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Modulation of Inflammation as a Way of Delaying Alzheimer's Disease Progression: The Diet's Role

[ Vol. 15 , Issue. 4 ]

Author(s):

R. Businaro*, M. Corsi, R. Asprino, C. Di Lorenzo, D. Laskin, R.M. Corbo, S. Ricci and A. Pinto   Pages 363 - 380 ( 18 )

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.

Keywords:

Alzheimer's disease, nutrition inflammation, cytokines, polyphenols, fatty acids, central nervous system.

Affiliation:

Department of Medico-Surgical Sciences and Biotechnologies, Sapienza University of Rome, Rome, Department of Medico-Surgical Sciences and Biotechnologies, Sapienza University of Rome, Rome, Department of Experimental Medicine, Medical Physiopathology, Food Science and Endocrinology Section, Sapienza University of Rome, Rome, Don Carlo Gnocchi Onlus Foundation, Milan, Departments of Pharmacology and Toxicology, Ernest Mario School of Pharmacy, Rutgers University, Piscataway, NJ, Department of Biology and Biotechnology "Charles Darwin", Sapienza University of Rome, Rome, Department of Anatomical Sciences, Histological, Legal Medicine and Locomotor Apparatus, Sapienza University of Rome, Rome, Department of Experimental Medicine, Medical Physiopathology, Food Science and Endocrinology Section, Sapienza University of Rome, Rome



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