Decreased Opa1 Expression Increases Neuronal Vulnerability To Ischaemic Stroke During Ageing: Role Of Timm8B As A Therapeutic Target
As we age, our bodies undergo various changes, and unfortunately, this can increase our vulnerability to serious health issues like ischemic stroke, a condition where blood flow to the brain is interrupted. This type of stroke is a leading cause of death and disability worldwide, with older individuals often experiencing more severe outcomes.
A key player in both the damage caused by stroke and the aging process itself is the mitochondria, often called the “powerhouses” of our cells. When mitochondria don’t function properly, brain cells become more susceptible to harm.
Recent research has shed light on a specific protein called OPA1, which is crucial for maintaining healthy mitochondrial function. Scientists observed that levels of OPA1 naturally decline with age and drop even further after an ischemic stroke. This reduction in OPA1 was linked to increased mitochondrial damage and worse recovery outcomes in aged animal models of stroke.
Interestingly, another protein, Timm8b, was also found to be reduced when OPA1 levels were low. The exciting discovery was that by increasing the amount of Timm8b, researchers could protect mitochondria, help restore OPA1’s normal function, and significantly reduce the damage in aged brains following a stroke.
These findings suggest a novel pathway where aging makes brain cells more vulnerable to stroke by affecting mitochondrial health through OPA1. Crucially, they highlight Timm8b as a promising new target for developing treatments to protect older adults from the devastating effects of ischemic stroke.
Source: link to paper