Title:Modulation of Inflammation as a Way of Delaying Alzheimer's Disease Progression: The Diet's Role
Volume: 15
Issue: 4
Author(s): R. Businaro*, M. Corsi, R. Asprino, C. Di Lorenzo, D. Laskin, R.M. Corbo, S. Ricci and A. Pinto
Affiliation:
- Department of Medico-Surgical Sciences and Biotechnologies, Sapienza University of Rome, Rome,Italy
Keywords:
Alzheimer's disease, nutrition inflammation, cytokines, polyphenols, fatty acids, central nervous system.
Abstract: Background: Most of the recent reports suggest that inflammatory mediators play a central
role in the etiopathogenesis of Alzheimer's disease (AD) and that the conditions leading to a chronic
low-grade inflammation, such as stress, depression, obesity and metabolic syndrome, increase the odds
of developing Mild Cognitive Impairment (MCI) and AD. Microglia cells are the main actors in the AD
process: stimuli from the microenvironment may induce microglia cells to switch to a classically activated
inflammatory phenotype M1, or, on the contrary to an alternatively activated M2 phenotype characterized
by the secretion of different types of cytokines. Many attempts are currently being made in
order to delay the progression of AD by reducing inflammatory mechanisms underlying the disease.
Several studies support a relationship among neuroinflammation and nutrients, foods or dietary patterns,
taking into account the synergistic or antagonistic biochemical interactions among nutrients as well as
the different food sources of the same nutrient. Natural antioxidant and anti-inflammatory compounds
found in plant foods, such as fruits, particularly berries (such as strawberry, blueberry, blackcurrant,
blackberry, blueberry and mulberry) have been shown to exert neuroprotective activity. It is still unclear
whether the dietary bioactive compounds enter the Blood Brain Barrier (BBB) playing a direct antiinflammatory
or pro-inflammatory effect on microglia and/or other Central Nervous System (CNS)
cells. Another hypothesis is that they may trigger a peripheral reaction that induce indirectly a CNS' response.
The subsequent synthesis of cytokines may drive microglia polarization by different ways. So,
via an indirect route microglia detects and responds to immune-to-brain signaling.
Conclusion: This review summarizes current evidence about the potential mechanisms of the interaction
among diet, neuroinflammation and AD.
