Alzheimer’s disease poses a significant threat to quality of life, and while a definitive cure remains elusive, researchers are actively seeking ways to mitigate its symptoms and explore preventive measures. A recent study by Massachusetts General Hospital (MGH)-led research team, sheds light on the potential role of exercise in preventing Alzheimer’s disease through the production of a hormone called irisin.
THE POWER OF EXERCISE
Exercise, a familiar ally in promoting overall health, emerges as a key player in the fight against Alzheimer’s disease. It triggers the production of irisin, a hormone with intriguing implications for Alzheimer’s prevention.
IRISIN’S ROLE IN THE BATTLE
Irisin, the muscle-derived hormone, takes centre stage in this study. It demonstrates the potential to enhance neprilysin, a vital enzyme that combats the brain-damaging protein known as amyloid beta, a primary culprit in Alzheimer’s disease.
RESEARCH INSIGHTS
The Massachusetts General Hospital (MGH)-led research team unveils compelling findings that underscore the promise of irisin-based therapies in the battle against Alzheimer’s disease.
While previous research indicated that exercise could reduce amyloid beta deposits in Alzheimer’s mouse models, the precise mechanisms remained elusive. However, the study reveals that exercise elevates irisin levels, providing a potential breakthrough.
THE BRAIN’S ALLY: IRISIN
Irisin, once produced in response to exercise, may become a powerful ally in Alzheimer’s prevention. It regulates glucose and lipid metabolism, increases energy expenditure, and promotes the transformation of white fat tissue into brown fat tissue.
REDUCING AMYLOID BETA: A KEY OBJECTIVE
The study unravels the presence of irisin in both human and mouse brains. Notably, its levels tend to decrease in individuals with Alzheimer’s disease and in mouse models of the condition.
To establish irisin’s causal role in the connection between exercise and reduced amyloid beta, researchers apply the hormone to a 3D cell culture model of Alzheimer’s disease, yielding promising results.
Irisin treatment demonstrates a remarkable reduction in amyloid beta pathology, attributed to increased neprilysin activity. Neprilysin, secreted by astrocytes in the brain, plays a pivotal role in breaking down amyloid beta.
CRITICAL SIGNALING PATHWAYS
Additionally, the research highlights how irisin’s binding to this receptor reduces the signalling of two crucial proteins: extracellular signal-regulated kinase (ERK) and signal activator of transcription 3 (STAT3). This reduction in ERK-STAT3 signalling proves critical for irisin-induced enhancement of neprilysin.
