21^st Annual European Pharma Congress

Biography

Biography: Judith Miklossy

Abstract

Strong epidemiologic evidence and common molecular mechanisms support an association between Alzheimer’s disease (AD), type 2‐diabetes and several other chronic inflammatory disoders. Local inflammation and amyloidosis occur in both diseases and are associated with periodontitis and various infectious agents. Here we discuss accumulated evidence for the presence of local inflammation and bacteria in Alzheimer’s disease and type 2 diabetes and discuss host pathogen interactions in chronic inflammatory disorders. Spirochetes, Chlamydophyla pneumoniae and Helicobacter pylori are demonstrated in association with dementia and brain lesions in AD and islet lesions in type 2 diabetes. The presence of pathogens in host tissues activates immune responses through Toll‐like receptor signaling pathways. Evasion of pathogens from complement‐mediated attack results in persistent infection, inflammation and amyloidosis. Amyloid beta and the pancreatic amyloid called amylin bind to lipid bilayers and produce Ca(2+) influx and bacteriolysis. Similarly to AD, accumulation of amylin deposits in type 2 diabetes may result from an innate immune response to chronic bacterial infection, which are known to be associated with amyloidosis. Further research based on an infectious origin of both AD and type 2 diabetes will lead to novel treatment strategies.