Parkinson's disease (PD) is a neurodegenerative movement disorder characterised by a loss of dopaminergic neurons in the substantia nigra and formation of fibrillar intraneuronal inclusions, so called Lewy bodies. There is evidence that aggregation of ?-Synuclein plays a central role in human PD. The objective of this study is a detailed characterisation of a transgenic mouse line over expressing human ?-Synuclein bearing the A53T mutation, which is considered to be an animal model of human Parkinson?s disease. Male and female A53T transgenic (tg) mice and non-transgenic (ntg) littermates were tested at three ages (3, 6 and 9 months) by a behavioural test battery, including the Irwin test, Open Field test, Nest Building Behaviour test, Beam Walk test, RotaRod test, Two Choice Swim test and Fear Conditioning test. Additionally, a quantitative histological analysis of the murine (endogenous) and human (transgenic) ?-Synuclein levels was performed. The results show that the A53T tg and ntg animals were healthy and that the sensorimotor reflexes and motor abilities were normal. The body weight measurement showed a normal and healthy growth of mice from both genotypes. Starting at 6 months of age A53T tg mice show severe motor deficits as analysed with the Beam Walk test and the RotaRod test. Analysis of animals in the Two Choice Swim test and the Fear Conditioning test up to an age of 9 months revealed no cognitive deficits. These results apply to both genders. Histological analyses showed expression and distribution of murine and human ?-Synuclein throughout different regions of the mouse brain. In summary, the A53T tg mouse presented here is a suitable model for ?-Synuclein dependent Parkinson?s disease research, since it illustrates major behavioural hallmarks of PD.