They find a promising molecular mechanism useful for treating Alzheimer’s disease.
Neurological diseases already affect more than 3.4 billion people, representing more than 43% of the world’s population, and in 2021 they were responsible for more than 11 million deaths, more than 168 million years lived with disability, and more than 275 million life years lived with disability. lives lost around the world. Among them is Alzheimer’s disease, a neurodegenerative disease that, according to the Spanish Society of Neurology (SEN), More than 800,000 Spaniards suffer from it.
In this scenario, continued research is critical. A good example of this is work carried out by a research group from Institute of Neurosciences of the University of Barcelona (UBneuro), who conducted a study describing New molecular mechanism that influences RNA processing and alters protein synthesis in the brains of Alzheimer’s patientswhich could help develop future treatments for this disease.
Research supported by Christina Malaguelladadirector of operations and Genis Campoy-Campos As first author, member of the Network Biomedical Research Center for Neurodegenerative Diseases (CIBERNED) and published in the journal Nucleic Acids Research, a hitherto unknown role is revealed RTP801 proteina stress response factor that is abundant in patients with neurodegenerative diseases such as Alzheimer’s disease. According to the findings, this protein are able to alter the molecular mechanisms that help neurons survive by affecting the translation of RNA into proteins.
A promising find
Research Director, Christina Malaguelladaexplained that “until now, we knew that the protein RTP801, which is found in hippocampal neurons, is involved in Alzheimer’s disease, and we already published this in a previous paper. At that time, We found that levels of this protein were significantly increased in both mouse models of Alzheimer’s disease. as in postmortem patient samples, and these values correlated with disease progression.
In this regard, researchers have already noticed that reducing the expression of RTP801 prevents cognitive deficits and inflammation. Specifically, the present study describes how RTP801 negatively regulates the activity of the tRNA ligase complex (tRNA-LC), which is critical for the processing of RNA molecules. In the context of Alzheimer’s disease, higher levels of RTP801 may inhibit this complex and cause problems with RNA ligation and subsequent production of related proteins such as brain-derived neurotrophic factor (BDNF), which exacerbates cognitive problems in the Alzheimer’s mouse model. Campoy-Campos, for his part, emphasizes that “in this study we confirmed that high levels of RTP801 interfere with the tRNA ligase complex, which is responsible for RNA processing.especially during the process of ligation of its exons after excision of introns. This process occurs both in messenger RNA (which contains information for building a protein) and in transport RNA, which includes amino acids for its translation. The researcher emphasizes that “this process is necessary for the proper synthesis of proteins in ribosomes, the cellular organelles where RNA is translated into proteins.”
“If we can develop inhibitors of the RTP801 protein or preserve the activity of the tRNA ligase complex, “We could specifically block the most toxic functions of this factor and preserve important neuronal processes.”Malaguelada emphasized. This will open up opportunities for treating not only Alzheimer’s disease, but also for treating neurodegenerative pathologies and preserving brain function and neuronal health.