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
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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.
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.
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