies, there are a large number of questions that need to be answered before such approaches can be considered in the clinic.
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The above story is reprinted from materials provided by Journal of Clinical Investigation, via EurekAlert!, a service of AAAS.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal Reference:
- Brochard et al. Infiltration of CD4 lymphocytes into the brain contributes to neurodegeneration in a mouse model of Parkinson disease
. Journal of Clinical Investigation, 2008; DOI: 10.1172/JCI36470
Note: If no author is given, the source is cited instead.
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