Abstract
The blood–brain barrier (BBB) is a network of specialized endothelial cells that regulates substrate entry into the central nervous system (CNS). Acting as the interface between the periphery and the CNS, the BBB must be equipped to defend against oxidative stress and other free radicals generated in the periphery to protect the CNS. There are unique features of brain endothelial cells that increase the susceptibility of these cells to oxidative stress. Insulin signaling can be impacted by varying levels of oxidative stress, with low levels of oxidative stress being necessary for signaling and higher levels being detrimental. Insulin must cross the BBB in order to access the CNS, levels of which are important in peripheral metabolism as well as cognition. Any alterations in BBB transport due to oxidative stress at the BBB could have downstream disease implications. In this review, we cover the interactions of oxidative stress at the BBB, how insulin signaling is related to oxidative stress, and the impact of the BBB in two diseases greatly affected by oxidative stress and insulin resistance: diabetes mellitus and Alzheimer’s disease.
Highlights
The blood–brain barrier (BBB) helps to separate the periphery from the central nervous system (CNS)
Oxidative stress can occur in any organ throughout the body and each organ has its own unique response to combat the production of oxidative stress
Oxidative stress is known to impact the gut microbiome, which can indirectly lead to alterations at the BBB through release of circulatory factors and have been linked to neurodegenerative and metabolic disease [111,112]
Summary
The blood–brain barrier (BBB) helps to separate the periphery from the central nervous system (CNS). As is well known, it links the periphery to the CNS through the impact of glucose, requiring high peripheral glucose to elicit a greater effect in the brain due to loss of the astrocytic insulin receptor It connects insulin receptor signaling on one cell type (astrocytes) to the communication with another cell type (neurons) and the potential impact on oxidative stress. As is well known, it links the periphery to the CNS through endothelial NOS and inducible NOS indirectly stimulates insulin transport, whereas NO the impact of glucose, requiring high peripheral glucose to elicit a greater effect in the released by nNOS acts directly on BECs to block insulin transport in a region-specific brain due to These loss ofdata thesupport astrocytic insulin receptor.insulin. Apolipoprotein E (apoE) is one protein linked to insulin resistance, oxidative stress, and AD
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