| First Author | Tofaris GK | Year | 2006 |
| Journal | J Neurosci | Volume | 26 |
| Issue | 15 | Pages | 3942-50 |
| PubMed ID | 16611810 | Mgi Jnum | J:108310 |
| Mgi Id | MGI:3623673 | Doi | 10.1523/JNEUROSCI.4965-05.2006 |
| Citation | Tofaris GK, et al. (2006) Pathological changes in dopaminergic nerve cells of the substantia nigra and olfactory bulb in mice transgenic for truncated human alpha-synuclein(1-120): implications for Lewy body disorders. J Neurosci 26(15):3942-50 |
| abstractText | Dysfunction of the 140 aa protein alpha-synuclein plays a central role in Lewy body disorders, including Parkinson's disease, as well as in multiple system atrophy. Here, we show that the expression of truncated human alpha-synuclein(1-120), driven by the rat tyrosine hydroxylase promoter on a mouse alpha-synuclein null background, leads to the formation of pathological inclusions in the substantia nigra and olfactory bulb and to a reduction in striatal dopamine levels. At the behavioral level, the transgenic mice showed a progressive reduction in spontaneous locomotion and an increased response to amphetamine. These findings suggest that the C-terminal of alpha-synuclein is an important regulator of aggregation in vivo and will help to understand the mechanisms underlying the pathogenesis of Lewy body disorders and multiple system atrophy. |
