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bcl-2 protein expression in aged brain and neurodegenerative diseases.

Authors
  • Migheli, A
  • Cavalla, P
  • Piva, R
  • Giordana, M T
  • Schiffer, D
Type
Published Article
Journal
Neuroreport
Publisher
Ovid Technologies (Wolters Kluwer) - Lippincott Williams & Wilkins
Publication Date
Oct 03, 1994
Volume
5
Issue
15
Pages
1906–1908
Identifiers
PMID: 7841373
Source
Medline
License
Unknown

Abstract

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.

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