Fig 11. Schematic illustration of age-related changes in the neurovascular unit that are prevented by exercise.Fig 11. Schematic illustration of age-related changes in the neurovascular unit that are prevented by exercise. Credit: Gareth R. Howell, Et al.

Working in Gareth R. Howell’s lab at Bar Harbor’s Jackson Laboratory led Grabowska to become a co-author of the paper. The rewarding research has the potential to change the way we approach Alzheimer’s disease and other age-related cognitive issues.

Grabowska’s work at the Jackson Lab is supported with both academic year and summer study fellowships from the Maine IDeA Network of Biomedical Research Excellence (INBRE). These grants support support student research and training at 12 Maine scientific and education institutions, including College of the Atlantic.

The program is led by the MDI Biological Laboratory and sponsored by the the National Institute of General Medical Sciences at the National Institutes of Health.

 

APOE Stabilization by Exercise Prevents Aging Neurovascular Dysfunction and Complement Induction

By Ileana Soto, Leah C. Graham, Hannah J. Richter, Stephen N. Simeone, Jake E. Radell, Weronika Grabowska, W. Keith Funkhouser, Megan C. Howell, Gareth R. Howell.   

Published: October 29, 2015   DOI: 10.1371/journal.pbio.1002279   PLOS Biology 

Weronika Grabowska ’17Weronika Grabowska ’17Author Summary

Aging is frequently accompanied with frailty and cognitive decline. In recent years, increasing evidence has linked physical inactivity with the development of dementias such as Alzheimer’s disease. In fact, it is recognized that exercise combats frailty and cognitive decline in older adults, but the biological mechanisms involved are not completely known.

Understanding the biological changes that trigger cognitive deterioration during aging and the mechanisms by which exercise improves health and brain function is key to ensuring the quality of life of the elderly population and to reducing risk of dementias such as Alzheimer’s disease.

Here, we show that the cerebrovascular system in mice significantly deteriorates with age, and the structure and function of the blood brain barrier is progressively compromised. These age-related neurovascular changes are accompanied by neuroinflammation and deficits in common and spontaneous behaviors in mice. We found, however, that exercise from middle to older age preserves the cerebrovascular health, prevents behavioral deficits and reduces the age-related neuroinflammation in the cortex and hippocampus in aged mice. Mice deficient in Apoe, a gene associated with longevity and Alzheimer’s disease, are resistant to the beneficial effects of exercise, suggesting a possible mediating role for APOE in the maintenance and function of the neurovascular system during aging.

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