| Autor: |
C.S. Casley, J.M. Land, M.A. Sharpe, J.B. Clark, M.R. Duchen, L. Canevari |
| Jazyk: |
angličtina |
| Rok vydání: |
2002 |
| Předmět: |
|
| Zdroj: |
Neurobiology of Disease, Vol 10, Iss 3, Pp 258-267 (2002) |
| Druh dokumentu: |
article |
| ISSN: |
1095-953X |
| DOI: |
10.1006/nbdi.2002.0516 |
| Popis: |
β-Amyloid deposition and compromised energy metabolism both occur in vulnerable brain regions in Alzheimer's disease. It is not known whether β-amyloid is the cause of impairment of energy metabolism, nor whether impaired energy metabolism is specific to neurons. Our results, using primary neuronal cultures, show that 24-h incubation with Aβ25–35 caused a generalized decrease in the specific activity of mitochondrial enzymes per milligram of cellular protein, induced mitochondrial swelling, and decreased total mitochondrial number. Incubation with Aβ25–35 decreased ATP concentration to 58% of control in neurons and 71% of control in astrocytes. Levels of reduced glutathione were also lowered by Aβ25–35 in both neurons (from 5.1 to 2.9 nmol/mg protein) and astrocytes (from 25.2 to 14.9 nmol/mg protein). We conclude that 24-h treatment with extracellular Aβ25–35 causes mitochondrial dysfunction in both astrocytes and neurons, the latter being more seriously affected. In astrocytes mitochondrial impairment was confined to complex I inhibition, whereas in neurons a generalized loss of mitochondria was seen. |
| Databáze: |
Directory of Open Access Journals |
| Externí odkaz: |
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