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Amyotrophic lateral sclerosis: the involvement of intracellular Ca2+and protein kinase C

Authors
Journal
Trends in Pharmacological Sciences
0165-6147
Publisher
Elsevier
Publication Date
Volume
17
Issue
3
Identifiers
DOI: 10.1016/0165-6147(96)10004-3
Disciplines
  • Biology
  • Medicine

Abstract

Abstract The neurodegenerative disease, amyotrophic lateral sclerosis (ALS), is characterized by the selective death of motoneurones and corticospinal tract neurones. Abnormalities in excitatory amino acids and their receptors, as well as disordered function of voltage-dependent Ca 2+ channels and superoxide dismutase have been reported in ALS patients. Furthermore, the activity of protein kinase C (PKC), a Ca 2+, phospholipid-dependent enzyme, is also substantially increased in tissue from ALS patients, suggesting that alterations in intracellular free Ca 2+ may be central to many of the diverse pathogenic mechanisms potentially responsible for ALS as discussed here by Charles Krieger and colleagues. Increased PKC activity, in turn, may have direct or indirect effects on neuronal viability and influence the pathogenic process in ALS by modifying the phosphorylation of voltage-dependent Ca 2+ channels, neurotransmitter receptors and structural proteins.

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