Abstract
Recent studies have shown that amyloid β-peptide (Aβ) can be directly neurotoxic by a mechanism related to secondary structure of the peptide, and mediated by free radical production and an increase in the concentration of intracellular free calcium ([Ca2+]i). We now report that staurosporine and K-252 compounds, low molecular weight alkaloids of bacterial origin, can protect cultured rat hippocampal neurons against the toxicity of Aβ in a concentration-dependent manner. The alkaloids also protected neurons against iron-induced (free radical-mediated) injury. Measurements of [Ca2+]i using fura-2 imaging revealed that the elevation of [Ca2+]i that occurred in response to long-term exposure to Aβ was attenuated in neurons treated with staurosporine and K-252 compounds. These findings indicate that staurosporine and K-252 compounds can interupt a neurodegenerative pathway relevant to the pathophysiology of Alzheimer's disease.
Original language | English (US) |
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Pages (from-to) | 170-174 |
Number of pages | 5 |
Journal | Brain Research |
Volume | 650 |
Issue number | 1 |
DOIs | |
State | Published - Jul 4 1994 |
Externally published | Yes |
Keywords
- Alkaloid
- Alzheimer's disease
- Calcium
- Free radical
- Fura-2
- Neurodegeneration
- Neurotrophic factor
- Phosphorylation
ASJC Scopus subject areas
- Developmental Biology
- Molecular Biology
- Clinical Neurology
- General Neuroscience