Neurodegeneráció: öregedés és demencia. Elektrontranszport-zavar, mint etiopatogenetikai tényezó. Terápiás lehetóségek.

Translated title of the contribution: Neurodegeneration: aging and dementia. Etiopathogenic role of electron transport disorders. Therapeutic possibilities

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

The neurodegenerative disorders (Parkinson's disease, Alzheimer's dementia, Huntington's disease, cerebellar degeneration) are common medical and social problems. The late onset diseases and slow neurodegeneration is connected with excitotoxins and alteration of mitochondrial electron transport chain. In elderly, congenital and acquired defects of mitochondrial complexes cause formation of free radicals. The overstimulation of excitatory amino acid receptors interfere with the cellular energy metabolism and also forming reactive oxygen species. The impaired energy metabolism make neuronal cells vulnerable to the excitotoxic damage. In these ways, excitotoxicity may be the final common pathway of neuronal death in a variety of neurodegenerative diseases. Potential therapeutic strategies would be use receptor antagonist or drugs to bypass energetic defects.

Original languageHungarian
Pages (from-to)331-335
Number of pages5
JournalOrvosi Hetilap
Volume138
Issue number6
Publication statusPublished - Feb 9 1997

Fingerprint

Electron Transport
Neurodegenerative Diseases
Energy Metabolism
Dementia
Huntington Disease
Social Problems
Neurotoxins
Glutamate Receptors
Free Radicals
Parkinson Disease
Reactive Oxygen Species
Alzheimer Disease
Therapeutics
Pharmaceutical Preparations
Late Onset Disorders

ASJC Scopus subject areas

  • Medicine(all)

Cite this

@article{852925588e224f4c83c0d4ff55c3d60d,
title = "Neurodegener{\'a}ci{\'o}: {\"o}reged{\'e}s {\'e}s demencia. Elektrontranszport-zavar, mint etiopatogenetikai t{\'e}nyez{\'o}. Ter{\'a}pi{\'a}s lehet{\'o}s{\'e}gek.",
abstract = "The neurodegenerative disorders (Parkinson's disease, Alzheimer's dementia, Huntington's disease, cerebellar degeneration) are common medical and social problems. The late onset diseases and slow neurodegeneration is connected with excitotoxins and alteration of mitochondrial electron transport chain. In elderly, congenital and acquired defects of mitochondrial complexes cause formation of free radicals. The overstimulation of excitatory amino acid receptors interfere with the cellular energy metabolism and also forming reactive oxygen species. The impaired energy metabolism make neuronal cells vulnerable to the excitotoxic damage. In these ways, excitotoxicity may be the final common pathway of neuronal death in a variety of neurodegenerative diseases. Potential therapeutic strategies would be use receptor antagonist or drugs to bypass energetic defects.",
author = "P. Kliv{\'e}nyi and L. V{\'e}csei",
year = "1997",
month = "2",
day = "9",
language = "Hungarian",
volume = "138",
pages = "331--335",
journal = "Orvosi Hetilap",
issn = "0030-6002",
publisher = "Akademiai Kiado",
number = "6",

}

TY - JOUR

T1 - Neurodegeneráció

T2 - öregedés és demencia. Elektrontranszport-zavar, mint etiopatogenetikai tényezó. Terápiás lehetóségek.

AU - Klivényi, P.

AU - Vécsei, L.

PY - 1997/2/9

Y1 - 1997/2/9

N2 - The neurodegenerative disorders (Parkinson's disease, Alzheimer's dementia, Huntington's disease, cerebellar degeneration) are common medical and social problems. The late onset diseases and slow neurodegeneration is connected with excitotoxins and alteration of mitochondrial electron transport chain. In elderly, congenital and acquired defects of mitochondrial complexes cause formation of free radicals. The overstimulation of excitatory amino acid receptors interfere with the cellular energy metabolism and also forming reactive oxygen species. The impaired energy metabolism make neuronal cells vulnerable to the excitotoxic damage. In these ways, excitotoxicity may be the final common pathway of neuronal death in a variety of neurodegenerative diseases. Potential therapeutic strategies would be use receptor antagonist or drugs to bypass energetic defects.

AB - The neurodegenerative disorders (Parkinson's disease, Alzheimer's dementia, Huntington's disease, cerebellar degeneration) are common medical and social problems. The late onset diseases and slow neurodegeneration is connected with excitotoxins and alteration of mitochondrial electron transport chain. In elderly, congenital and acquired defects of mitochondrial complexes cause formation of free radicals. The overstimulation of excitatory amino acid receptors interfere with the cellular energy metabolism and also forming reactive oxygen species. The impaired energy metabolism make neuronal cells vulnerable to the excitotoxic damage. In these ways, excitotoxicity may be the final common pathway of neuronal death in a variety of neurodegenerative diseases. Potential therapeutic strategies would be use receptor antagonist or drugs to bypass energetic defects.

UR - http://www.scopus.com/inward/record.url?scp=17344378886&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=17344378886&partnerID=8YFLogxK

M3 - Article

C2 - 9082290

AN - SCOPUS:17344378886

VL - 138

SP - 331

EP - 335

JO - Orvosi Hetilap

JF - Orvosi Hetilap

SN - 0030-6002

IS - 6

ER -