| Autor: | Franz-Werner Schwaiger, Olaf Riess, Manuel B. Graeber, L. B. Moran, Georg W. Kreutzberg, S. Kösel, Christoph Spitzer |
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| Rok vydání: | 2001 |
| Předmět: |
Alpha-synuclein
Pathology medicine.medical_specialty Programmed cell death Histology Lewy body General Neuroscience medicine.medical_treatment Cell Neurodegeneration Cell Biology Biology medicine.disease Facial nerve Phenotype nervous system diseases chemistry.chemical_compound medicine.anatomical_structure nervous system chemistry medicine Anatomy Axotomy Neuroscience |
| Zdroj: | Journal of Neurocytology. 30:515-521 |
| ISSN: | 0300-4864 |
| Popis: | The discovery that missense mutations in the alpha-synuclein gene represent a rare genetic cause of Parkinson's disease (PD) has had significant impact on the development of research into neurodegenerative disorders. It is becoming increasingly clear that alpha-synuclein plays a central role in the pathological process, which causes Lewy body formation and neurodegeneration in PD. Importantly, there is evidence to suggest that mutated alpha-synuclein is toxic to both nerve cells and glia. However, the regulation and function of wild-type alpha-synuclein are as yet ill defined. Using the facial nerve axotomy model, we have addressed the question whether the expression of alpha-synuclein in nerve cells may change in response to injury. We were particularly interested in testing the hypothesis that the severity of neuronal injury had an effect on alpha-synuclein metabolism. Facial nerve cut and crush, respectively, were performed in adult rats where normal facial motoneurones do not express alpha-synuclein. Following axotomy, a subset of facial motoneurones newly expressed high levels of alpha-synuclein immunoreactivity in their cell body and, occasionally, their nucleus. Significantly more nerve cells were labelled following facial nerve transection than following facial nerve crush. Confocal microscopy revealed a granular pattern of alpha-synuclein aggregation in degenerating nerve cells. Interestingly, the observed cell death phenotype was clearly non-apoptotic and developed over days or weeks rather than hours. Thus, axotomy of adult rat facial motoneurones triggers de novo expression of alpha-synuclein and this expression is associated with a non-apoptotic, slow form a neurodegeneration. In addition, the extent of alpha-synuclein expression is related to the severity of neuronal injury. |
| Databáze: | OpenAIRE |
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