Skip to main content
Fig. 1 | Acta Neuropathologica Communications

Fig. 1

From: Upregulating β-hexosaminidase activity in rodents prevents α-synuclein lipid associations and protects dopaminergic neurons from α-synuclein-mediated neurotoxicity

Fig. 1

High molecular weight aSYN and ubiquitin accumulation accompany HEX-deficiencies in the Sandhoff mouse model. a Representative immunoblot of high molecular weight (HMW) aSYN in whole-brain homogenates from age-matched WT and SD mice. GAPDH is shown as loading control. b Densitometric quantifications of HMW-aSYN (>17kDA) of samples treated as in (a), normalized by GAPDH and expressed as folds of WT (*:p < 0.05, Welch’s t-test). c Densitometric quantifications of monomeric aSYN17 over GAPDH. d Representative immunoblot of ubiquitin in age-matched WT- and SD mouse whole-brain. GAPDH is shown as loading control. e Densitometric quantifications of total ubiquitin over GAPDH, expressed as folds of WT (***:p < 0.001, two-tailed t-test). Box plots show median, 95% CI and range, with individual data points shown for all graphs, n = 7–8 / group

Back to article page

Acta Neuropathologica Communications

ISSN: 2051-5960

Contact us