🔄FROM THE ARCHIVE: Some researchers suspect these bacterial ancestors living within our cells may contribute to a wide range of neurological and psychiatric disorders.
Long before the earliest animals swam through the water-covered surface of Earth’s ancient past, one of the most important encounters in the history of life took place. A primitive bacterium was engulfed by our oldest ancestor — a solo, free-floating cell. The two fused to form a mutually beneficial relationship that has lasted more than a billion years, with the latter providing a safe, comfortable home and the former becoming a powerhouse, fueling the processes necessary to maintain life.
There is one organ that appears to be particularly vulnerable to mitochondrial damage: our power-hungry brains. “The more energetically demanding a cell is, the more mitochondria they have, and the more critical that mitochondria health is — so there’s more potential for things to go wrong,” says Andrew Moehlman, postdoctoral researcher who studies neurodegeneration at the US National Institute of Neurological Disorders and Stroke .
Researchers have since linked dozens of disorders to alterations in mitochondrial DNA and nuclear DNA related to mitochondrial function — and interestingly, the majority of these are either neurological in nature or have some effect on the brain.
“It’s too soon to make any firm conclusions about a lot of this stuff, but it sure looks like the mitochondria are disrupted in many kids with autism,” Frye says. “And environmental exposures, especially early on, may be programming the mitochondria to have different types of respiratory physiology.”
Inflammation caused by the release of mitochondrial DNA may contribute to the damage found in neurodegenerative diseases such as Parkinson’s, Alzheimer’s and amyotrophic lateral sclerosis , according to a growing number of studies. In separate lines of research, scientists have linked these disorders with both inflammation and an inability to properly rid cells of defective mitochondria. Mitochondria-triggered inflammation may be the missing link between the two.
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