Cell death mechanisms of neurodegeneration

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

There are common mechanisms shared by genetically or pathologically distinct neurodegenerative diseases, such as excitotoxicity, mitochondrial deficits and oxidative stress, protein misfolding and translational dysfunction, autophagy and microglia activation. This indicates that although the original cause may differ in individual diseases or even subtypes of certain disorders, these disrupted common cell functions and signaling, together with aging, may lead to final execution of cell death through similar pathways. The variable neurodegenerative disease symptoms are probably caused by the type, location, and connection of the cell populations that suffer from dysfunction and loss. Besides apoptosis, necroptosis, and autophagy, an important form of death termed parthanatos plays a prominent role in stroke and several neurodegenerative diseases, which is due to PARP-1 overactivation, PAR accumulation, nuclear translocation of the mitochondria protein AIF, and large-scale DNA cleavage. Understanding the mechanisms and interactions of cell death signaling will not only help to develop neuroprotective strategies to halt neurodegeneration, but also provide biomarkers for monitoring disease progression and recovery.

Original languageEnglish (US)
Title of host publicationAdvances in Neurobiology
PublisherSpringer New York LLC
Pages403-425
Number of pages23
Volume15
DOIs
StatePublished - 2017

Publication series

NameAdvances in Neurobiology
Volume15
ISSN (Print)2190-5215

Keywords

  • AIF
  • Cell death
  • Excitotoxicity
  • Mitochondria
  • Neurodegenerative diseases
  • Nitric oxide
  • Oxidative stress
  • Parthanatos

ASJC Scopus subject areas

  • Biochemistry
  • Neurology
  • Developmental Neuroscience
  • Cellular and Molecular Neuroscience

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