Title

Chlamydia Pneumoniae as an Etiologic Agent for Late-Onset Alzheimer's Disease

Document Type

Chapter

Publication Date

2017

Abstract

Sporadic, late-onset Alzheimer's disease (LOAD) is a progressive neurodegenerative disease that is now the most common and severe form of dementia in the elderly. That dementia is thought to be a direct result of neuronal damage and loss associated with accumulations of abnormal protein deposits in the brain. Great strides have been made in the past 20 years with regard to understanding the pathological entities that arise in the AD brain, both for familial AD (~5% of all cases) and LOAD (~95% of all cases). The neuropathology observed includes: neuritic senile plaques (NSPs), neurofibrillary tangles (NFTs), neuropil threads (NPs), and often deposits of cerebrovascular amyloid. Genetic, biochemical, and immunological analyses have provided a relatively detailed knowledge of these entities, but our understanding of the 'trigger' events leading to the biological processes resulting in this pathology and neurodegeneration remains limited. For this reason, the etiology of AD, in particular LOAD, has remained elusive. However, a number of recent and ongoing studies have implicated infection in the etiology and pathogenesis of LOAD. This review focuses specifically on infection with Chlamydophila (Chlamydia) pneumoniae in LOAD and how this infection may function as a 'trigger or initiator' in the pathogenesis of this disease.

Publication Title

Advances in Alzheimer's Disease

Volume

5

First Page

41

Last Page

54

Comments

This article was published in Advances in Alzheimer's Disease, Volume 5, Pages 41-54.

The published version is available at http://dx.doi.org/10.3233/978-1-61499-706-1-41.

Copyright © 2017.

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