Long-term Aerobic Exercise Prevents Age-Related Brain Changes
Here’s one more good reason to get up and get moving! Structural Deterioration associated with old age can be prevented by long-term aerobic exercise starting in mid-life, according to the authors of a research article published in the Open Access journal PLOS Biology on October 29th 2015. Gareth Howell, Ileana Soto, and their colleagues at The Jackson Laboratory in Bar Harbor, Maine (USA) found that structural changes that make the blood-brain barrier leaky and result in inflammation of brain tissues in old mice can be mitigated by allowing the animals to run regularly, thus providing a potential explanation for the beneficial effects of exercise on dementia in humans.
A release from the publisher notes that old age is the major risk factor for Alzheimer’s disease, like many other diseases. Age-related cognitive deficits are due partly to changes in neuronal function, but also correlate with deficiencies in the blood supply to the brain and with low-level inflammation. In this study, the authors set out to investigate the changes in the brains of normal young and aged laboratory mice by comparing by their gene expression profiles using a technique called RNA sequencing, and by comparing their structures at high-resolution by using fluorescence microscopy and electron microscopy. The gene expression analysis indicated age-related changes in the expression of genes relevant to vascular function (including focal adhesion, vascular smooth muscle and ECM-receptor interactions), and inflammation (especially related to the complement system, which clears foreign particles) in the brain cortex. These changes were accompanied by a decline in the function of astrocytes (key support cells in brain) and loss of pericytes (the contractile cells that surround small capillaries and venules and maintain the blood-brain barrier) and of major components of the basement membrane, which forms an integral part of the blood-brain barrier, as well as an increase in the density and functional activation of the immune cells known as microglia/monocytes, which scavenge the brain for infectious agents and damaged cells. Dr. Soto, lead author on the study, says: “Collectively, our data suggests that normal aging causes significant dysfunction to the cortical neurovascular unit, including basement membrane reduction and pericyte loss. These changes correlate strongly with an increase in microglia/monocytes in the aged cortex,”