Impact Factor 3.582

The world's most-cited Neurosciences journals

Review ARTICLE Provisionally accepted The full-text will be published soon. Notify me

Front. Aging Neurosci. | doi: 10.3389/fnagi.2018.00302


 Alan P. Hudson1*, Judith W. Hudson1,  Brian J. Balin2, Christine J. Hammond2, Susan T. Hingley2, Christopher S. Little2, Zein Al-Atrache2 and Denah M. Appelt2
  • 1Biochemistry, Microbiology, and Immunology, Wayne State University School of Medicine, United States
  • 2Biomedical Sciences, Philadelphia College of Osteopathic Medicine, United States

Late-onset Alzheimer’s disease is a progressive neurodegenerative condition now recognized as the single most common, severe form of dementia in the elderly. The condition is sporadic and has been attributed to neuronal damage and loss, both of which have been linked to the accumulation of protein deposits in the brain. Significant progress has been made over the past two decades regarding our overall understanding of the apparently pathogenic entities that arise in the affected brain, both for early-onset disease, which constitutes approximately 5% of all cases, as well as late-onset disease, which constitutes the remainder of cases. Observable neuropathology includes: neurofibrillary tangles, neuropil threads, neuritic senile plaques, and often deposits of amyloid around the cerebrovasculature. Although many studies have provided a relatively detailed knowledge of these putatively pathogenic entities, understanding of the events that initiate and support the biological processes generating them and the subsequent observable neuropathology and neurodegeneration remain limited. This is especially true in the case of late-onset disease. Although early-onset Alzheimer’s disease has been shown conclusively to have genetic roots, the detailed etiologic initiation of late-onset disease without such genetic origins has remained elusive. Several studies over the last 15 years, including both current and ongoing work, have implicated infection in the etiology and pathogenesis of late-onset dementia. Infectious agents reported to be associated with disease initiation are various, including several viruses and pathogenic bacterial species. We have reported extensively regarding an association between late-onset disease and infection with the obligate intracellular bacterial pathogen Chlamydia pneumoniae. In this article, we review previously published data and recent results that support involvement of this unusual respiratory pathogen in disease induction and development. We further suggest several areas for future research that should elucidate details relating to those processes, and we argue for a change in the designation of the disease based on increased understanding of its clinical attributes.

Keywords: Late-onset dementia, Alzheimer’s disease, Amyloid, APOE, Chlamydia pneumoniae, etiology, Infection, Neuroinflammation

Received: 19 Mar 2018; Accepted: 13 Sep 2018.

Edited by:

Judith Miklossy, Prevention Alzheimer International Foundation, Switzerland

Reviewed by:

Michael Lardelli, University of Adelaide, Australia
Robert V. Schoborg, East Tennessee State University, United States  

Copyright: © 2018 Hudson, Hudson, Balin, Hammond, Hingley, Little, Al-Atrache and Appelt. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Dr. Alan P. Hudson, Wayne State University School of Medicine, Biochemistry, Microbiology, and Immunology, Detroit, 48201, MI, United States,