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Fig. 4 | Molecular Neurodegeneration

Fig. 4

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. 4

Associations of M18 splice variants with Alzheimer’s disease pathology, global cognition and clinical dementia. a Contour plots illustrating MAP participants’ (n = 308) global cognition (z-score) as a function of M18L or M18S DLPFC immunodensities, and Alzheimer’s disease (AD) pathology. Only AD pathology × M18L (r =−0.251, p < 0.001), AD pathology × global cognition (r =−0.545, p < 0.001), and M18L × global cognition (r = 0.373, p < 0.001) were significantly correlated. b Regression analyses predicting global cognition as a function of AD pathology in groups of MAP participants having M18L or M18S immunodensities above 90th (green), between 10th and 90th (blue), or below 10th percentile (red). Lines represent best-fit curves and 95 % confident intervals. For M18L, significant correlations between AD pathology and global cognitive function were observed for participants among the lowest (r =−0.735, p < 0.001, n = 31) and intermediate (r =−0.512, p < 0.001, n = 243), but not the highest (r =−0.399, p = 0.074, n = 31), M18L groups. For M18S, statistically significant correlations were seen in all three M18S ranked groups: low (r =−0.460, p = 0.036, n = 31), intermediate (r =−0.559, p < 0.001, n = 245) and high (r =−0.509, p = 0.021, n = 29). c Whiskers represent 10th and 90th percentiles of M18L or M18S values, with boxed interquartile ranges crossed by the median, in participants with no- (NCI, n = 90), or mild-cognitive impairment (MCI, n = 86), or with dementia (DEM, n = 132). One-way ANOVA detected a significant effect only for M18L (F(2305) = 8.77, p < 0.001). *p < 0.05 and ***p < 0.001, ANOVA followed by Bonferroni’s test. d Representative immunoblots of M18L/S and β-actin, with various participants and standard (std) samples. Masses are indicated in kDa

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