With the in-depth research on neuroinflammation in the scientific community, people are increasingly aware of the importance of microglia in the central nervous system. These resident immune cells are activated when the nervous system is injured or infected, demonstrating their powerful immune response. However, activation of microglia may also trigger harmful inflammation, thereby exacerbating nerve damage. This makes us wonder, are microglia protectors or destroyers?
Microglia are the main immune cells of the central nervous system, responsible for scanning their surrounding environment and responding to nerve damage. When the nervous system is traumatized, these cells rapidly deform and release inflammatory factors. Activation of microglia is part of the acute inflammatory response and is primarily used in response to acute injury.
Over time, however, the persistence of chronic inflammation can cause further damage to neural tissue.
Neuroinflammation is generally considered chronic inflammation, as opposed to acute inflammation, which generally occurs immediately upon pigment removal or trauma. Common factors that cause chronic neuroinflammation include aging, autoimmune diseases, viral infections, and environmental pollution. These factors not only trigger an immune response but also lead to permanent activation of microglia.
When microglial hormones are activated, they release a variety of cytokines, most of which promote inflammation, including tumor necrosis factor (TNF-α) and interleukin- 1β(IL-1β). While increasing the local inflammatory response, these factors may have toxic effects on neurons and cause secondary tissue damage.
In the process of treating neurodegenerative diseases, mediating the regulation of microglia in the choroid may become an effective strategy.
Microglia are associated with a variety of neurodegenerative diseases. Taking Alzheimer's disease as an example, studies have shown that the number of activated microglia increases significantly in the brain tissue of patients. These microglia are unable to effectively clear beta-amyloid, triggering accumulation and ultimately neuronal loss.
Chronic inflammation is considered to be one of the main causes of impaired cognitive function as we age. Chronically high levels of pro-inflammatory cytokines are common in the aged brain, which further contributes to neurological degeneration. For example, increases in interleukin-6 (IL-6) in the elderly are thought to be closely related to the development of neurodegenerative diseases.
These findings highlight the potential role of microglia in the aging process. Will there be long-term effects on cognitive function?
As the understanding of the role of microglia increases, the scientific community is increasingly interested in how to modulate the behavior of these cells to combat neurodegenerative diseases. Treatment includes the use of anti-inflammatory medications, increased exercise, and other lifestyle improvements. These strategies aim to reduce chronic inflammation and promote neuronal survival and repair.
Although microglia play an important role in protecting the nervous system, their overreactivity and continued activation may lead to nerve damage. This makes microglia a contradictory and balanced existence. Future research will need to explore how to effectively exploit the drug target functions of microglia to improve our therapeutic strategies for neurodegenerative diseases. And whether we can turn the duality of microglia into a therapeutic advantage is still worth thinking about, because it is related to our possibility of fighting a series of neurological diseases that plague humans.