RNA interference is the process by which RNA molecules regulate gene expression. In general, interfering RNA (RNAi) binds specific mRNA, inducing either translation inhibition or mRNA cleavage. This thesis investigates a specific type of RNAi: miRNAs, which are involved in the regulation of several biological processes, including inflammatory response. In particular, this work focuses on miRNA-146a and its involvement in the regulation of inflammatory pathway, with evidences on Alzheimer’s Disease (AD) and Multiple Sclerosis (MS). MiRNA-146a is well-established to be implicated in autoimmunity and inflammation, acting as a negative feedback regulator in MyD88 inflammatory pathway, targeting adapter proteins in this signalling cascade. Dysregulation of miRNA-146a expression may contribute to the onset and progression of inflammatory disease, such as AD and MS, due to the uncontrolled production of pro-inflammatory molecules.

RNA interference is the process by which RNA molecules regulate gene expression. In general, interfering RNA (RNAi) binds specific mRNA, inducing either translation inhibition or mRNA cleavage. This thesis investigates a specific type of RNAi: miRNAs, which are involved in the regulation of several biological processes, including inflammatory response. In particular, this work focuses on miRNA-146a and its involvement in the regulation of inflammatory pathway, with evidences on Alzheimer’s Disease (AD) and Multiple Sclerosis (MS). MiRNA-146a is well-established to be implicated in autoimmunity and inflammation, acting as a negative feedback regulator in MyD88 inflammatory pathway, targeting adapter proteins in this signalling cascade. Dysregulation of miRNA-146a expression may contribute to the onset and progression of inflammatory disease, such as AD and MS, due to the uncontrolled production of pro-inflammatory molecules.

Role of miRNA-146a in inflammatory pathway: evidences in Alzheimer's Disease and Multiple Sclerosis

VACCARO, ALESSIA
2023/2024

Abstract

RNA interference is the process by which RNA molecules regulate gene expression. In general, interfering RNA (RNAi) binds specific mRNA, inducing either translation inhibition or mRNA cleavage. This thesis investigates a specific type of RNAi: miRNAs, which are involved in the regulation of several biological processes, including inflammatory response. In particular, this work focuses on miRNA-146a and its involvement in the regulation of inflammatory pathway, with evidences on Alzheimer’s Disease (AD) and Multiple Sclerosis (MS). MiRNA-146a is well-established to be implicated in autoimmunity and inflammation, acting as a negative feedback regulator in MyD88 inflammatory pathway, targeting adapter proteins in this signalling cascade. Dysregulation of miRNA-146a expression may contribute to the onset and progression of inflammatory disease, such as AD and MS, due to the uncontrolled production of pro-inflammatory molecules.
Role of miRNA-146a in inflammatory pathway: evidences in Alzheimer's Disease and Multiple Sclerosis
RNA interference is the process by which RNA molecules regulate gene expression. In general, interfering RNA (RNAi) binds specific mRNA, inducing either translation inhibition or mRNA cleavage. This thesis investigates a specific type of RNAi: miRNAs, which are involved in the regulation of several biological processes, including inflammatory response. In particular, this work focuses on miRNA-146a and its involvement in the regulation of inflammatory pathway, with evidences on Alzheimer’s Disease (AD) and Multiple Sclerosis (MS). MiRNA-146a is well-established to be implicated in autoimmunity and inflammation, acting as a negative feedback regulator in MyD88 inflammatory pathway, targeting adapter proteins in this signalling cascade. Dysregulation of miRNA-146a expression may contribute to the onset and progression of inflammatory disease, such as AD and MS, due to the uncontrolled production of pro-inflammatory molecules.
GIUSTETTO, MAURIZIO
Autorizzo consultazione esterna dell'elaborato
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.14240/8281