Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.

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.

Original publication

DOI

10.1523/JNEUROSCI.4965-05.2006

Type

Journal article

Journal

J Neurosci

Publication Date

12/04/2006

Volume

26

Pages

3942 - 3950

Keywords

Animals, Dopamine, Humans, Lewy Bodies, Lewy Body Disease, Mice, Mice, Inbred C57BL, Mice, Inbred CBA, Mice, Transgenic, Neurons, Olfactory Bulb, Parkinson Disease, Promoter Regions, Genetic, Rats, Substantia Nigra, Tyrosine 3-Monooxygenase, alpha-Synuclein