Abstract

This study aims to quantitate Chlamydia pneumoniae (Cpn) and Aβ amyloid plaques throughout the limbic system in brains from individuals diagnosed with late-onset dementia/Alzheimer's disease (AD) and non-demented conditions. The amount of deposition of amyloid relative to Cpn may further implicate Chlamydia's role as a trigger for neuroinflammation leading to the pathology observed in late-onset disease. Sporadic late-onset Alzheimer's disease (LOAD) is the most common form of dementia, affecting ~55 million individuals worldwide. Despite the prevalence of the disease the etiology of LOAD remains unknown. In recent years, significant attention has been given to the role of infection in the onset and pathogenesis of late-onset dementia/AD. The Cpn pathogen has been an organism of particular focus since the seminal study by Balin et. al 1998 which found that Cpn DNA was present in 90% of brain samples taken from patients diagnosed with LOAD.

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