Calcium: The Darth Vader of ALS Review uri icon

Overview

MeSH Major

  • Amyotrophic Lateral Sclerosis
  • Calcium

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.

publication date

  • March 2001

Research

keywords

  • Review

Identity

Language

  • eng

PubMed ID

  • 11465925

Additional Document Info

start page

  • S47

end page

  • 54

volume

  • 2

number

  • SUPPL. 1