New Study Discusses Molecular Mechanism in Alzheimer’s Disease
The Institute of Neurosciences at the University of Barcelona has conducted a new study that has led to the discovery of a new molecular mechanism that affects RNA processing and alters the process of protein synthesis in the brains of those suffering from Alzheimer’s disease. The study was conducted using post-mortem samples of patients and animal models of the disease. The research will improve the creation of future therapies to address the treatment of dementia and other neurological disorders.
Understanding the mechanism
Alzheimer’s disease is the most common type of dementia. It causes a gradual decline in cognition, memory, and language skills, as well as emotional and psychiatric disorders. It is characterized by the accumulation of β-amyloid plaques outside neurons and hyperphosphorylated tau protein inside neurons, which alter brain function and cause cell death.
The new study revealed a previously unknown role for the RTP801 protein, a stress response factor that is abundant in patients with neurodegenerative diseases such as Alzheimer’s disease and other forms of dementia. According to the study, this protein can alter the molecular mechanisms that support neuronal survival by affecting the translation of RNA into proteins.
According to the study authors, “until now, we knew that the RTP801 protein, which is found in hippocampal neurons, was involved in the pathology of Alzheimer’s, as we published in a previous article (Cell Death and Disease, 2021). Back then, we discovered that levels of this protein were significantly elevated in both mouse models of Alzheimer’s and in post-mortem samples from patients, and these values correlated with disease progression”.
“On a mechanistic level, we observed that reducing RTP801 expression prevented cognitive deficits and inflammation, especially by mitigating the activation of the hippocampal inflammasome, i.e. the machinery that processes cytokines in inflammatory responses and drives gliosis (reactivation and proliferation of glial cells)”.
Why is this mechanism crucial to brain health?
According to the study, the RTP801 factor negatively regulates the activity of the tRNA ligase complex (tRNA-LC), which the study says is critical for processing RNA molecules. In terms of Alzheimer’s disease, higher levels of RTP801 can inhibit this complex and cause problems in RNA splicing and the production of important proteins, which makes cognitive problems worse in a mouse model of Alzheimer’s disease.
One of the study’s authors notes that “in this study, we have found that high levels of RTP801 interfere with the tRNA ligase complex, which is responsible for RNA processing, specifically in the process of ligation of its exons, once the introns have been cleaved. This process takes place both in the messenger RNA — which contains the information to build the protein — and in the transfer RNAs, which carry the amino acids to translate it”. The researcher stresses that “this process is vital for the correct synthesis of proteins at the ribosome, the cell organelles where the translation of RNA into proteins takes place”.
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Source:
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