Physical Exercise Inhibits Inflammation and Microglial Activation

Abstract

Accumulating evidence indicates that exercise can enhance brain function and attenuate neurodegeneration. Besides improving neuroplasticity by altering the synaptic structure and function in various brain regions, exercise also modulates multiple systems that are known to regulate neuroinflammation and glial activation. Activated microglia and several pro-inflammatory cytokines play active roles in the pathogenesis of neurodegenerative diseases, such as Alzheimer’s disease and Parkinson’s disease. The purpose of this review is to highlight the impacts of exercise on microglial activation. Possible mechanisms involved in exercise-modulated microglial activation are also discussed. Undoubtedly, more studies are needed in order to disclose the detailed mechanisms, but this approach offers therapeutic potential for improving the brain health of millions of aging people where pharmacological intervention has failed.

Physical exercise promotes astrocyte coverage of microvessels in a model of chronic cerebral hypoperfusion

“…Treatment during this period can trigger and promote neuroprotective mechanisms that will assist in the recovery of neuronal functions [12][13][14][15]. Among new therapeutic strategies being pursued to minimize cognitive damage, physical exercise has been shown to support brain health and function, with an impact on neurogenesis [16,17], reducing neuroinflamation [14,18] and oxidative stress [14,19]. Moreover, regular physical exercise is able to improve cognitive function in animals [20,21], and in adult and elderly populations [22][23][24].…”

The Immunomodulary Effects of Systematic Exercise in Older Adults and People with Parkinson’s Disease

“…Secretion of neurotrophic factors such as brain-derived neurotrophic factor (BDNF), glial cell-derived neurotrophic factor (GDNF), nerve growth factor (NGF), insulin-like growth factor 1 (IGF-1) or the vascular endothelial growth factor (VEGF) by microglia is neuroprotective. In the healthy brain, microglia exist in a resting state, but when exposed to pathological insult, microglia transform from resting to a spectrum of activated stages [5]. The classical activation state (M1) is associated with a pro-inflammatory phenotype having enhanced production of the tumour necrosis factor (TNF), interleukins 6 (IL-6), IL-12, IL-1β and several chemokines such as chemokine (C-C motif) ligand 2 (CCL2) and the human interferon-inducible protein 10 (IP-10 or CXCL10).…”

“…The activity of microglia can be inhibited by anti-inflammatory molecules [5]. One of them is fractalkine, which has been reported to inhibit the release of inflammatory cytokines while reducing microglia activation [8].…”

Sexually dimorphic microglia and ischemic stroke

“…Microglia are known as the resident brain macrophages and comprise about 5%‐12% of total brain cells, depending on the brain region . Under normal conditions, microglia exist in a resting state under what is known as a ramified morphology . They are involved in regulating neuronal excitability, synaptic activity, connectivity, neurogenesis, and clearance of apoptotic cells in the healthy adult brain .…”

“…8 Under normal conditions, microglia exist in a resting state under what is known as a ramified morphology. 9 They are involved in regulating neuronal excitability, synaptic activity, connectivity, neurogenesis, and clearance of apoptotic cells in the healthy adult brain. 10 In this review, we will focus on the role of microglia as a modulator of the differences in the inflammatory response and outcomes poststroke.…”