AMPK in Neurodegenerative Diseases.

Exp Suppl

Univ. Lille, Inserm, CHU Lille, UMR-S 1172 - JPArc - Centre de Recherche Jean-Pierre AUBERT, F-59000, Lille, France.

Published: June 2017

AI Article Synopsis

  • Alzheimer's, Parkinson's, Huntington's, and ALS are neurodegenerative diseases that progressively damage nerve cells, leading to dementia, but they affect different parts of the nervous system and exhibit unique symptoms.
  • Despite their differences, these diseases share common features like problems with energy metabolism, oxidative stress, and excitotoxicity, which may be linked to the malfunctioning of a key protein called AMPK.
  • AMPK, which helps regulate energy in the brain, has shown overactivation in people with these disorders, and while its exact role is still being studied, it is believed to play a significant part in the pathways contributing to disease progression.

Article Abstract

Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis are neurodegenerative disorders that are characterized by a progressive degeneration of nerve cells eventually leading to dementia. While these diseases affect different neuronal populations and present distinct clinical features, they share in common several features and signaling pathways. In particular, energy metabolism defects, oxidative stress, and excitotoxicity are commonly described and might be correlated with AMP-activated protein kinase (AMPK) deregulation. AMPK is a master energy sensor which was reported to be overactivated in the brain of patients affected by these neurodegenerative disorders. While the exact role played by AMPK in these diseases remains to be clearly established, several studies reported the implication of AMPK in various signaling pathways that are involved in these diseases' progression. In this chapter, we review the current literature regarding the involvement of AMPK in the development of these diseases and discuss the common pathways involved.

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Source
http://dx.doi.org/10.1007/978-3-319-43589-3_7DOI Listing

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