Type of contract CDD
Location Valbonne, France
Statut Available
Key Words Alzheimer's disease, mitochondria, neuroscience
Details of the offer
Place of work: CNRS / the Institute of Molecular and Cellular Pharmacology (IPMC)
Missions:
Alzheimer's disease (AD) is characterized by the spread of toxic proteins (Tau and Aβ) via exosomes, contributing to disease progression. Similarly, extracellular vesicles containing mitochondria (EVMs) may facilitate the transfer of dysfunctional mitochondria between brain cells, thereby accelerating neurodegeneration. However, the role of EVMs in AD remains poorly understood.
Our recent findings (manuscript under revision) have, for the first time, revealed that dysfunctional mitochondria in AD model cells, induced by the accumulation of C-terminal fragments of APP (APP-CTFs), trigger the secretion of EVMs carrying dysfunctional mitochondria. Moreover, AD-derived EVMs actively contribute to the transfer of mitochondrial pathology between cells in vitro.
Based on these observations, this project aims to explore how EVMs mediate the transfer of dysfunctional mitochondria from a neuronal perspective and how they influence neuronal function, plasticity, and cognition in AD.
The development of this project builds on our expertise in mitochondrial structure and function, as well as on validated protocols we have recently established protocols for the study of extracellular vesicles. Our team has long-standing experience in studying AD using both cellular and mouse models. This project will enhance our understanding of intercellular communication in AD by identifying EVMs as key mediators of mitochondrial dysfunction and synaptic alterations, potentially uncovering new therapeutic targets.
Type of job
Type of contract CDD
Application deadline
Employment start date 01/10/2025
Contact