Rheumatoid Arthritis and Alzheimer Disease: Possible Cellular and Molecular Links

Abstract

Alzheimer disease (AD) is the most common form of dementia of the old population over 85 years. AD pathogenesis is multifactorial and several findings support the neuroinflammatory pathogenetic hypothesis. There is an inverse relationship between AD and Rheumatoid arthritis (RA) due to different factors. Among them, NSAIDs use acting both on amyloid formation and COX enzymes has been supposed to play a protective role on AD risk. Moreover, new insights on colony stimulating factors (GM-CSF, M-CSF and G-CSF) pathways in immune cells differentiation suggested a possible cellular link between AR and the AD onset. Alzheimer disease (AD) is the most common form of dementia, accounts for 50-60% of all dementia cases. It interests about 20-40% of the old population over 85 years and is characterized by cognitive dysfunction as memory loss, language difficulties, visuospatial deficits, impairment in judgment and decision-making, deficit in higher and subsequently in basic daily activities, behavioral disturbances and psychiatric alterations. The classical AD pathologic hallmarks are senile plaques made by extracellular amyloid beta (Aβ) deposition and neurofibrillary tangles made of hyperphosphorylated Tau proteins [1].