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Fig. 4 | Alzheimer's Research & Therapy

Fig. 4

From: Thiamine diphosphate reduction strongly correlates with brain glucose hypometabolism in Alzheimer’s disease, whereas amyloid deposition does not

Fig. 4

Amyloid deposition does not enhance the vulnerability of brain glucose hypometabolism. a Representative cortical or hippocampal slices of 6-month-old amyloid precursor protein/presenilin-1 (APP/PS1) transgenic and wild-type (WT) mice following thiamine deficiency (TD) or control diet with immunostaining for β-amyloid (Aβ; green) and TO-PRO (blue; Thermo Fisher Scientific). b–e The area and intensity of amyloid plaques in cortex and hippocampus were significantly elevated in APP/PS1 transgenic mice as compared with age-matched WT mice. Thiamine diphosphate (TDP) reduction significantly enhanced the area and intensity of amyloid plaques in cortex and hippocampus of 6-month-old APP/PS1 transgenic mice (P < 0.001, P < 0.01, or P < 0.05, respectively; two-way analysis of variance (ANOVA) with Tukey’s multiple comparisons posttest; n = 5 or 6). f–i TDP reduction induced a similar reduction of glucose metabolism in representative brain regions in APP/PS1 transgenic and WT mice. There were no significant interactions between TDP reduction and amyloid plaques (F1,19 = 0.15, P > 0.05 for cortex; F1,19 = 0.66, P > 0.05 for hippocampus; F1,19 = 0.39, P > 0.05 for thalamus; F1,19 = 0.00, P > 0.05 for striatum; P < 0.001, P < 0.01, or P < 0.05, respectively; two-way ANOVA with Tukey’s multiple comparisons posttest; n = 5 or 6). SUV Standardized uptake value. *P < 0.05, **P < 0.01, and ***P < 0.001

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