4.7 Review

Defects of Nutrient Signaling and Autophagy in Neurodegeneration

期刊

出版社

FRONTIERS MEDIA SA
DOI: 10.3389/fcell.2022.836196

关键词

neurodegenerative diseases; autophagy; nutrient sensing pathways; mitochondrial metabolism; lipid metabolism; glucose metabolism; mTORC1 (mechanistic target of rapamycin complex 1); AMPK

资金

  1. Instituto de Salud Carlos III
  2. FEDER [PI19/01637]
  3. Basque Country Government
  4. Eusko Jaurlaritzako Osasun Saila [2018111042]
  5. Fundacio La Marato [fmarato20/001]
  6. Basque Country PhD fellowships [PRE_2018_1_0095, PRE_2020_1_0122, PRE_2020_1_0191]
  7. Margaretha af Ugglas (MAU) Foundation
  8. MAU foundation
  9. Swedish Alzheimer's Foundation (Alzheimerfonden)
  10. FG-B by Roche Stop Fuga de cerebros [BIO19/ROCHE/017/BD]
  11. Juan de la Cierva-Incorporacion (Agencia Estatal de Investigacion, Ministerio de Ciencia e innovacion, Gobierno de Espana) [IJC 2019-039965I]
  12. Biodonostia Health Research Institute, Donostia/San Sebastian, Spain

向作者/读者索取更多资源

Neurons rely on autophagy to maintain cellular energy balance and proper functioning during energy scarcity. Defects in autophagy can lead to neurodegenerative diseases such as Parkinson's disease, frontotemporal dementia, amyotrophic lateral sclerosis, or Alzheimer's disease.
Neurons are post-mitotic cells that allocate huge amounts of energy to the synthesis of new organelles and molecules, neurotransmission and to the maintenance of redox homeostasis. In neurons, autophagy is not only crucial to ensure organelle renewal but it is also essential to balance nutritional needs through the mobilization of internal energy stores. A delicate crosstalk between the pathways that sense nutritional status of the cell and the autophagic processes to recycle organelles and macronutrients is fundamental to guarantee the proper functioning of the neuron in times of energy scarcity. This review provides a detailed overview of the pathways and processes involved in the balance of cellular energy mediated by autophagy, which when defective, precipitate the neurodegenerative cascade of Parkinson's disease, frontotemporal dementia, amyotrophic lateral sclerosis or Alzheimer's disease.

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