Skip to main content
Fig. 5 | Molecular Neurodegeneration

Fig. 5

From: Loss of Munc18-1 long splice variant in GABAergic terminals is associated with cognitive decline and increased risk of dementia in a community sample

Fig. 5

M18 splice variants are not altered in APP23 mice. a Immunodensities of M18L/S splice variants were quantified by Western blotting in brain homogenates (frontal cortex) from adult (12-month-old; T12) and aged (22-month-old; T22) wild type (WT) and APP23 transgenic mice. Columns are immunodensity mean values ± standard error (normalized by β-actin) of n = 6 mice per group, and represented in percentage to control (T12–WT) animals. Two-way ANOVA only detected a significant effect for genotype (but not age) on M18S (F(1,20) = 4.51, p = 0.0462), and a borderline age (but not genotype) effect on M18L (F(1,20) = 3.44, p = 0.0784), without specific between-group differences in the following Dunnett’s post hoc tests. b Representative immunoblots of M18L, M18S and β-actin, with one sample per group. Masses (in kDa) of proximal prestained markers are indicated on the left side of immunoblots

Back to article page