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von Lewinski, F; Keller, BU.
Ca2+, mitochondria and selective motoneuron vulnerability: implications for ALS.
Trends Neurosci. 2005; 28(9):494-500
Doi: 10.1016/j.tins.2005.07.001
Web of Science
PubMed
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- Führende Autor*innen der Med Uni Graz
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von Lewinski Friederike
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- Abstract:
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Motoneurons are selectively damaged in amyotrophic lateral sclerosis (ALS), a fatal neurodegenerative disorder. Although the underlying mechanisms are not completely understood, increasing evidence indicates that motoneurons are particularly sensitive to disruption of mitochondria and Ca(2+)-dependent signalling cascades. Comparison of ALS-vulnerable and ALS-resistant neurons identified low Ca(2+)-buffering capacity and a strong impact of mitochondrial signal cascades as important risk factors. Under physiological conditions, weak Ca(2+) buffers are valuable because they facilitate rapid relaxation times of Ca(2+) transients in motoneurons during high-frequency rhythmic activity. However, under pathological conditions, weak Ca(2+) buffers are potentially dangerous because they accelerate a vicious circle of mitochondrial disruption, Ca(2+) disregulation and excitotoxic cell damage.
- Find related publications in this database (using NLM MeSH Indexing)
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Amyotrophic Lateral Sclerosis - metabolism
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Amyotrophic Lateral Sclerosis - pathology
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Animals -
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Brain - metabolism
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Brain - pathology
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Calcium - metabolism
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Humans -
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Mitochondria - metabolism
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Mitochondria - pathology
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Models, Neurological -
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Motor Neurons - metabolism
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Motor Neurons - pathology
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Reactive Oxygen Species -
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Spinal Cord - metabolism
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Spinal Cord - pathology