Based on the results of the present study, we infer that CAP37, an established inflammatory mediator previously shown to activate microglial cells, may mediate the chronic neuroinflammation associated with AD from within the brain parenchyma.
Finally we will present an integrated model of how aldosterone may mediate effects of chronic stress on CVD, recommend new directions for research, and identify important methodological and design issues for this work.
There is a growing understanding that insulin resistance may mediate the relationship between chronic high-fat diets and reduced cognition, both in rat models and in humans with type 2 diabetes, while at the same time contributing to cardiovascular disease, depression and hypertension [ 35].
In addition, physical activity may mediate the negative association between chronic conditions and health outcomes by reducing the likelihood of acquiring additional chronic conditions and delaying the progression of current chronic condition(s).
Chronic inflammation may mediate risk of colorectal cancer (CRC); however, the association between circulating inflammatory markers and risk of CRC has been inconsistent.
A single exposure to cocaine does not alter sirtuin activity; however, upregulation of the sirtuins after chronic cocaine may mediate the stable neuroadaptive changes involved in maintaining addiction.
There is indication that chronic inflammation may mediate obesity and cancer 12. Interestingly, a role of leptin in inflammation has been suggested 13, as shown by a linear association between leptin and markers of inflammation 14.
These data provide strong epidemiologic evidence linking overall dietary patterns, inflammation, and diabetes risk, suggesting that chronic inflammation may mediate the association between a Western dietary pattern and risk of type 2 diabetes.
Further adjustment for inflammatory factors, but not for adipokines and elevated hepatic enzymes, substantially attenuated the associations for metabolic syndrome and most of its components, suggesting that chronic inflammation may mediate the effects of innate immune response induced by LPS-LBP.
32 A number of chronic maternal diseases may mediate the association, including the metabolic syndrome.
