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Fig. 6 | Alzheimer's Research & Therapy

Fig. 6

From: Normal levels of KIF5 but reduced KLC1 levels in both Alzheimer disease and Alzheimer disease in Down syndrome: evidence suggesting defects in anterograde transport

Fig. 6

KLC1 was reduced in the frontal cortex of both AD and AD-DS brains, but not in the brains of Dp16 or J20 mouse models. Aa EGFP-KLC1 was transiently expressed in HEK293T cells for 36 h; after cell lysis, the soluble proteins were submitted to Western blotting to evaluate the specificity of the KLC1 antibody. Ab A goat IgG antibody to cathepsin D (CD) was used to further test the specificity of the KLC1 antibody in mouse brain lysate. B Western blotting analysis of KLC1 levels in protein extracts from the frontal cortex of patients with AD and from C/AD. For quantitation, the intensity of the doublet band at 75 kD and the band at ~ 65 kD were combined. C Quantitation and statistical analysis of KLC1 in AD and C/AD. D Statistical analysis of KLC1 levels in females and in males from AD and C/AD. E Western blotting of KLC1 levels in protein extracts from the frontal cortex of patients with AD-DS and C/AD-DS. F Quantitation and statistical analysis of the levels of KLC1 in AD-DS and C/AD-DS. G Statistical analysis of the levels of KLC1 in both females and males from AD-DS and C/AD-DS. H–J Western blotting analysis of KLC1 levels in the brains from 4- or 16-month-old Dp16 and 6-month-old J20 mice. n = 3–7 mice for each category. β-Actin or GAPDH was employed as an internal control for all panels. Mann-Whitney test; *P < 0.05, **P < 0.01, ***P < 0.001. n.s., non-significant; F, female; M, male

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