The senescence accelerated mouse (SAMP8) as a model for oxidative stress and Alzheimer's disease
| Autor: | H. J. Armbrecht, Vijaya B. Kumar, Susan A. Farr, John E. Morley |
|---|---|
| Rok vydání: | 2012 |
| Předmět: |
Senescence
Aging Antioxidant Amyloid beta medicine.medical_treatment Mitochondrion Blood–brain barrier medicine.disease_cause Amyloid beta-Protein Precursor Mice Senescence accelerated mouse (SAMP8) Hormesis Alzheimer Disease mental disorders Oxidative damage medicine Amyloid precursor protein Animals Molecular Biology Melatonin biology Brain Alzheimer's disease Mitochondria Cell biology Disease Models Animal Oxidative Stress medicine.anatomical_structure Biochemistry biology.protein Molecular Medicine Amyloid-beta Oxidative stress |
| Zdroj: | Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease. 1822(5):650-656 |
| ISSN: | 0925-4439 |
| DOI: | 10.1016/j.bbadis.2011.11.015 |
| Popis: | The senescence accelerated mouse (SAMP8) is a spontaneous animal model of overproduction of amyloid precursor protein (APP) and oxidative damage. It develops early memory disturbances and changes in the blood–brain barrier resulting in decreased efflux of amyloid-β protein from the brain. It has a marked increase in oxidative stress in the brain. Pharmacological treatments that reduce oxidative stress improve memory. Treatments that reduce amyloid-β (antisense to APP and antibodies to amyloid-β) not only improve memory but reduce oxidative stress. Early changes in lipid peroxidative damage favor mitochondrial dysfunction as being a trigger for amyloid-β overproduction in this genetically susceptible mouse strain. This sets in motion a cycle where the increased amyloid-beta further damages mitochondria. We suggest that this should be termed the Inflammatory-Amyloid Cycle and may well be similar to the mechanisms responsible for the pathophysiology of Alzheimer's disease. This article is part of a Special Issue entitled: Antioxidants and Antioxidant Treatment in Disease. |
| Databáze: | OpenAIRE |
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