|
Post by LymeEnigma on Jun 3, 2008 8:57:55 GMT -8
Beta-amyloid deposition and Alzheimer's type changes induced by Borrelia spirochetes Judith Miklossya, b, Corresponding Author Contact Information, E-mail The Corresponding Author, Andras Kisc, Alexandra Radenovicc, Lisa Millerd, Laszlo Forroc, Ralph Martinse, Krzysztof Reissf, Nune Darbinianf, Pushpa Darekarb, Laszlo Mihalyg and Kamel Khalili Abstract: The pathological hallmarks of Alzheimer's disease (AD) consist of β-amyloid plaques and neurofibrillary tangles in affected brain areas. The processes, which drive this host reaction are unknown. To determine whether an analogous host reaction to that occurring in AD could be induced by infectious agents, we exposed mammalian glial and neuronal cells in vitro to Borrelia burgdorferi spirochetes and to the inflammatory bacterial lipopolysaccharide (LPS). Morphological changes analogous to the amyloid deposits of AD brain were observed following 2–8 weeks of exposure to the spirochetes. Increased levels of β-amyloid presursor protein (AβPP) and hyperphosphorylated tau were also detected by Western blots of extracts of cultured cells that had been treated with spirochetes or LPS. These observations indicate that, by exposure to bacteria or to their toxic products, host responses similar in nature to those observed in AD may be induced. www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T09-4G5BJ7S-1&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=47b89ea7bb5d63df414830564e0d79de
|
|
|
Post by LymeEnigma on Sept 2, 2008 11:47:24 GMT -8
J Alzheimers Dis. 2008 May;13(4):381-91. Chronic inflammation and amyloidogenesis in Alzheimer's disease -- role of Spirochetes. Miklossy J. University of British Columbia, Kinsmen Laboratory of Neurological Research, Vancouver, BC, Canada. judithmiklossy@bluewin.ch Alzheimer's disease (AD) is associated with dementia, brain atrophy and the aggregation and accumulation of a cortical amyloid-beta peptide (Abeta). Chronic bacterial infections are frequently associated with amyloid deposition. It had been known from a century that the spirochete Treponema pallidum can cause dementia in the atrophic form of general paresis. It is noteworthy that the pathological hallmarks of this atrophic form are similar to those of AD. Recent observations showed that bacteria, including spirochetes contain amyloidogenic proteins and also that Abeta deposition and tau phosphorylation can be induced in or in vivo following exposure to bacteria or LPS. Bacteria or their poorly degradable debris are powerful inflammatory cytokine inducers, activate complement, affect vascular permeability, generate nitric oxide and free radicals, induce apoptosis and are amyloidogenic. All these processes are involved in the pathogenesis of AD. Old and new observations, reviewed here, indicate that to consider the possibility that bacteria, including several types of spirochetes highly prevalent in the population at large or their persisting debris may initiate cascade of events leading to chronic inflammation and amyloid deposition in AD is important, as appropriate antibacterial and antiinflammatory therapy would be available to prevent dementia. PMID: 18487847 [PubMed - indexed for MEDLINE] www.ncbi.nlm.nih.gov/pubmed/18487847?ordinalpos=38&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSumiospress.metapress.com/content/k4t8m7ql69174775/
|
|