Interplay Of Oxidative Stress And Neuroinflammation In Alzheimer’S: Insights Into Age-Driven Pathogenesis
As we age, our brains become more susceptible to conditions like Alzheimer’s disease. Recent research sheds light on how the aging process itself contributes to this devastating condition. It highlights a critical trio of factors: an imbalance of damaging molecules (known as oxidative stress), persistent inflammation in the brain, and the accumulation of “aged” cells that no longer function properly.
At the heart of this process are the cell’s powerhouses, mitochondria. When these energy factories malfunction, they produce an excess of harmful molecules, leading to oxidative stress. This stress damages our genetic material and contributes to the buildup of sticky proteins, a hallmark of Alzheimer’s, ultimately impairing our thinking abilities.
Furthermore, the brain’s immune cells, called microglia and astrocytes, can become chronically overactive, leading to a state of constant brain inflammation. This inflammation damages the connections between brain cells and worsens the accumulation of another problematic protein associated with the disease. Adding to this complexity, old, dysfunctional brain cells release substances that further fuel inflammation and oxidative damage.
While promising treatments like compounds that target mitochondria or remove these aged cells are being explored, getting them to work effectively in humans presents challenges. A proposed strategy emphasizes closely monitoring markers of oxidative stress and inflammation, using a combination of therapies, and tailoring treatments to each individual to strengthen the aging brain and potentially delay the onset of Alzheimer’s.
Source: link to paper