Calcium: The Darth Vader of ALS

Stanley H. Appel, David Beers, Laszlo Siklos, Joseph I. Engelhardt, Dennis R. Mosier

Research output: Contribution to journalArticle

50 Citations (Scopus)

Abstract

Motor neuron dysfunction and loss in amyotrophic lateral sclerosis (ALS) have been attributed to several different mechanisms, including increased intracellular calcium, glutamate excitotoxicity, oxidative stress and free radical damage, mitochondrial dysfunction, and neurofilament aggregation and dysfunction of transport mechanisms. These alterations are not mutually exclusive, and increased calcium could be a common denominator. Furthermore, the selective vulnerability of spinal motor neurons and the relative sparing of eye motor neurons represent striking features of both sporadic and familial ALS. Here we review the evidence that calcium homeostasis is altered in ALS, and that low levels of the calcium binding proteins parvalbumin and calbindin-D28K contribute to selective vulnerability by decreasing the ability of motor neurons to handle an increased calcium load, with cell injury and death as the consequence.

Original languageEnglish
Pages (from-to)47-54
Number of pages8
JournalAmyotrophic Lateral Sclerosis and Other Motor Neuron Disorders
Volume2
Issue numberSUPPL. 1
DOIs
Publication statusPublished - Mar 2001

Keywords

  • ALS
  • Calcium
  • Calcium binding
  • Motor neurons
  • Parvalbumin
  • Proteins
  • Selective vulnerability

ASJC Scopus subject areas

  • Clinical Neurology

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