Abstract
Many chronic diseases, including those classified as cardiovascular, neurodegenerative, or autoimmune, are characterized by persistent inflammation. The origin of this inflammation is mostly unclear, but it is typically mediated by inflammatory biomarkers, such as cytokines, and affected by both environmental and genetic factors. Recently circulating bacterial inflammagens such as lipopolysaccharide (LPS) have been implicated. We used a highly selective mouse monoclonal antibody to detect bacterial LPS in whole blood and/or platelet poor plasma of individuals with Parkinson’s Disease, Alzheimer’s type dementia, or Type 2 Diabetes Mellitus. Our results showed that staining is significantly enhanced (P < 0.0001) compared to healthy controls. Aberrant blood clots in these patient groups are characterized by amyloid formation as shown by the amyloid-selective stains thioflavin T and Amytracker™ 480 or 680. Correlative Light-Electron Microscopy (CLEM) illustrated that the LPS antibody staining is located in the same places as where amyloid fibrils may be observed. These data are consistent with the Iron Dysregulation and Dormant Microbes (IDDM) hypothesis in which bacterial inflammagens such as LPS are responsible for anomalous blood clotting as part of the aetiology of these chronic inflammatory diseases.
Highlights
Antibody staining is located in the same places as where amyloid fibrils may be observed
In this hypothesis we argue that microorganisms and their circulating products represent an important external stimulus in inflammatory conditions such as Parkinson’s Disease (PD), Alzheimer’s Disease (AD), Type 2 Diabetes (T2D) as well as in other diseases such as pre-eclampsia[34,35], overlaid on any genetic disease predisposition and exposure to environmental stressors
Healthy individuals and individuals diagnosed with PD, AD and T2D were age-correlated and participants included both genders (Table 1)
Summary
Antibody staining is located in the same places as where amyloid fibrils may be observed These data are consistent with the Iron Dysregulation and Dormant Microbes (IDDM) hypothesis in which bacterial inflammagens such as LPS are responsible for anomalous blood clotting as part of the aetiology of these chronic inflammatory diseases. In inflammatory conditions, including PD, AD and T2D, a changed erythrocyte and platelet structure, together with close interactions with pathological fibrin (atypical fibrin fibre formation), were previously reported[48,49,50,51] Such a hypercoagulable state and anomalous blood clotting go hand in hand[37,52,53], resulting in pathological clotting, and is one of the main causes contributing to myocardial infarction and thrombo-embolic strokes[54,55]. This is consistent with the view that LPS and/or LTA have a causal role in these diseases
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
