Abstract

The immune system and the central nervous system message each other to preserving central homeostasis. Both systems undergo changes during aging that determine central age-related defects. Ellagic acid (EA) is a natural product which is beneficial in both peripheral and central diseases, including aging. We analyzed the impact of the oral administration of a new oral ellagic acid micro-dispersion (EAm), that largely increased the EA solubility, in young and old mice. Oral EAm did not modify animal weight and behavioral skills in young and old mice, but significantly recovered changes in “ex-vivo, in vitro” parameters in old animals. Cortical noradrenaline exocytosis decreased in aged mice. EAm administration did not modify noradrenaline overflow in young animals, but recovered it in old mice. Furthermore, GFAP staining was increased in the cortex of aged mice, while IBA-1 and CD45 immunopositivities were unchanged when compared to young ones. EAm treatment significantly reduced CD45 signal in both young and old cortical lysates; it diminished GFAP immunopositivity in young mice, but failed to affect IBA-1 expression in both young and old animals. Finally, EAm treatment significantly reduced IL1beta expression in old mice. These results suggest that EAm is beneficial to aging and represents a nutraceutical ingredient for elders.

Highlights

  • Aging is a progressive physio-pathological process that provokes an array of both central and peripheral complications

  • GFAP staining was increased in the cortex of aged mice, while IBA-1 and CD45 immunopositivities were unchanged when compared to young ones

  • ellagic acid micro-dispersion (EAm) treatment significantly reduced IL1beta expression in old mice. These results suggest that EAm is beneficial to aging and represents a nutraceutical ingredient for elders

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Summary

Introduction

Aging is a progressive physio-pathological process that provokes an array of both central and peripheral complications. Learning and memory impairments as well as mood disorders and anxiety mainly rely on alteration of the chemical neurotransmission in selected regions of the central nervous system (CNS), affecting the catecholaminergic, the cholinergic and the GABAergic pathways. These systems are selected targets of aging processes, as the efficiency of the synthesis and the release of these neuromodulators, as well as the expression of the corresponding membrane receptors, result in impairments in old brains [1,2,3,4,5,6]. The growing confidence in the promise of new actions/interventions that could in part restore the neuronal damages and/or delay their progression is so far unanswered and, despite expectations, the need of therapeutics remains unmet

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