What Fuels Brain Damage in MS? Scientists Find Clues

A new study reveals how mitochondrial failure in brain cells may be behind motor dysfunction in multiple sclerosis, offering hope for targeted treatment breakthroughs.

Highlights:

Mitochondrial failure found to drive nerve cell loss in MS
Balance and coordination issues linked to Purkinje cell damage
Mouse model confirms early energy loss precedes brain cell death

A groundbreaking study published in Proceedings of the National Academy of Sciences sheds light on why people with multiple sclerosis (MS) often suffer from severe movement and coordination problems. The culprit? Mitochondria, the tiny energy factories inside brain cells, may be failing as a result of inflammation and nerve damage in the cerebellum ().

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The brain's energy factories could shape future MS care #mitochondriainms #brainhealthbreakthrough #medindia

What the Numbers Say

MS affects around 2.3 million people worldwide, with about 80% experiencing inflammation in the cerebellum, the brain region responsible for movement and balance. This can lead to tremors, poor coordination, and difficulty walking, symptoms that can worsen over time. Researchers found that Purkinje cells, large neurons essential for motor control, are damaged and dying due to mitochondrial dysfunction, disrupting the brain’s ability to send proper movement signals.

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What Are Purkinje Cells?

These special neurons in the cerebellum act like control towers for motor functions. They help us perform everything from walking to dancing with precision. When they malfunction or die, as seen in MS, the results can be devastating; a condition known as ataxia, where balance and coordination deteriorate significantly.

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How Mitochondria Become the Weak Link

The UC Riverside team observed that chronic inflammation and loss of myelin (the protective coating around nerves) lead to reduced activity in a key mitochondrial protein called COXIV. This protein is vital for energy production in brain cells. Without it, Purkinje cells become weak and eventually die, contributing to long-term disability in MS patients.

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Mouse Model Confirms Human Findings

Using a mouse model of MS called EAE (experimental autoimmune encephalomyelitis) , researchers found similar patterns of Purkinje cell loss and mitochondrial breakdown. These mice showed early signs of myelin damage, disrupted energy supply, and eventual neuronal death, mirroring what occurs in the human brain. This makes EAE a powerful model for studying MS and testing future treatments.

Energy Loss Leads to Brain Decline

Mitochondria aren’t just passive players. According to the study author, the loss of energy inside brain cells is not just a symptom, but a key driver of disease progression in MS. Early damage to the myelin sheath and energy-producing structures can trigger a domino effect, leading to worsening neurological symptoms over time.

Can We Protect the Brain Before It’s Too Late?

The next step, the team says, is to explore whether other brain cells like astrocytes and oligodendrocytes also suffer from mitochondrial problems in MS. If researchers can find ways to boost cellular energy, repair myelin, or calm the immune system early, it may be possible to delay or prevent the damage seen in MS.

Why This Matters for MS Patients

For many with MS, the gradual decline in movement and coordination can be one of the most frustrating aspects of the disease. This study provides a new perspective on how and why this happens, highlighting mitochondria as a promising target for therapies. It also reinforces the importance of early diagnosis and intervention before irreversible brain damage sets in.

These findings don’t just deepen our understanding of MS. They open the door to treatments that go beyond managing symptoms and instead focus on protecting and energizing brain cells at the root of the disease. The possibility of restoring balance and movement for millions of people is no longer a distant dream but a scientific goal within reach.

If we can give brain cells the power they need to survive, we may finally give MS patients a future with hope and stability.

Reference:

Decreased mitochondrial activity in the demyelinating cerebellum of progressive multiple sclerosis and chronic EAE contributes to Purkinje cell loss - (https://www.pnas.org/doi/10.1073/pnas.2421806122)

Source-Medindia