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. 2014 Aug;35(8):1821–1832. doi: 10.1016/j.neurobiolaging.2014.02.010

Table 2.

A high-fat diet had no effect on Alzheimer's disease neuropathology in 3xTgAD mice

Cortex
Hippocampus
Amygdala
Control High-fat Control High-fat Control High-fat
 Plaque burden
 3–4 mo nd nd nd nd nd nd
 7–8 mo nd nd nd nd nd nd
 11–12 mo nd nd 680 ± 183 585 ± 264 nd nd
 15–16 mo nd nd 2713 ± 458 6177 ± 1845 nd nd
 Oligomers (nmol/L)
 3–4 mo 2.7 ± 0.4 3.9 ± 0.4
 7–8 mo 4.2 ± 0.4 3.1 ± 0.2
 11–12 mo 3.6 ± 0.4 3.1 ± 0.3
 15–16 mo 3.8 ± 0.5 4.1 ± 0.4
Tau
 3–4 mo nd nd nd nd nd nd
 7–8 mo nd nd 1 ± 1 nd 2 ± 2 1 ± 1
 11–12 mo nd nd 7 ± 1 8 ± 3 2 ± 1 1 ± 1
 15–16 mo nd nd 8 ± 6 3 ± 1 9 ± 4 12 ± 5

3xTgAD mice were maintained on a control or high-fat diet for those aged 3–4, 7–8, 11–12, and 15–16 months. Immunohistochemistry for Aβ or hyperphosphorylated tau was performed using 6E10 and AT8 antibodies, respectively. The average number of cells per section positive for tau were counted in the cortex, hippocampus, and amygdala. The extracellular Aβ plaque burden in the hippocampus was assessed and data are expressed as average plaque area/section (μm2). The expression of Aβ oligomers was analyzed by ELISA in the hippocampus. Data are mean ± SEM, n = 6–12/group.

Key: Aβ, amyloid beta; ELISA, enzyme-linked immunosorbent assay; nd, none detected; —, not analyzed; SEM, standard error of the mean.