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正文
The metabolic decline is one of the most common features of aging, and it is closely involved in developing multiple neurodegenerative diseases (NDDs), including ALS and FTD. Genetic mutation-associated or aging-associated metabolic decline can be a powerful mechanism to trigger defective signal transductions, intracellular stress build-up, and protein homeostasis collapse, ultimately leading to neuronal cell death in ALS/FTD. We will leverage multiple model systems to identify how the metabolic decline is induced in the process of ALS/FTD and through which pathways the metabolic decline triggers the molecular cascades of neuronal death.
Our recent research interests include:
1. Uncovering the underlying mechanisms and critical regulators for mitochondrial dysregulation and metabolic disturbance in ALS/FTD.
2. Elucidating the interplay between metabolic disturbance and pathological alternations during the development of NDDs.

Email:15659706031@163.com
Research Direction:Cellular stress response and neurodegenerative diseases

Email:ntguling@163.com
Research Direction:Metabolic regulation in mitochondria

Email:22111520040@m.fudan.edu.cn
Research Direction:Cellular stress response and neurodegenerative diseases

Email:22211520009@m.fudan.edu.cn
Research Direction:The dynamic regulatory mechanism of protein homeostasis

Email:23111530005@m.fudan.edu.cn
Research Direction:Regulation and homeostasis of protein synthesis

Email:wuyou_9602@163.com
Research Direction:Regulation and homeostasis of protein synthesis

Email:24111530020@fudan.edu.cn
Research Direction:Regulation of neuronal metabolism in neurodegeneration
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