Abstract
Stroke is a life-threatening condition that is characterized by secondary cell death processes that occur after the initial disruption of blood flow to the brain. The inability of endogenous repair mechanisms to sufficiently support functional recovery in stroke patients and the inadequate treatment options available are cause for concern. The pathology behind oxidative stress in stroke is of particular interest due to its detrimental effects on the brain. The oxidative stress caused by ischemic stroke overwhelms the neutralization capacity of the body’s endogenous antioxidant system, which leads to an overproduction of reactive oxygen species (ROS) and reactive nitrogen species (RNS) and eventually results in cell death. The overproduction of ROS compromises the functional and structural integrity of brain tissue. Therefore, it is essential to investigate the mechanisms involved in oxidative stress to help obtain adequate treatment options for stroke. Here, we focus on the latest preclinical research that details the mechanisms behind secondary cell death processes that cause many central nervous system (CNS) disorders, as well as research that relates to how the neuroprotective molecular mechanisms of pituitary adenylate cyclase-activating polypeptides (PACAPs) could make these molecules an ideal candidate for the treatment of stroke.
Highlights
Stroke is a potentially fatal interference in the normal blood supply to the brain that precipitates debilitating sequelae including visual deficits, cognitive decline, and paresis.The two major subtypes of stroke are ischemic and hemorrhagic, the former is profoundly more common and accounts for nearly 85% of total stroke events worldwide [1]
Exhibited significantly higher levels of oxidative metabolites in the findings suggest that pituitary adenylate cyclase-activating polypeptides (PACAPs) functions as an antioxidant under oxidaplasma compared to wild-type mice; the difference in treatment, younger mice was notmice as tive stress conditions
mitogen-activated protein kinases (MAPK) and P1kK signaling play a role in PACAP-induced neuroprotection in models of Alzheimer’s Disease (AD) via α-secretase cleavage of APP, which is a precursor of Aβ [95]
Summary
Nadia Sadanandan , Blaise Cozene, You Jeong Park, Jeffrey Farooq , Chase Kingsbury, Zhen-Jie Wang, Alexa Moscatello , Madeline Saft, Justin Cho, Bella Gonzales-Portillo and Cesar V. Antioxidants 2021, Abstract: Stroke is a life-threatening condition that is characterized by secondary cell death processes that occur after the initial disruption of blood flow to the brain. The inability of endogenous repair mechanisms to sufficiently support functional recovery in stroke patients and the inadequate treatment options available are cause for concern. The oxidative stress caused by ischemic stroke overwhelms the neutralization capacity of the body’s endogenous antioxidant system, which leads to an overproduction of reactive oxygen species (ROS) and reactive nitrogen species (RNS) and eventually results in cell death. We focus on the latest preclinical research that details the mechanisms behind secondary cell death processes that cause many central nervous system (CNS) disorders, as well as research that relates to how the neuroprotective molecular mechanisms of pituitary adenylate cyclase-activating polypeptides (PACAPs) could make these molecules an ideal candidate for the treatment of stroke.
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