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Neurovascular MedicinePursuing Cellular Longevity for Healthy Aging$
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Kenneth Maiese

Print publication date: 2009

Print ISBN-13: 9780195326697

Published to Oxford Scholarship Online: January 2010

DOI: 10.1093/acprof:oso/9780195326697.001.0001

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Protein Misfolding, Mitochondrial Disturbances, And Kynurenines In The Pathogenesis Of Neurodegenerative Disorders

Protein Misfolding, Mitochondrial Disturbances, And Kynurenines In The Pathogenesis Of Neurodegenerative Disorders

Chapter:
(p.452) Chapter 18 Protein Misfolding, Mitochondrial Disturbances, And Kynurenines In The Pathogenesis Of Neurodegenerative Disorders
Source:
Neurovascular Medicine
Author(s):

Gabriella Gárdián

Katalin Sas

József Toldi

László Vécsei

Publisher:
Oxford University Press
DOI:10.1093/acprof:oso/9780195326697.003.0018

As a population ages, neurodegenerative diseases become increasingly prevalent. These are different clinical entities, though they display many common features in their clinical, biochemical, and morphological appearance. The majority of them have both genetic and environmental components in their pathomechanism. The genetic background involves a single gene mutation (for example, spinocerebellar ataxias 1, 2, and 3 and Huntington's disease [PD]), heterozygote gene modifications following the patterns of the Mendelian laws (familial Parkinson's disease [PD] and familial Alzheimer's disease [AD]), multiple predisposing genes (sporadic PD and sporadic AD), or mitochondrial DNA defects. Protein misfolding, mitochondrial impairment, oxidative stress, endoplasmic reticulum stress, excitotoxicity, caspase cascade activation, and apoptosis are common mechanisms acknowledged to lead to cell death in the different neurodegenerative disorders.

Keywords:   protein misfolding, endoplasmic reticulum stress, apoptosis, neurodegenerative disorders, oxidative stress, excitotoxicity

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