Frequency of LATE neuropathologic change across the spectrum of Alzheimer's disease neuropathology: combined data from 13 community-based or population-based autopsy cohorts.
Previously, we reported that intracranial inoculation of brain homogenate from multiple system atrophy (MSA) patient samples produces neurological disease in the transgenic (Tg) mouse model TgM83 +/− , which uses the prion protein promoter to express human α-synuclein harboring the A53T mutation found in familial Parkinson's disease (PD). In our studies, we inoculated MSA and control patient samples into Tg mice constructed using a P1 artificial chromosome to express wildtype (WT), A30P, and A53T human α-synuclein on a mouse α-synuclein knockout background [Tg(SNCA +/+)Nbm, Tg(SNCA*A30P +/+)Nbm, and Tg(SNCA*A53T +/+)Nbm]. In contrast to studies using TgM83 +/− mice, motor deficits were not observed by 330 to 400 days in any of the *
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