Inflammation: major denominator of obesity, Type 2 diabetes and Alzheimer’s disease-like pathology?

Abstract

Abstract Adipose tissue is an active metabolic organ that contributes to processes such as energy storage and utilization and to the production of a number of metabolic agents, such as adipokines, which play a role in inflammation. In this review, we try to elucidate the connections between peripheral inflammation at obesity and Type 2 diabetes and the central inflammatory process. Multiple lines of evidence highlight the importance of peripheral inflammation and its link to neuroinflammation, which can lead to neurodegenerative diseases such as dementia, Alzheimer’s disease (AD) and Parkinson’s disease. In addition to the accumulation of misfolded amyloid beta (Aβ) peptide and the formation of the neurofibrillary tangles of hyperphosphorylated tau protein in the brain, activated microglia and reactive astrocytes are the main indicators of AD progression. They were found close to Aβ plaques in the brains of both AD patients and rodent models of Alzheimer’s disease-like pathology. Cytokines are key players in pro- and anti-inflammatory processes and are also produced by microglia and astrocytes. The interplay of seemingly unrelated pathways between the periphery and the brain could, in fact, have a common denominator, with inflammation in general being a key factor affecting neuronal processes in the brain. An increased amount of white adipose tissue throughout the body seems to be an important player in pro-inflammatory processes. Nevertheless, other important factors should be studied to elucidate the pathological processes of and the relationship among obesity, Type 2 diabetes and neurodegenerative diseases.