Adult hippocampal neurogenesis (AHN) is impaired before the onset of Alzheimer’s disease (AD) pathology. We found that exercise provided cognitive benefit to 5×FAD mice, a mouse model of AD, by inducing AHN and elevating levels of brain-derived neurotrophic factor (BDNF). Neither stimulation of AHN alone, nor exercise, in the absence of increased AHN, ameliorated cognition. We successfully mimicked the beneficial effects of exercise on AD mice by genetically and pharmacologically inducing AHN in combination with elevating BDNF levels. Suppressing AHN later led to worsened cognitive performance and loss of preexisting dentate neurons. Thus, pharmacological mimetics of exercise, enhancing AHN and elevating BDNF levels, may improve cognition in AD. Furthermore, applied at early stages of AD, these mimetics may protect against subsequent neuronal cell death.
This blog reports new ideas and work on mind, brain, behavior, psychology, and politics - as well as random curious stuff. (Try the Dynamic Views at top of right column.)
Tuesday, September 11, 2018
How exercise slows Alzheimer’s disease.
Wow…if I ever needed more encouragement to keep up my exercise routines (mainly swimming, biking, and a few weights) Choi et al. provide it by demonstrating that in a mouse model of Alzheimer's disease, exercise improves memory through a combination of encouraging the generation of new nerve cells in the hippocampus and increasing the levels of brain-derived neurotrophic factor (BDNF) that supports neuronal growth and survival. Their abstract:
Subscribe to:
Post Comments (Atom)
Great article post.Really thank you! Really Cool.
ReplyDelete