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[Oxidative stress in the pathogenesis of Alzheimer's disease and antioxidant neuroprotection].
Fortschr Neurol Psychiatr. 1998 Mar; 66(3):113-21.FN

Abstract

Alzheimer's disease (AD) is one of the most frequent causes of dementia in the aged. The elucidation of the pathomechanisms of this neurodegenerative disease with age, as the only risk factor for the majority of cases, is in the centre of the efforts of molecular and cellular neurobiology in preclinical research. Various findings point to the involvement of the amyloid beta protein (A beta) in the pathogenesis and progression of AD. Precipitated A beta aggregates are found in the brain of AD patients post mortem in the so-called plaques, a major histopathological hallmark of this progressive destructive disease. A beta can be toxic to cultivated neuronal cells only in its aggregated fibril form. After interaction with the neuronal cell membrane, these aggregates can induce intracellular oxidative events and can lead to the release of so-called free radicals. This is just one important finding for the involvement of oxidative events in the nerve cell degeneration in AD supporting the oxidative stress hypothesis. Furthermore, different neurochemical methods revealed many additional traits and scars of oxidative reactions in the brain of AD patients. Inflammatory events also seem to take part in the generation of an oxidative environment and therefore in nerve cell death as well. In addition, various age-dependent pathophysiological changes can increase neuronal vulnerability. Different antioxidants can protect cultivated neurons against A beta toxicity, but also against other oxidative stressors relevant to the disease. Besides the classical lipophilic antioxidant vitamin E, the female sex hormone oestrogen could also play an important neuroprotective role as an antioxidant, as was shown recently. Oestrogen, oestrogen derivatives, but also other potential free radical scavengers could block the accumulation of oxidative events on the long run and could, therefore, possibly slow down or prevent progressive nerve cell death of AD, which occurs over decades. If future clinical trials using antioxidants as neuroprotectants in AD would also support the oxidative stress hypothesis of the aetiopathogenesis of AD, antioxidants identified in the laboratory could then find their way more and more into the clinical treatment of Alzheimer's dementia.

Authors+Show Affiliations

Max-Planck-Institut für Psychiatrie, Klinisches Institut, München. chris@mpipsykl.mpg.deNo affiliation info available

Pub Type(s)

English Abstract
Journal Article
Review

Language

ger

PubMed ID

9565761

Citation

Behl, C, and F Holsboer. "[Oxidative Stress in the Pathogenesis of Alzheimer's Disease and Antioxidant Neuroprotection]." Fortschritte Der Neurologie-Psychiatrie, vol. 66, no. 3, 1998, pp. 113-21.
Behl C, Holsboer F. [Oxidative stress in the pathogenesis of Alzheimer's disease and antioxidant neuroprotection]. Fortschr Neurol Psychiatr. 1998;66(3):113-21.
Behl, C., & Holsboer, F. (1998). [Oxidative stress in the pathogenesis of Alzheimer's disease and antioxidant neuroprotection]. Fortschritte Der Neurologie-Psychiatrie, 66(3), 113-21.
Behl C, Holsboer F. [Oxidative Stress in the Pathogenesis of Alzheimer's Disease and Antioxidant Neuroprotection]. Fortschr Neurol Psychiatr. 1998;66(3):113-21. PubMed PMID: 9565761.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Oxidative stress in the pathogenesis of Alzheimer's disease and antioxidant neuroprotection]. AU - Behl,C, AU - Holsboer,F, PY - 1998/5/5/pubmed PY - 1998/5/5/medline PY - 1998/5/5/entrez SP - 113 EP - 21 JF - Fortschritte der Neurologie-Psychiatrie JO - Fortschr Neurol Psychiatr VL - 66 IS - 3 N2 - Alzheimer's disease (AD) is one of the most frequent causes of dementia in the aged. The elucidation of the pathomechanisms of this neurodegenerative disease with age, as the only risk factor for the majority of cases, is in the centre of the efforts of molecular and cellular neurobiology in preclinical research. Various findings point to the involvement of the amyloid beta protein (A beta) in the pathogenesis and progression of AD. Precipitated A beta aggregates are found in the brain of AD patients post mortem in the so-called plaques, a major histopathological hallmark of this progressive destructive disease. A beta can be toxic to cultivated neuronal cells only in its aggregated fibril form. After interaction with the neuronal cell membrane, these aggregates can induce intracellular oxidative events and can lead to the release of so-called free radicals. This is just one important finding for the involvement of oxidative events in the nerve cell degeneration in AD supporting the oxidative stress hypothesis. Furthermore, different neurochemical methods revealed many additional traits and scars of oxidative reactions in the brain of AD patients. Inflammatory events also seem to take part in the generation of an oxidative environment and therefore in nerve cell death as well. In addition, various age-dependent pathophysiological changes can increase neuronal vulnerability. Different antioxidants can protect cultivated neurons against A beta toxicity, but also against other oxidative stressors relevant to the disease. Besides the classical lipophilic antioxidant vitamin E, the female sex hormone oestrogen could also play an important neuroprotective role as an antioxidant, as was shown recently. Oestrogen, oestrogen derivatives, but also other potential free radical scavengers could block the accumulation of oxidative events on the long run and could, therefore, possibly slow down or prevent progressive nerve cell death of AD, which occurs over decades. If future clinical trials using antioxidants as neuroprotectants in AD would also support the oxidative stress hypothesis of the aetiopathogenesis of AD, antioxidants identified in the laboratory could then find their way more and more into the clinical treatment of Alzheimer's dementia. SN - 0720-4299 UR - https://www.unboundmedicine.com/medline/citation/9565761/[Oxidative_stress_in_the_pathogenesis_of_Alzheimer's_disease_and_antioxidant_neuroprotection]_ L2 - http://www.thieme-connect.com/DOI/DOI?10.1055/s-2007-995246 DB - PRIME DP - Unbound Medicine ER -