From Necroptosis To Neuroinflammation: Unraveling Mechanisms And Therapeutic Targets In Age-Related Cognitive Decline
As we age, our immune system can become less effective, leading to a persistent, low-level inflammation throughout the body, including the brain. This chronic inflammation, sometimes called “inflammaging,” can damage our nervous system and speed up the progression of conditions like Alzheimer’s and Parkinson’s disease, ultimately affecting our thinking and memory abilities.
Recent research points to a specific process called necroptosis as a crucial player in this connection between inflammation and brain degeneration. Necroptosis is a form of programmed cell death, meaning cells are instructed to die in a controlled way. However, when this process is overactive, it can be detrimental.
Scientists have found that certain molecules central to necroptosis, such as RIPK1, RIPK3, and MLKL, become more active in older brain tissues. This heightened activity triggers the release of harmful signals that further intensify inflammation, increase damaging oxidative stress, and compromise the protective barrier around the brain. This cascade of events contributes to the loss of brain cells and the decline in cognitive function seen in aging and neurodegenerative diseases.
Understanding this mechanism opens new avenues for addressing age-related cognitive decline. Researchers are exploring ways to detect this harmful process early, potentially through specific markers in the blood. Furthermore, developing treatments, including both medications and nutritional supplements, that specifically target and inhibit necroptosis could offer promising strategies to protect brain health and combat neurodegeneration.
Source: link to paper