It would help predict Parkinson’s

BARCELONA (EFE).— A study determined that alterations in the DNA of mitochondria, the organelles responsible for supplying energy to cells, may be a way to predict Parkinson’s.

Parkinson’s is associated with a dysfunction in the mitochondria, as some studies have shown that in the cerebrospinal fluid of people with this degenerative disease there is mitochondrial DNA that has defects, which would be an indicator of this malfunction. But what is not clear is whether this mitochondrial dysfunction is a consequence of Parkinson’s or if it is prior, that is, if it is a cause of the disease.

This is what a team led by Ramón Trullas, professor at the Higher Center for Scientific Research at the Barcelona Biomedical Research Institute, together with other experts, tried to elucidate.

In the work, which is published in the journal “eBioMedicine” (from the group “The Lancet”) and carried out with funding from the Michael J. Fox Foundation of the United States, the researchers studied a group of people with sleep behavior disorder during the REM phase. This disorder consists of an alteration of the deep sleep phase that is characterized by lack of muscle relaxation and the execution of sudden and violent movements of the extremities and trunk, which may be related to aggressive dreams.

Many patients with REM sleep behavior disorder eventually develop Parkinson’s, a brain disorder that causes involuntary or uncontrollable movements—such as tremors, rigidity, and difficulty with balance and coordination—or Lewy body dementia, which can cause alterations in thinking, movement, behavior and mood.

In both, round, abnormal protein deposits (called Lewy bodies) form in the brain associated with the death of neurons.

In collaboration with the Sleep Disorders Unit of the Hospital Clínic of Barcelona, ​​the team analyzed samples from 71 people.

Of them, 34 were diagnosed with sleep behavior disorder during the REM phase and years later developed Parkinson’s or Lewy body dementia; 17 were also diagnosed with REM sleep behavior disorder but remained disease-free, and 20 formed a control group without sleep behavior disorder or Parkinson’s.

“We have found that patients with REM sleep behavior disorder have higher levels of mitochondrial DNA with deletions compared to the control group,” reported Ramón Trullas.

Deletions are alterations of the mitochondrial DNA that involve the loss of genetic material in the DNA sequence.

The survival of neurons, unlike most cells in the body, depends largely on the energy provided by mitochondria.

The presence of circulating mitochondrial DNA with deletions indicates that mitochondria cannot provide sufficient energy for neurons to maintain their activity and long-term survival.

In this study, “patients with REM sleep behavior disorder, both those who subsequently developed Parkinson’s and those who did not, presented more circulating mitochondrial DNA with deletions—that is, those who have lost some fragment of genetic material—in the cerebrospinal fluid than the control group”, according to the first author of the work, Margalida Puigròs.

In addition, the researchers observed that the amount of DNA with deletions is related to the time it will take for patients with sleep behavior disorder to manifest clinical symptoms of Parkinson’s disease.

This means that the more deletions, the sooner the disease will appear, suggesting that mitochondrial DNA dysfunction is a mechanism that precedes the complete motor and cognitive clinical manifestation of Parkinson’s.

Thus, deletions could be a marker to predict serious brain diseases during the follow-up of patients with sleep disorders, considered the initial state of Parkinson’s disease.