Cited by 77Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

Chlamydia pneumoniae: An Etiologic Agent for Late-Onset Dementia

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Balin, Brian J., Hammond, Christine J., Little, Christopher Scott, Hingley, Susan T., Al-Atrache, Zein, Appelt, Denah M., Whittum-Hudson, Judith A., Hudson, Alan P.·2018·Frontiers in Aging Neuroscience

Abstract

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.

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Cited by

Sorted by citations

Authors
Balin, B. J., Hammond, C. J., Little, C. S., Hingley, S. T., Al-Atrache, Z., Appelt, D. M., Whittum-Hudson, J. A., & Hudson, A. P.
Affiliations
  • Philadelphia College of Osteopathic Medicine (US)
  • Wayne State University (US)
Corresponding author
Hudson, Alan P.
Venue
Frontiers in Aging Neuroscience
Published
2018-10-09
Volume
10
Pages
302-302
ISSN
1663-4365 (ISSN-L)
OpenAlex
W2898002943
Cited by
77
References
9
Citations by year
2026: 6 · 2025: 6 · 2024: 7 · 2023: 9 · 2022: 15 · 2021: 17 · 2020: 13 · 2019: 4
FWCI
1.12
Type
journal article
Language
en
Open access
Locations
  • Frontiers in Aging Neuroscience (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Digital Commons - PCOM (Philadelphia College of Osteopathic Medicine) (submittedVersion, cc-by)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
Funders
National Institutes of Health (44055)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
Chlamydia pneumoniae, late-onset Alzheimer's disease, dementia etiology, neurofibrillary tangles, neuritic plaques, amyloid deposition, bacterial infection, disease nomenclature

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