Chapters authored
The Role of NO/cGMP Signaling on Neuroinflammation: A New Therapeutic Opportunity
The nitric oxide/cyclic guanosine monophosphate (NO/cGMP) signaling appears to play a key role in inhibiting neuroinflammation and preventing the activation of a proapoptotic pathway, thereby promoting neural cell survival. In addition, evidence indicates that cGMP/protein kinase G (PKG) pathway is involved in the modulation of glial cell activity. Phosphodiesterase 5 (PDE5), which hydrolyzes cGMP in the inactive form, 5ʹGMP, is present throughout the body and brain and has emerged as a potential therapeutic target for diseases related to neuroinflammatory and neurodegenerative processes, since their inhibition leads to accumulation of cGMP. The objective of this chapter is to review current knowledge of NO/cGMP signaling pathways on neuroinflammation and the potential therapeutic use of PDE5 inhibitors (PDE5-Is) in neurological diseases. The extensive, while recent, literature on the effects of PDE-Is on Alzheimer’s disease (AD), multiple sclerosis (MS), Parkinson’s disease (PD), Huntington’s disease (HD), and stroke has been reviewed.
Part of the book: Mechanisms of Neuroinflammation
Involvement of Astrocytes in the Process of Metabolic Syndrome
Astrocytes constitute a very heterogeneous population of cells, which regulate pH, extracellular levels of ions and neurotransmitters, and energy metabolism in addition to actively participating in neurotransmission. In situations of damage to the CNS, the typical response is the degree of reactive gliosis, which can form glial scars. On the other hand, chronic diseases such as obesity, type 2 diabetes, hypertension, and atherosclerosis have been causally related to low-grade chronic inflammation in various metabolic tissues. It has been pointed out that the identification of hypothalamic inflammatory alterations are triggered by overnutrition, orchestrated by the hypothalamic immune system, and sustained by the pathophysiology associated with the metabolic syndrome. We discuss here the effects of astrocytes and the main astrocyte mechanisms involved in the metabolic syndrome and its comorbidities.
Part of the book: Glia in Health and Disease