Abstract
Traumatic
brain injury (TBI) is a major health problem in the United States,
which affects about 1.7 million people each year. Glial cells, T-cells,
and mast cells perform specific protective functions in different
regions of the brain for the recovery of cognitive and motor functions
after central nervous system (CNS) injuries including TBI. Chronic
neuroinflammatory responses resulting in neuronal death and the
accompanying stress following brain injury predisposes or accelerates
the onset and progression of Alzheimer’s disease (AD) in high-risk
individuals. About 5.7 million Americans are currently living with AD.
Immediately following brain injury, mast cells respond by releasing
prestored and preactivated mediators and recruit immune cells to the
CNS. Blood-brain barrier (BBB), tight junction and adherens junction
proteins, neurovascular and gliovascular microstructural rearrangements,
and dysfunction associated with increased trafficking of inflammatory
mediators and inflammatory cells from the periphery across the BBB leads
to increase in the chronic neuroinflammatory reactions following brain
injury. In this review, we advance the hypothesis that neuroinflammatory
responses resulting from mast cell activation along with the
accompanying risk factors such as age, gender, food habits, emotional
status, stress, allergic tendency, chronic inflammatory diseases, and
certain drugs can accelerate brain injury-associated neuroinflammation,
neurodegeneration, and AD pathogenesis.
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