Potential Involvement of Retroviral Elements in Human Dementias

  1. Greg Bock Organizer and
  2. Joan Marsh
  1. Laura Manuelidis,
  2. Geoffrey Murdoch and
  3. Elias E. Manuelidis

Published Online: 28 SEP 2007

DOI: 10.1002/9780470513613.ch8

Ciba Foundation Symposium 135 - Novel Infectious Agents and the Central Nervous System

Ciba Foundation Symposium 135 - Novel Infectious Agents and the Central Nervous System

How to Cite

Manuelidis, L., Murdoch, G. and Manuelidis, E. E. (2007) Potential Involvement of Retroviral Elements in Human Dementias, in Ciba Foundation Symposium 135 - Novel Infectious Agents and the Central Nervous System (eds G. Bock and J. Marsh), John Wiley & Sons, Ltd., Chichester, UK. doi: 10.1002/9780470513613.ch8

Author Information

  1. Neuropathology Section, Yale University, School of Medicine, PO Box 3333, 333 Cedar Street, New Haven, Connecticut 06510, USA

Publication History

  1. Published Online: 28 SEP 2007

ISBN Information

Print ISBN: 9780471915126

Online ISBN: 9780470513613

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Keywords:

  • potential involvement;
  • retroviral elements;
  • human dementias;
  • alzheimer's disease;
  • oncogenic retroviruses

Summary

Creutzfeldt-Jakob disease (CJD) is a dementia of humans caused by a class of infectious agents with several biological properties similar to those of conventional viruses. The molecular nature of this group of agents is enigmatic, for neither an agent-specific nucleic acid nor a non-host protein has yet been identified. Recent transmissions of familial CJD dementias to rodents suggest that this class of agent can be integrated into the germline. Furthermore, tissue culture studies indicate that CJD causes transformation of cells in a manner reminiscent of slowly oncogenic retroviruses. Currently characterized retroviral-like elements include many forms that do not have ‘typical’ retroviral ultra-structural morphology; several forms are also known to be resistant to various types of standard physicochemical inactivation. We suggest that CJD agents are either constituted by retroviral-like nucleic acids or interact with endogenous retroviral sequences to elicit a slowly progressive disease of the central nervous system. Several overlapping properties between infectious CJD and ‘non-infectious’ dementias, such as Alzheimer's disease, implicate potential common pathogenic mechanisms.