Carmen Fernandez Barcelona

Barcelona

Updated Saturday, March 30, 2024-01:59

Finding out who is more likely to develop Parkinson's is a challenge for medicine. In some neurodegenerative disorders, they begin inside the body years before manifesting themselves externally. Many

clues lie in imperceptible genetic changes

and cellular alterations. To do this, scientists need time and volume of patients in which to test their hypotheses.

The Neurology Service of the Hospital Clínic-Idibaps of Barcelona develops a broad line of research that since 2006 has allowed it to publish up to 70 articles on the relationship between

idiopathic behavioral disorder in the REM phase of sleep

(those who suffer from it have nightmares in which they are attacked and persecuted, with the particularity that they express them with screams, crying, hitting and kicking) and neurodegenerative diseases such as

Lewy body dementia or Parkinson's disease

.

His first work (2006) showed that 45% of patients who suffer from this type of sleep behavior disorder develop Parkinson's disease and other neurodegenerative diseases.

In 2013, in the study of a cohort of people with the aforementioned sleep behavior disorder recruited between 1991 and 2003, he concluded that this problem is a strong candidate to study early events and the

progression of that prodromal phase

(initial symptoms that precede to the development of the disease), and to test modifying strategies that slow or stop the neurodegenerative process.

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And the latest article on the matter, published this month in

eBioMedicine

(from The Lancet group), provides evidence that

deletions in mitochondrial DNA

make it possible to predict Parkinson's before the appearance of its symptoms. It indicates, specifically, that the presence of mitochondrial DNA with mutations in which one or more bases of the DNA sequence is lost in the cerebrospinal fluid is a predictor of the appearance of the motor and cognitive symptoms of Parkinson's.

The research, carried out with funding from the Michael J. Fox Foundation of the United States, was led by

Ramon Trullàs

, researcher at the Barcelona Biomedical Research Institute of the CSIC (IIBB-CSIC), and

Alex Iranzo

, from the Neurology Service of the Hospital Clínic. from Barcelona, ​​head of the Clinical Neurophysiology research group at Idibaps and professor at the Faculty of Medicine and Health Sciences of the University of Barcelona (UB); both linked to the CIBER of Neurodegenerative Diseases (CiberNED).

DYSFUNCTION OF THE MITOCHONDRIA

Iranzo has explained to this newspaper that Parkinson's is associated with a dysfunction in the mitochondria (intracellular organelles that have their own DNA to function correctly and are responsible, among other things, for supplying energy to the cells): "They perform a very important function, like

lung,

for the neurons, but in this case they function poorly", and cannot provide enough energy for the

nerve cells

to maintain their activity and long-term survival.

This leading clinical researcher in the field has also reported that up to 90% of patients with the aforementioned sleep behavior disorder

end up developing, after about 15 years, either Parkinson's or Lewy body dementia

, which is why It is considered that this problem could be an early stage of these neurodegenerative diseases. In both, round, abnormal protein deposits (Lewy bodies) form in the brain associated with the death of neurons.

The authors studied, on this occasion, a cohort of

71 patients

with the aforementioned sleep behavior disorder; Of them, 34 were diagnosed with this disorder and years later developed Parkinson's or Lewy body dementia; 17 were diagnosed with the disorder but remained free of neurodegenerative disease, and 20 formed the control group (without disorder or parkinsonism).



And thanks to that sample they observed that

patients with specific sleep behavior disorder have higher levels of mitochondrial DNA with deletions

compared to the control group.

According to Margalida Puigròs, researcher at the IIBB-CSIC, Ciberned and the Institute of Neurosciences of the UB (UBneuro) and first author of this work, she highlighted, for her part, that "patients with sleep behavior disorder in the REM phase , both those who subsequently developed Parkinson's and those who did not, presented more circulating mitochondrial DNA with deletions - that is, they have lost some fragment of genetic material - in the cerebrospinal fluid than the control group. But the most relevant finding is that we have 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.

A PHYSIOPATHOLOGICAL CASCADE

The authors of the study suggest that mitochondrial DNA dysfunction would, therefore, be a primary molecular mechanism of the pathophysiological cascade that precedes the complete motor and cognitive clinical manifestation of Parkinson's.

And Iranzo has stressed that all the evidence allows us to think about the possibility of

designing and developing a neuroprotective therapy aimed at stopping or slowing down the neurodegenerative process

before the development of parkinsonism and dementia. When this treatment exists, he pointed out, it will be relevant to be able to analyze in patients with idiopathic behavioral disorder in the REM phase of sleep (the incidence is 0.7% of the population over 60 years of age) whether they present deletions in Mitochondrial DNA predictors of Parkinson's.