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Massachusetts General Hospital (MGH) research team finds that neurogenesis -inducing the production of new neurons in the brain structure in which memories are encoded can improve cognitive function in a mouse model of Alzheimer’s disease. Beneficial effects on cognition can be blocked by the hostile inflammatory environment present in the brain of patients with Alzheimer’s disease, physical exercise can clean up the brain and allows new nerve cells to survive, thrive and improve cognition in the Alzheimer’s mice.
Exercise is one of the best ways to turn on neurogenesis, adult neurogenesis is the production of new neurons occurring after the embryonic. In some animals, neonatal periods takes place in the hippocampus and another brain structure-the striatum. While adult hippocampal neurogenesis is essential to learning and memory. The MGH team set out to investigate how impairment of adult hippocampal neurogenesis (AHN) contributed to Alzheimer’s disease pathology and cognitive function in a mouse model and whether increasing AHN could reduce symptoms.
Their experiments showed that AHN could be induced in the model either by exercise or by treatment with drugs and gene therapy that promoted the birth of neural progenitor cells. Behavioral testing of animals revealed limited cognitive benefits for animals in which neurogenesis had been induced pharmacologically and genetically. But animals in which AHN was induced by exercise showed improved cognitive performance and reduced levels of beta-amyloid.
Trying to achieve that result by using gene therapy and drugs did not work because newly born neurons, induced by drugs and gene therapy, were not able to survive in brain regions already ravaged by Alzheimer’s pathology, particularly neuroinflammation. The key difference was that exercise also turned on the production of brain-derived neurotrophic factor or BDNF known to be important for the growth and survival of neurons which created a more hospitable brain environment for the new neurons to survive. Blocking neurogenesis in young Alzheimer’s mice shortly after birth led to more pronounced cognitive deficits later in life.