Chronic inflammation and innate immunity in Alzheimer’s Disease : role of diet

The immune system utilizes an army of cellular and molecular agents to protect against adverse effects of chronic diseases. The immune surveillance of the brain is mediated by cell types specific to the brain but responsive to the same effector species as the peripheral immune system, which can circulate across the blood-brain barrier and influence its inflammation status. In the presence of peripheral chronic disease, proinflammatory mediators produced in the periphery can mediate a proinflammatory response in the brain. This can explain why antiinflammatory therapies, including protective dietary patterns, taken in midlife, may be protective against development of Alzheimer's disease (AD) in later life. Regulation of peripheral inflammation may thus suppress proinflammatory immune signaling to the brain and delay neurodegeneration. However, in symptomatic mild cognitive impairment and AD, when the perpetual cycle of damage-associated molecular patterns (DAMPs) generate localized inflammation, stimulation and not suppression of the peripheral immune system may be theoretically required to promote phagocytosis of amyloid by macrophages, seeking to resolve the inflammation cycle. However, the AD brain also requires local immunesuppression to circumvent the DAMP cycle. Consumption of immunomodulatory dietary factors offers potential for regulation of chronic inflammation.