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Fig. 4 | Molecular Neurodegeneration

Fig. 4

From: VPS35 and α-Synuclein fail to interact to modulate neurodegeneration in rodent models of Parkinson’s disease

Fig. 4

Absence of retromer deficiency in brains from human A53T-α-Syn transgenic mice. A) Western blot analysis of retromer subunits and αSyn (total or pS129) in Triton-soluble extracts from spinal cord, brain stem, ventral midbrain and striatum of 6-month old pre-symptomatic hemizygous A53T-αSyn transgenic mice and their non-transgenic littermates (n = 3–4 animals/group). B) Similar Western blot analysis of spinal cord and brain stem extracts from symptomatic end-stage hemizygous A53T-αSyn mice (~ 12–13 months) and their non-transgenic littermates (n = 6 animals/group). C) Densitometric analysis of VPS35, VPS29 or VPS26 levels in the spinal cord and brain stem of end-stage A53T-αSyn transgenic and non-transgenic mice normalized to β-tubulin levels. Data are expressed as a percent of non-transgenic mice with bars representing the mean ± SEM (n = 6 animals/group). n.s., non-significant by unpaired two-tailed Student’s t-test

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