bcl-2 protein expression in aged brain and neurodegenerative diseases

Neuroreport. 1994 Oct 3;5(15):1906-8. doi: 10.1097/00001756-199410000-00016.


The proto-oncogene bcl-2 is involved in the regulation of cell death and is able to block apoptosis in neurones through reduced generation of reactive oxygen species (ROS). We have studied the immunohistochemical expression of bcl-2 protein in the aged brain and in various human neurodegenerative diseases. In all cases, bcl-2 was strongly enriched within lipofuscin and autophagic vacuoles of neurones, glial and vascular cells. Our data show that accumulation of bcl-2 is not disease-specific and represents a general cellular response which accompanies the increased formation of lipofuscin. Since oxidative stress is directly involved in lipofuscinogenesis, accumulation of bcl-2 may reflect a mechanism for counterbalancing ROS-mediated damage, or it might represent the impairment of bcl-2-dependent protection from ROS.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aging / metabolism*
  • Alzheimer Disease / metabolism
  • Alzheimer Disease / pathology
  • Amyotrophic Lateral Sclerosis / metabolism
  • Amyotrophic Lateral Sclerosis / pathology
  • Brain / pathology
  • Brain Chemistry / physiology*
  • GTP-Binding Proteins / biosynthesis*
  • Gerstmann-Straussler-Scheinker Disease / metabolism
  • Gerstmann-Straussler-Scheinker Disease / pathology
  • Humans
  • Immunohistochemistry
  • Lipofuscin
  • Nervous System Diseases / metabolism*
  • Proto-Oncogene Mas
  • Proto-Oncogene Proteins / biosynthesis*
  • Proto-Oncogene Proteins c-bcl-2
  • Spinal Cord / metabolism
  • Spinal Cord / pathology


  • Lipofuscin
  • MAS1 protein, human
  • Proto-Oncogene Mas
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • GTP-Binding Proteins

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