Mutations in human SNCA that result in aberrant polymerization and fibrillar aggregations are associated with neurodegenerative synucleinopathies, such as Parkinson's disease and multiple system atrophy. These BAC-aSyn120 mice express a conditional mutant human synuclein, alpha (non A4 component of amyloid precursor), SNCA, gene directed by the human SNCA promoter/enhancer regions that produces a C-terminal truncated protein (amino acids are deleted after residue 120). In addition, the BAC-aSyn120 transgene contains loxP sites flanking exon 2 including the translation initiation codon. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 2 of SNCA deleted in the cre-expressing tissues. Deletion of exon 2 allows expression of human aSyn to be turned off. The transgene expression mimics the endogenous mouse Snca expression pattern. Human SNCA protein levels are one fold higher than the endogenous mouse Snca protein levels. By 12 months of age, BAC-aSyn120 transgenic mice exhibit abnormal gait, increased activity in an open field test, increased immobility in a forced swimming test, and reduced anxiety behavior. Histological analysis reveals an accumulation of proteinase K-resistant SNCA protein in the brain (hippocampus CA2/CA3, cortex, brain stem and amygdala). Vacuoles and dystrophic neurites are observed in neurons of the cortex and hippocampus. Mice that are hemizygous for the transgene are viable and fertile. BAC-aSyn120 transgenic mice and BAC-aSyn transgenic mice (Stock No. <a href="https://www.jax.org/strain/028806">028806</a>) express human SNCA at similar levels. When bred to a strain with Cre recombinase expression in neurons of the CNS and PNS (see Stock No. <a href="https://www.jax.org/strain/003771">003771</a> for example), the resulting mice exhibit reduced expression of human SNCA protein.
 Distribution of this strain was supported by the Michael J. Fox Foundation for Parkinson's Research.

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These BAC-aSyn120 mice express a conditional mutant human synuclein, alpha (non A4 component of amyloid precursor), SNCA, gene directed by the human SNCA promoter/enhancer regions on the BAC transgene that produces a C-terminal truncated protein. These mice may be useful for studying SNCA function and the pathogenesis of Parkinson's disease.

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