A recent study led by two members of Mental Health Research Centre (MHRC) including Prof. Hector Tsang, Chair Professor of Rehabilitation Sciences (RS) and Prof. Sonata Yau, Associate Professor of RS, has identified a novel biological pathway that explains how physical exercise mitigates the risk of Alzheimer’s disease (AD). Published in the prestigious journal Aging Cell, the research provides a detailed look at how exercise protects the brain from the damaging effects of chronic stress and cognitive decline.
The team discovered that physical activity triggers the release of adiponectin, a hormone secreted by fat tissue, which acts as a critical messenger to the brain. This hormone activates a protective enzyme called Protein Phosphatase 2A (PP2A) in the hippocampus—a key brain region for mood regulation for memory formation. By activating PP2A, exercise effectively prevents Tau hyperphosphorylation, a pathological process where proteins become “tangled” and cause the neuronal damage typically seen in Alzheimer’s patients.
Significantly, the study found that while chronic stress accelerates harmful brain changes and suppresses PP2A activity, regular exercise effectively counteracts this damage. By experimentally reducing adiponectin levels or PP2A activity, the researchers demonstrated that the neuroprotective benefits of exercise were completely abolished. The study further revealed that exercise-induced PP2A activation is strictly dependent on the presence of adiponectin. These results prove that the adiponectin–PP2A axis is essential for brain health and highlight it as a promising therapeutic target for treating stress-related cognitive impairment and Alzheimer’s disease
Read the full research paper: https://onlinelibrary.wiley.com/doi/full/10.1111/acel.70447
| Research Units | Mental Health Research Centre |
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