Chlamydia pneumoniae induces Alzheimer-like amyloid plaques in brains of BALB/c mice

Abstract

Amyloid deposits resembling plaques found in Alzheimer's disease (AD) brains were formed in the brains of non-transgenic BALB/c mice following intranasal infection with Chlamydia pneumoniae. The mice were infected at 3 months of age with C. pneumoniae isolated from an AD brain. Infection was confirmed by light and electron microscopy in olfactory tissues of the mice. C. pneumoniae was still evident in these tissues 3 months after the initial infection indicating that a persistent infection had been established. Amyloid beta (A␤) 1-42 immunoreactive deposits were identified in the brains of infected BALB/c mice up to 3 months post-infection with the density, size, and number of deposits increasing as the infection progressed. A subset of deposits exhibited thioflavin-s labeling. Intracellular A␤1-42 labeling was observed in neuronal cells. Experimental induction of amyloid deposition in brains of non-transgenic BALB/c mice following infection with C. pneumoniae may be a useful model for furthering our understanding of mechanisms, linked to infection, involved in the initiation of the pathogenesis of sporadic AD.

Beta-amyloid deposition and Alzheimer's type changes induced by Borrelia spirochetes

“…These observations are in line with the present findings showing that A␤ formation may be induced in vitro following exposure of mammalian cells to B. burgdorferi. Recently, the formation of amyloid deposits resembling AD plaques was induced in the brains of mice following intranasal infection with another bacterium, Chlamydia pneumoniae [17].…”

Pathogenesis of Chlamydia pneumonia Persistent Illnesses in Autoimmune Diseases

“…Infection was confirmed by light and electron microscopy in olfactory tissues of the mice. C. pneumoniae was still evident in these tissues 3 months after the initial infection indicating that a persistent infection had been established [41].…”

“…The results of Balin study demonstrated the frequent infection of microglia and astroglia with C. pneumoniae in the AD-affected brain [7]. Intriguingly, an animal model, in which low-dose infusion of LPS has been used, revealed remarkable parallels with AD inflammation including APP induction, increased cytokine production with microglial reactivity, and temporal lobe pathology [41].…”

“…Further immunolabelling studies confirmed the organisms' intracellular presence primarily in areas of neuropathology in the AD brain. Thus, C. pneumoniae is present, viable, and transcriptionally active in areas of neuropathology in the AD brain, possibly suggesting that infection with the organism is a risk factor for late-onset AD [41]. In other study, Immunohistochemical analyses showed that astrocytes, microglia, and neurons all served as host cells for C. pneumoniae in the AD brain, and that infected cells were found in close proximity to both neuritic senile plaques and neurofibrillary tangles in the AD brain [26,41].…”

The human genome is composed of viral DNA: Viral homologues of the protein products cause Alzheimer's disease and others via autoimmune mechanisms.

“…These features, including betaamyloid deposition, tau phosphorylation 35 59,75 , entorhinal and hippocampal cell loss and cerebral shrinkage 4 can all be induced by Herpes simplex viral infection in mice. Several hundred genes have been implicated in the disease 8 (see http://www.polygenicpathways.co.uk/alzpolys.html , and a number of environmental risk factors including viral infection (Herpes viruses HSV-1 36,37 and the cytomegalovirus) , and bacterial and parasitic infection (C.Pneumoniae 17,49 , Borrelia Burgdorferri 53 and Helicobacter pylori) have also been shown to promote risk 31 . Indeed eradication of H.Pylori has been reported to improve cognitive performance 44 .…”