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SHR Neuro Krebs Kardio Lipid Stoffw Microb

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
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Führende Autor*innen der Med Uni Graz
von Lewinski Friederike
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Abstract:
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)
Amyotrophic Lateral Sclerosis - metabolism
Amyotrophic Lateral Sclerosis - pathology
Animals -
Brain - metabolism
Brain - pathology
Calcium - metabolism
Humans -
Mitochondria - metabolism
Mitochondria - pathology
Models, Neurological -
Motor Neurons - metabolism
Motor Neurons - pathology
Reactive Oxygen Species -
Spinal Cord - metabolism
Spinal Cord - pathology

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