Assessment of the peripheral immune response profile in the neurodegeneration process due to intestinal inflammation PI Sérgio Andrade

The predominant hypothesis for Alzheimer's disease (AD) is amyloid, which establishes changes in the proteolytic processing of amyloid precursor protein resulting in the accumulation of amyloid beta peptide (Aβ), forming amyloid plaques, which trigger an immunological response that promotes neuroinflammation and neurodegeneration. However, the association between genetic and non-genetic risk factors for the development of neuroinflammatory diseases, mainly AD, has been widely discussed in the scientific community and much is said about the influence of the intestinal microbiota in modulating neuro-immune functions. and strong evidence reinforcing the gut-brain link has emerged in recent decades.

Therefore, endotoxins, especially lipopolysaccharide (LPS), have been adopted as a strong non-genetic risk factor for AD neurodegeneration as they promote activation of both systemic and central pro-inflammatory pathways, in addition to having already been documented. presence of LPS in Aβ peptides in amyloid plaques and vascular endothelium of patients with AD. Based on the above, this research proposal aims to elucidate through which neuro-immune or systemic mechanisms an inflammatory bowel disease can influence cognitive decline and a neuroinflammatory process.