Can our mitochondria help to beat long Covid? - The Guardian

This line of research could help provide much-needed treatments for people with long Covid, as well as revolutionising our understanding of everything from neurodegenerative illnesses such as Parkinson’s disease to the ageing process.

It is thought that some Parkinson’s patients have genetic mutations that prevent damaged mitochondria being eliminated and replaced with healthy versions – a process called autophagy.

While hacking the mitochondrial genome could change healthcare in years to come, finding more immediate ways of improving mitochondrial health could help the millions of people with long Covid and chronic fatigue syndrome, also known as ME/CFS.

The idea that mitochondria may be involved in the ailments of some of those with long Covid arises from research conducted by Raman and others on patients who find themselves chronically exhausted by exercise following Covid-19, despite showing no obvious heart or lung abnormalities.

This symptom is often referred to as post-exertional malaise (PEM), and is also experienced by people with genetic mitochondrial diseases?

David Systrom, a pulmonary and critical care doctor at Brigham & Women’s Hospital, Boston, believes he has found answers through studying patients with ME/CFS, an illness that in many cases is precipitated by viral infections such as Epstein-Barr and bears many similarities to long Covid.

When Systrom studied the mitochondrial DNA of these patients it appeared to be normal, but after taking a deep look and conducting muscle biopsies, he identified abnormalities at the electron level, deep within the mitochondria.

“In both ME/CFS and long Covid it’s most likely that these are acquired forms of mitochondrial dysfunction, perhaps related to the initial infection itself or an autoimmune response to a virus or both,” Systrom says.

Systrom is now running his own clinical trial in both ME/CFS and long Covid patients, in partnership with Japanese drug company Astellas, which has developed a drug that aims to restore normal mitochondrial metabolism.

Both Raman and Systrom agree that mitochondrial dysfunction is only likely to be a factor in a subset of long Covid and ME/CFS patients.

A common ailment reported by people with long Covid and ME/CFS is dysautonomia, a peculiar condition that causes a rapid increase in heartbeat and lightheadedness when patients attempt any form of activity.

As a result, if mitochondrial drugs prove effective in long Covid and ME/CFS, they may have applications in other illnesses, while mitochondrial DNA editing to understand the effects of various mutations could shed further light on how the ageing process manifests in our cells.

Scientists are also taking some more left-field approaches to finding ways to improve mitochondrial health.

This is already taking place in clinical trials, which have found that the dietary supplement urolithin A seems to improve mitochondrial health in older adults.

Studies have also shown that exercise itself can improve mitochondrial health in older adults who lead sedentary lifestyles, triggering proteins in mitochondria to cluster together in ways that allow them to pass electrons more efficiently