Older adults who lose muscle mass and gain body fat through a condition called sarcopenic obesity could risk developing chronic, age-related conditions such as Alzheimer\u2019s disease. Brock University PhD student Emily Copeland (BSc \u201920, MSc \u201922) is determined to understand why.<\/p>\n
Copeland is the lead author on a recently published research review exploring the impacts of a protein called brain derived neurotrophic factor (BDNF) on brain functioning, skeletal muscles and body fat.<\/p>\n
BDNF plays an important role in neuron development and other brain processes and is essential for learning and memory. The vital protein is lower in people living with Alzheimer\u2019s<\/a> and particularly in post-menopausal women<\/a>.<\/p>\n \u201cKnowing that BDNF declines with age and plays a role in both muscle and brain, we thought that it might be an important factor for healthy aging,\u201d Copeland says. \u201cSarcopenic obesity and Alzheimer\u2019s disease are two common age-related diseases, so we wanted to see how BDNF might be affected by them.\u201d<\/strong><\/p>\n The team \u2014 which also included co-leads Associate Professors of Kinesiology Val Fajardo and Health Sciences Rebecca MacPherson, who serve as Copeland\u2019s supervisors, as well as Professor of Health Sciences Paul LeBlanc and Assistant Professor of Psychology Paula \u00a0Duarte-Guterman \u2014 reviewed almost 100 scientific studies.<\/p>\n Copeland says the review shows how muscle wasting and weight gain associated with sarcopenic obesity contributes to Alzheimer\u2019s disease, and the role BDNF could play in treating these conditions.<\/p>\n \u201cIf you have more BDNF, you\u2019re more protected from developing Alzheimer\u2019s,\u201d she says. \u201cYou\u2019ll have better skeletal muscle health, and BDNF is linked to lower obesity as well.\u201d<\/p>\n Targeting BDNF-related pathways can inform both pharmacological and lifestyle interventions, including exercise, adds MacPherson.<\/p>\n \u201cExercise is one of the most robust physiological stimuli for increasing BDNF,\u201d she says. \u201cThe best part is that exercise is a simple strategy to boost brain health that is accessible to almost everyone.\u201d<\/p>\n \u00a0<\/strong>The review found that, in studies on animal models, higher levels of BDNF decreased overactivity of an enzyme called GSK3, leading to fewer beta amyloid and neurofibrillary tangles, which are evidence of Alzheimer\u2019s disease in the brain. These plaques and tangles increased in both animal and human tissues with lower levels of BDNF.<\/p>\n BDNF was also shown to repair muscle, burn fat and boost the performance of mitochondria \u2014 a sub-unit within a cell that regulates muscle endurance, insulin sensitivity and protein generation \u2014 in studies using animal models.<\/p>\n When muscles fibres are injured or break down because they aren\u2019t being used, skeletal muscle repair and regeneration take place by a type of stem cell called satellite cells. These mechanisms decline as the body ages.<\/p>\n For older adults grappling with sarcopenic obesity, this muscle repair doesn\u2019t function well. According to the team\u2019s review, research links this impairment to decreased BDNF levels.<\/p>\n With muscle wasting and insulin insensitivity, more body fat \u2014 called adipose tissue \u2014 is created, especially in the abdomen, leading to obesity, chronic low-grade inflammation and problems with metabolism.<\/p>\n \u201cAlzheimer\u2019s has become known as Type 3 diabetes,\u201d says Copeland. \u201cInflammation created with this type of insulin resistance in adipose tissue throughout the body crosses over into the brain. When the brain becomes resistant to insulin, it can increase amyloid beta production and overload the brains inflammatory response, putting the brain at higher risk for Alzheimer\u2019s disease.\u201d<\/p>\n Animal model studies reviewed by the team showed BDNF injections reduced body weight and the amount of adipose tissue that, in turn, reduced inflammation and improves insulin sensitivity.<\/p>\n