PT  - JOURNAL ARTICLE
AU  - Keomanivong, Cameron
AU  - Schamp, Josephine
AU  - Tabakovic, Ervina
AU  - Thangavel, Ramasamy
AU  - Aldridge, Georgina
AU  - Pieper, Andrew A.
AU  - Narayanan, Nandakumar S.
TI  - Mice Expressing A53T/A30P Mutant Alpha-Synuclein in Dopamine Neurons Do Not Display Behavioral Deficits
AID  - 10.1523/ENEURO.0170-23.2023
DP  - 2024 Feb 01
TA  - eneuro
PG  - ENEURO.0170-23.2023
VI  - 11
IP  - 2
4099  - http://www.eneuro.org/content/11/2/ENEURO.0170-23.2023.short
4100  - http://www.eneuro.org/content/11/2/ENEURO.0170-23.2023.full
SO  - eNeuro2024 Feb 01; 11
AB  - Alpha-synuclein has been implicated in neurodegenerative diseases such as Parkinson's disease and dementia with Lewy bodies, with A53T and A30P mutations shown to be disease causing. It has been reported that hemizygous transgenic mice with tyrosine hydroxylase promotor-driven expression of A53T/A30P mutant alpha-synuclein in dopamine neurons provide a useful preclinical model of these conditions by virtue of developing behavioral deficits. Here, we report a lack of replication of this finding. Despite detecting robust overexpression of A53T/A30P mutant alpha-synuclein in dopamine neurons, we did not observe decreased tyrosine hydroxylase immunofluorescence or behavioral deficits in these mice. Our results demonstrate that preclinical models of synucleinopathy need careful validation in the field.