Running exercise delays neurodegeneration in amygdala and hippocampus of Alzheimer’s disease (APP/PS1) transgenic mice

Is your doctor going to figure out a way for you to get some kind of running exercise to counteract your 33% chance of getting dementia post-stroke?
Even though this is just in mice what is the downside of doing this for stroke survivors? Keep demanding answers from your doctors, they are supposed to be helping you recover.
http://www.sciencedirect.com/science/article/pii/S1074742714002196 

• Tzu-Wei Lin^a,
• Yao-Hsiang Shih^a,
• Shean-Jen Chen^{b, c, d},
• Chi-Hsiang Lien^b,
• Chia-Yuan Chang^b,
• Tung-Yi Huang^e,
• Shun-Hua Chen^{a, f},
• Chauying J. Jen^{a, e},
• Yu-Min Kuo^{a, g, ,}

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doi:10.1016/j.nlm.2014.12.005

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Highlights

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Neurodegeneration occurs in the hippocampus and amygdala of young transgenic mice.

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Neurodegeneration in the amygdala is more severe than that in the hippocampus.

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Exercise counteracts the transgene-induced neurodegeneration.

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Exercise enhances the BDNF signaling pathways and Aβ clearance.

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Abstract

Alzheimer’s disease (AD) is an age-related neurodegenerative disease. Post-mortem examination and brain imaging studies indicate that neurodegeneration is evident in the hippocampus and amygdala of very early stage AD patients. Exercise training is known to enhance hippocampus- and amygdala-associated neuronal function. Here, we investigated the effects of exercise (running) on the neuronal structure and function of the hippocampus and amygdala in APP/PS1 transgenic (Tg) mice. At 4-months-old, an age before amyloid deposition, the amygdala-associated, but not the hippocampus-associated, long-term memory was impaired in the Tg mice. The dendritic complexities of the amygdalar basolateral neurons, but not those in the hippocampal CA1 and CA3 neurons, were reduced. Furthermore, the levels of BDNF-TrkB signaling molecules (i.e. p-TrkB, p-Akt and p-PKC) were reduced in the amygdala, but not in the hippocampus of the 4-month-old Tg mice. The concentrations of Aβ₄₀ and Aβ₄₂ in the amygdala were higher than those in the hippocampus. Ten weeks of treadmill training (from 1.5- to 4-month-old) increased the hippocampus-associated memory and dendritic arbor of the CA1 and CA3 neurons, and also restored the amygdala-associated memory and the dendritic arbor of amygdalar basolateral neurons in the Tg mice. Similarly, exercise training also increased the levels of p-TrkB, p-Akt and p-PKC in the hippocampus and amygdala. Furthermore, exercise training reduced the levels of soluble Aβ in the amygdala and hippocampus. Exercise training did not change the levels of APP or RAGE, but significantly increased the levels of LRP-1 in both brain regions of the Tg mice. In conclusion, our results suggest that tests of amygdala function should be incorporated into subject selection for early prevention trials. Long-term exercise protects neurons in the amygdala and hippocampus against AD-related degeneration, probably via enhancements of BDNF signaling pathways and Aβ clearance. Physical exercise may serve as a means to delay the onset of AD.