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Abstract
Cellular senescence may play a significant role in the pathogenesis of Alzheimer's disease.
- In Alzheimer's disease, various brain cells, including neurons and glial cells, show signs of premature aging.
- Senescent cells in the brain become inactive but can still release harmful substances that affect nearby cells.
- These substances can worsen neurotoxicity related to amyloid-beta and tau proteins, leading to increased inflammation in the brain.
- The presence of senescent cells may disrupt the blood-brain barrier, contributing to a cycle of neurodegeneration.
- Current therapies targeting amyloid-beta and tau have limited success, indicating a need for new treatment strategies.
- Potential new treatments may include approaches that target senescent cells to mitigate their harmful effects.
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