Mouse: asyn-/- CB57BL6
Expression of the mutated (A30P) human alpha-synuclein protein using the bacterial artificial chromosome (BAC).
Endogenous alpha-synuclein: No
Corresponding human genotype: Autosomal dominant mutation in PD patients (PARK1/PARK4)
Transgene insertion: chromosome 15
- 3 months: Transgene expression is observed in the cortex, as well as in TH-positive neurons in the SN and VTA.
- Expression of transgene restores sensitivity to MPTP treatment which is usually absent in mice lacking endogenous alpha-synuclein.
- Up to 18 months: No neurodegeneration is observed in transgenic mice.
- Up to 24 months: no loss of dopamine is detected in the SN and locus coeruleus.
- 3 months: a decrease in evoked dopamine release is observed in the striatum.
- Up to 24 months: no pathological expression of alpha-synuclein is observed
Test results from BAC-hsynA30P mice are compared to those of wild type animals lacking endogenous alpha-synuclein
- Up to 18 months: no novelty-induced motor deficits and no changes in forepaw stride length are observed. No deficits in rotarod test are present.
Response to L-DOPA treatment
- Not reported
Non motor Behaviours
Tests results from BAC-hsynA30P mice are compared to those of wild type animals lacking endogenous alpha-synuclein
- No anxiety-type phenotype is observed
- No differences in circadian rhythm activity are detected although a specific increase in wheel running at dark can be detected.
- Gastrointestinal disturbances are not detected.
- Not reported
- Up to 24 months: No gliosis is observed