Issue title: Chronic Inflammation and Amyloidogenesis in Alzheimer's Disease: The Emerging Role of Infection
Guest editors: Judith Miklossyx and Ralph N. Martinsy
Article type: Research Article
Authors: Balin, Brian J.a; b; * | Little, C. Scotta; b | Hammond, Christine J.a; b | Appelt, Denah M.b; c | Whittum-Hudson, Judith A.d | Gérard, Hervé C.d | Hudson, Alan P.d
Affiliations: [a] Department of Pathology, Microbiology, Immunology and Forensic Medicine, Philadelphia PA, USA | [b] Center for Chronic Disorders of Aging, Philadelphia College of Osteopathic Medicine, Philadelphia PA, USA | [c] Department of Neuroscience, Pharmacology, and Physiology, Philadelphia PA, USA | [d] Department of Immunology and Microbiology, Wayne State University School of Medicine, Detroit MI, USA | [x] The University of British Columbia, Kinsmen Laboratory of Neurological Research, Vancouver, BC, Canada | [y] Sir James McCusker Alzheimer's Disease Research Unit, University of Western Australia, Hollywood Private Hospital, 115 Monash Avenue, Nedlands, Perth, WA 6009, Australia
Correspondence:
[*]
Corresponding author: Dr. Brian J. Balin, Department of Pathology, Microbiology, Immunology and Forensic Medicine, and the Center for Chronic Disorders of Aging, Philadelphia College of Osteopathic Medicine, 4170 City Avenue, Philadelphia, PA 19131, USA. Tel.: +1 215 871 6862; Fax: +1 215 871 6869; E-mail: Brianba@pcom.edu.
Abstract: Sporadic, late-onset Alzheimer's disease (LOAD) is a non-familial, progressive neurodegenerative disease that is now the most common and severe form of dementia in the elderly. That dementia is 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 many cascades resulting in this pathology and neurodegeneration is still quite 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.
Keywords: Alzheimer's disease, amyloid, animal models antibiotic, APOE, Chlamydia pneumoniae, etiology, infection, LOAD, neuroinflammation
DOI: 10.3233/JAD-2008-13403
Journal: Journal of Alzheimer's Disease, vol. 13, no. 4, pp. 371-380, 2008
