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

Fingerprint

Neurodegenerative diseases
Cell death
Neurodegenerative Diseases
Cell Death
Autophagy
DNA Cleavage
Mitochondria
Oxidative stress
Microglia
Biomarkers
Protein Transport
Heat-Shock Proteins
Disease Progression
Oxidative Stress
Aging of materials
Chemical activation
Stroke
Cells
Apoptosis
Recovery

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

Cite this

Fan, J., Dawson, T. M., & Dawson, V. (2017). Cell death mechanisms of neurodegeneration. In Advances in Neurobiology (Vol. 15, pp. 403-425). (Advances in Neurobiology; Vol. 15). Springer New York LLC. https://doi.org/10.1007/978-3-319-57193-5_16

Cell death mechanisms of neurodegeneration. / Fan, Jing; Dawson, Ted M; Dawson, Valina.

Advances in Neurobiology. Vol. 15 Springer New York LLC, 2017. p. 403-425 (Advances in Neurobiology; Vol. 15).

Research output: Chapter in Book/Report/Conference proceedingChapter

Fan, J, Dawson, TM & Dawson, V 2017, Cell death mechanisms of neurodegeneration. in Advances in Neurobiology. vol. 15, Advances in Neurobiology, vol. 15, Springer New York LLC, pp. 403-425. https://doi.org/10.1007/978-3-319-57193-5_16
Fan J, Dawson TM, Dawson V. Cell death mechanisms of neurodegeneration. In Advances in Neurobiology. Vol. 15. Springer New York LLC. 2017. p. 403-425. (Advances in Neurobiology). https://doi.org/10.1007/978-3-319-57193-5_16
Fan, Jing ; Dawson, Ted M ; Dawson, Valina. / Cell death mechanisms of neurodegeneration. Advances in Neurobiology. Vol. 15 Springer New York LLC, 2017. pp. 403-425 (Advances in Neurobiology).
@inbook{f43675b2070345ddb146f69ed4dc0e5b,
title = "Cell death mechanisms of neurodegeneration",
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.",
keywords = "AIF, Cell death, Excitotoxicity, Mitochondria, Neurodegenerative diseases, Nitric oxide, Oxidative stress, Parthanatos",
author = "Jing Fan and Dawson, {Ted M} and Valina Dawson",
year = "2017",
doi = "10.1007/978-3-319-57193-5_16",
language = "English (US)",
volume = "15",
series = "Advances in Neurobiology",
publisher = "Springer New York LLC",
pages = "403--425",
booktitle = "Advances in Neurobiology",

}

TY - CHAP

T1 - Cell death mechanisms of neurodegeneration

AU - Fan, Jing

AU - Dawson, Ted M

AU - Dawson, Valina

PY - 2017

Y1 - 2017

N2 - 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.

AB - 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.

KW - AIF

KW - Cell death

KW - Excitotoxicity

KW - Mitochondria

KW - Neurodegenerative diseases

KW - Nitric oxide

KW - Oxidative stress

KW - Parthanatos

UR - http://www.scopus.com/inward/record.url?scp=85021999939&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85021999939&partnerID=8YFLogxK

U2 - 10.1007/978-3-319-57193-5_16

DO - 10.1007/978-3-319-57193-5_16

M3 - Chapter

C2 - 28674991

AN - SCOPUS:85021999939

VL - 15

T3 - Advances in Neurobiology

SP - 403

EP - 425

BT - Advances in Neurobiology

PB - Springer New York LLC

ER -