T cell response to amyloid-beta and to mitochondrial antigens in Alzheimer's disease

Dement Geriatr Cogn Disord. 2003;16(1):35-8. doi: 10.1159/000069991.

Abstract

Despite the vast amount of literature on non-specific immune mechanisms in Alzheimer's disease (AD), little is known about the role of antigen-specific immune responses. We investigated T cell reactivity to fragment 1-42 of amyloid-beta (Abeta) and to N-terminal peptides of human mitochondrial and control microbial proteins. Thirty subjects with a diagnosis of probable AD according to NINCDS-ADRDA criteria and 30 sex- and age-matched healthy controls were enrolled. T cell responses to Abeta fragment showed no significant differences between AD patients and controls. By contrast, the mean number of positive T cell responses to both human mitochondrial and microbial peptides was significantly decreased in AD patients compared to control subjects. No significant correlation was found between T cell responses and both the severity of cognitive impairment and duration of the disease. Our results suggest that antigen-specific immune responses are impaired in AD. Protective immune responses to harmful amyloidogenic substances may also be impaired, thus favoring their accumulation in the brain.

MeSH terms

  • Aged
  • Aged, 80 and over
  • Alzheimer Disease / immunology*
  • Amyloid beta-Peptides / immunology*
  • Amyloidosis / immunology
  • Autoantigens / immunology
  • Brain / immunology
  • Female
  • Humans
  • Male
  • Middle Aged
  • Mitochondria / immunology*
  • Peptide Fragments / immunology*
  • T-Lymphocytes / immunology*

Substances

  • Amyloid beta-Peptides
  • Autoantigens
  • Peptide Fragments
  • amyloid beta-protein (1-42)