A recent study appearing in the Journal of Neuroinflammation has brought further clarity to the role of astrocytes in the beneficial effects of voluntary exercise on patients with Alzheimer’s disease.
The effects of increased, voluntary physical exercise on cognitive functions in individuals with Alzheimer’s disease (AD) is well known. The underlying mechanisms, however, including the role of astrocytes, remain largely unexplored. Understanding these mechanisms, however, is crucial to developing more effective drugs and behavioral protocols for patients with AD.
Astrocytes are a type of glial cell—those that do not transmit electrochemical signals like neurons—present in the central nervous system that perform a variety of supportive functions, including blood-brain barrier maintenance, provision of nutrients, and neuronal repair.
For their study, the researchers subjected male mice of two groups to a series of behavioral tests and biochemical measurements to determine neuronal loss, impairment in neurogenesis, beta-amyloid (Aß) deposits, inflammation, and reductions in cognition and learning.
The first group included transgenic 5xFAD mice. 5xFAD refers to a series of mutations that produce cognitive and motor deficits and neuro-morphological changes that reproduce major features of AD in humans. The second group were wild-type, having no specific 5xFAD gene expressions, and served as a control.
The authors’ results are consistent with previous research in that physical exercise reversed cognitive impairment. More importantly, however, the researchers found that exercise had a significant effect on GFAP astrocytes. GFAP (glial fibrillary acidic protein) is a protein believed to contribute to astrocyte mechanical strength, morphology, and the general structure of the cytoskeleton.
5xFAD mice that were given the opportunity to exercise voluntarily demonstrated increased GFAP immunoreactivity, a greater overall number of GFAP-positive hippocampal astrocytes, and morphological changes among GFAP-astrocytes adjacent to Aß plaques.
Given that GFAP astrocytes are far more common in humans than rodents and, additionally, can interact with 10 times as many neurons, the implications for the treatment of AD in humans are all the more significant.
A better understanding of the role of exercise in slowing and even reversing the effects of Alzheimer’s disease is crucial to better using this treatment method, and may also lead to effective pharmaceutical approaches that reproduce its effects. The study’s findings, while preliminary, are promising and bear further exploration.
The study, “Astrocyte remodeling in the beneficial effects of long-term voluntary exercise in Alzheimer’s disease“, was authored by Irina Belaya, Mariia Ivanova, Annika Sorvari, Marina Ilicic, Sanna Loppi, Hennariikka Koivisto, Alessandra Varricchio, Heikki Tikkanen, Frederick R. Walker, Mustafa Atalay, Tarja Malm, Alexandra Grubman, Heikki Tanila, and Katja M. Kanninen.
