Abstract

Carnosine restores aging-induced elevation of corticosterone status and brain regional amyloid-beta in relation to down regulation of locomotor activity

Highlights

  • The aging process of living species makes the phenomena unique as its negative association with the ability to respond to stress-related physiological conditions [1]

  • The adrenal gland being the site of synthesis of corticosterone demands an attention for further study in relation to the plasma corticosterone level and brain regional Aβ deposition for plaque formation during aging

  • Since carnosine has (a) these unique properties, and (b) ability to attenuate the aging-induced brain regional deterioration in serotonergic activity [13,21], without any side effect [22], it is not unreasonable to assume that there may be a role of carnosine on aging-induced stress related to corticosterone status and brain regional Aβ deposition. Based on this correlative information, the present study has focused with the effect of carnosine on aginginduced changes in the plasma and adrenal corticosterone status as well as locomotor behaviour, and brain regional Aβ (1-42) levels including plaques

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Summary

Introduction

The aging process of living species makes the phenomena unique as its negative association with the ability to respond to stress-related physiological conditions [1]. Glucocorticoid receptors involved in the recovery from stress with an activation of a set of hormonal and neuronal responses and other mediators, such as neurotransmitters, cytokines to assist in adaptation to a new situation or challenge [6] This corticosterone has been found to be associated with the amyloid pathogenesis [7] and loss of neural integrity and functions of brain regions [8]. Weight of human brain and/or its volume has (have) been found to decline during aging [9] with production of a wide range of misfolded proteins, aggregation (proteinopathy) and loss of neuronal cells [10] It is well-known that deposition and formation of brain regional synaptic plaques are the major histopathological hallmark of brain aging [10]. The adrenal gland being the site of synthesis of corticosterone demands an attention for further study in relation to the plasma corticosterone level and brain regional Aβ deposition for plaque formation during aging

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