A groundbreaking study has revealed how microscopic energy failures inside your brain cells might be behind one of the most debilitating symptoms of multiple sclerosis — the slow, silent collapse of your ability to move.
Key Points at a Glance
- MS-related movement loss may stem from failing mitochondria in key brain cells
- Purkinje cells in the cerebellum are especially vulnerable to energy deficits
- Mouse models show early mitochondrial dysfunction even before brain cells die
- Targeting mitochondria could unlock new MS therapies
What if your brain’s power grid started to flicker and fail — not all at once, but cell by cell, until even simple movements like walking or balancing became a daily struggle? This is the invisible threat posed by multiple sclerosis (MS), and a new study from the University of California, Riverside offers a stunning new insight into why it happens.
For years, scientists have known that MS involves the immune system attacking myelin — the protective sheath that wraps nerve fibers. But now, researchers are peering deeper, into the cells themselves, and discovering that the mitochondria — tiny energy generators inside neurons — are breaking down long before neurons die. And this malfunction may be the key to understanding a particularly cruel feature of MS: the loss of motor control.
Published in the *Proceedings of the National Academy of Sciences*, the study zeroes in on the cerebellum, the brain’s coordination command center. It’s where balance, rhythm, and fine motor skills are fine-tuned — from walking and running to dancing or even typing. In MS patients, nearly 80% experience inflammation in this region, leading to the progressive loss of Purkinje cells, large neurons critical for motor control. And that loss? It’s not just structural — it’s energetic.
“We found a sharp drop in a key mitochondrial protein, COXIV, inside these demyelinated neurons,” says lead researcher Seema Tiwari-Woodruff. “This suggests a devastating energy crisis right where it matters most — in the brain cells that keep us coordinated.”
The research team didn’t stop at analyzing human brain tissue. They turned to experimental autoimmune encephalomyelitis (EAE), a mouse model that mimics many MS symptoms. The parallels were striking: the mice lost Purkinje cells over time, and the remaining cells showed failing mitochondria and early myelin damage. In essence, the disease doesn’t wait until neurons die — it erodes their energy, function, and connections long before that.
Understanding this energy drain opens powerful new possibilities. If mitochondria can be protected or restored, it might be possible to halt or even reverse the cascade of damage before symptoms become severe. “This brings us a step closer to therapies that don’t just mask symptoms,” says Tiwari-Woodruff, “but actually preserve brain function.”
It’s a breakthrough that could redefine how we understand — and treat — MS. The researchers are already looking at other cerebellar cells, like oligodendrocytes and astrocytes, to see if they, too, suffer mitochondrial dysfunction. If so, the implications could stretch far beyond Purkinje cells — and offer a unified target for therapies aimed at slowing or stopping this relentless disease.
At a time when research funding is under threat, Tiwari-Woodruff offers a poignant reminder: “Scientific progress is our best hope. Without it, we leave millions to struggle in the dark.”
Source: UC Riverside News
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