Pilot for David Fardo: Inflammation and Alzheimer's Disease: AGenome-wide Investigation of Interrelated Pathways

Chronic inflammation (CI) has been associated with numerous conditions throughout the body including: aging disorders (Premature aging, Dementia, Alzheimer’s Disease, AD), dental disease (periodontitis, PD), autoimmune disorders (Rheumatoid Arthritis, RA; Sarcoidosis; Multiple Sclerosis) and multiple other disease states. While it is interesting that patients exhibiting one form of chronic inflammatory disease (CID) appear to be more prone to developing a second CID elsewhere within their body as has been observed with PD in conjunction with dementia and Alzheimer’s disease (AD), yet this phenomena is not well understood. This observation suggests that an unhealthy or “out-of-balance” systemic environment, primed for tissue damage exists in some individuals which facilitates the multiple tissue CID development. This observation also suggests that some individuals are inherently more prone to development of CIDs potentially due to genetic factors/variations can influence the generation or maintenance of the systemic environment imbalance. Chronic inflammation is an underlying feature of AD. We hypothesize that a pro-inflammatory genetic profile, generated by the aggregate presence and interaction of multiple pro-inflammatory markers, will predispose individuals to the generation of a systemic environment prone to CID development as observed in AD. We hypothesize that a panel of genetic markers, all with moderate roles in CIDs independently, will correlate with AD (and other CIDs) when present in aggregate and will prove to be a valuable source of potential AD drug targets.