S-100β protein is upregulated in astrocytes and motor neurons in the spinal cord of patients with amyotrophic lateral sclerosis

Antonio Migheli, Susanna Cordera, Caterina Bendotti, Cristiana Atzori, Roberto Piva, Davide Schiffer

Research output: Contribution to journalArticle

Abstract

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by progressive motor neuron loss and astrogliosis. We studied the immunohistochemical expression of S-100β, a calcium-binding protein with both neurotrophic and neurotoxic activities, in the spinal cord of patients with ALS. Adjacent sections were processed with an in situ end-labeling technique for the demonstration of apoptosis-related DNA fragmentation. In controls, low expression of S-100β was found in astrocytes but not motor neurons. Compared to controls, S-100β was overexpressed in ALS. Most stained cells were reactive astrocytes, but a minority of motor neurons was also labeled. Neuronal labeling was unrelated to the presence of signs of atrophy/degeneration. S-100β expression was also unrelated to neuronal or glial apoptosis. S-100β upregulation in ALS spinal cord suggests that the protein might be involved in cellular defense mechanisms against oxidative stress.

Original languageEnglish
Pages (from-to)25-28
Number of pages4
JournalNeuroscience Letters
Volume261
Issue number1-2
DOIs
Publication statusPublished - Feb 12 1999

Keywords

  • Amyotrophic lateral sclerosis
  • Apoptosis
  • Glia
  • Immunohistochemistry
  • Oxidative stress
  • S-100β

ASJC Scopus subject areas

  • Neuroscience(all)

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