Conicet scientists reveal therapeutic studies for Parkinson’s and Alzheimer’s

An in vitro investigation, led by Conicet experts, details a potential therapeutic target against Parkinson’s, Alzheimer’s, multiple sclerosis and other neurodegenerative conditions.

Although there are medical approaches available to improve the quality of life of those suffering from neurodegenerative diseases, detailed research is required to create more effective treatments.

In this scenario and through the execution of in vitro research, experts from the institution identified a potential therapeutic target against Parkinson’s, Alzheimer’s, multiple sclerosis, Huntington’s disease and other neurodegenerative conditions. The research is detailed in the scientific publication Biochimica et Biophysica Acta – Molecular Basis of Disease.

Carina Weissmann, researcher of the organism at the Institute of Physiology, Molecular Biology and Neurosciences, pointed out: “In our work we verified that different molecular mechanisms, which have been studied in parallel, actually interact and that this interaction could play an important role in different neurodegenerative pathologies. . Likewise, we identified a potential therapeutic target for those conditions,” she said.

The study

Different studies have indicated the reduction of the pH level (increased acidity) and the increase of a protein called interleukin 6, a key regulator of the immune system in the brain, during pathological neuroinflammation processes observed in neurodegenerative diseases.

Similarly, other works elucidated the mechanisms by which certain types of proteins, known as ASIC1a and widely present in neurons of the central nervous system, could play a crucial role in various neurodegenerative diseases.

In this recent work, Weissmann highlighted that they verified that the “molecular mechanisms studied in parallel (the activation of ASIC1 proteins, low pH conditions and interleukin 6) interact and that this interaction could play a relevant role in multiple neurodegenerative diseases.” .

What the research group managed to demonstrate, in tests carried out in cellular models, including human cells and mouse brain neurons, that mimic neuroinflammation processes, is that the increase in interleukin 6 leads to a relocation of the ASIC1a proteins. from intracellular compartments to the neuronal membrane.

“When the presence of ASIC1a proteins increases in the membrane of neurons, there is a greater entry of sodium and calcium into the intracellular environment and this activates other molecules. We were able to evaluate that in cells this caused alterations in morphology which leads to cell death. We were able to avoid these alterations by blocking the activation of the ASIC1a proteins,” explains Catalina Salinas, doctoral fellow at Conicet and author of the study. And she continues: “By blocking ASIC1a proteins, we prevent cell death.”

The results indicate that interactions between interleukin 6 and ASIC1a proteins trigger cellular cascades that could lead to cell death. However, blocking proteins prevents these harmful effects. Future studies will have to confirm this.