Neuroinflammation plays a significant role in memory loss by disrupting the normal functioning of brain cells involved in learning and memory. When the brain experiences injury, infection, or other harmful stimuli, immune cells in the brain called microglia and astrocytes become activated. While these cells usually protect the brain, their prolonged activation leads to the release of inflammatory molecules that can harm neurons and interfere with their communication.
Astrocytes, which normally support neurons by maintaining a healthy environment and helping form connections, can shift into a harmful state during neuroinflammation. In this state, they produce toxic substances and reactive oxygen species that damage neurons. They also release components of the complement system, such as complement 3, which bind to receptors on neurons and worsen their function. This process contributes to the breakdown of synapses—the connections between neurons essential for memory storage and retrieval.
Microglia, the brain’s resident immune cells, also contribute to this damaging cycle. When overactivated, they produce proinflammatory cytokines and enzymes that further injure neurons and promote synaptic loss. This inflammation-driven damage impairs the brain’s ability to retain and recall information, leading to memory decline.
In diseases like Alzheimer’s, neuroinflammation is a key factor that accelerates neurodegeneration and memory impairment. The inflammatory environment disrupts synaptic function and promotes the loss of neurons, which are critical for cognitive processes. Some experimental treatments aim to reduce neuroinflammation by targeting specific inflammatory pathways, showing promise in protecting memory and brain function.
Overall, neuroinflammation transforms protective brain cells into agents of damage, creating a harmful environment that undermines the neural networks responsible for memory. This understanding highlights the importance of controlling brain inflammation to preserve cognitive health.
