Molecular Mechanisms Of Age-Related Vulnerability To Traumatic Brain Injury
As we age, our brains become more susceptible to injuries like traumatic brain injury (TBI), often leading to more severe consequences and a tougher recovery. Researchers have delved into the microscopic, molecular changes that contribute to this heightened vulnerability. They’ve identified several key factors, including a reduction in the brain’s “white matter,” which acts like the wiring connecting different brain regions. The “blood-brain barrier,” a protective shield that regulates what enters the brain, can also become less effective. Inside brain cells, there can be an increase in “oxidative stress,” which is damage caused by unstable molecules, and the “mitochondria,” the cell’s powerhouses, may not function optimally. Additionally, older brains tend to experience more cell death and a loss of “synapses,” the vital connections between brain cells. The brain’s immune response can also become overactive, leading to prolonged “neuroinflammation,” or inflammation within the brain. The brain’s capacity for self-repair after injury can also be compromised, and systems responsible for clearing out damaged proteins might not work as efficiently, leading to a buildup of misfolded proteins. These age-related changes collectively impact how well an individual recovers from a brain injury, influencing their long-term brain function and behavior. Understanding these underlying mechanisms is essential for developing more effective treatments for TBI, particularly in older adults.
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