Abstract
Aging is the leading risk factor for neurodegenerative diseases and oxidative stress involved in the pathophysiology of these diseases. These changes increase during menopausal condition in females when the level of estradiol is decreased. The aim of the present study was to determine the effect of tachykinin neuropeptide, Neurokinin B (NKB) and Amyloid beta fragment Aβ (25 - 35) on 17β estradiol (E2) treated aging female rat synaptosomes of different age groups. Aging brain functions were assayed by measuring the activities of antioxidant enzymes—superoxide dismutase (SOD) and monoamine oxidase (MAO) with neuropeptides. An in-vitro incubation of Aβ (25 - 35) in E2 treated brain synaptosomes showed toxic effects on all the parameters. However, NKB and NKB combined with Aβ (25 35) showed stimulating effects in E2 treated rat brain synaptosomes. In the present study, an increase in activity of SOD and decrease in the level of MAO, in the presence of NKB and combined NKB and Aβ in E2 treated brain synaptosomes of aging rats. This study elucidates that treatment of NKB and Aβ with E2 incombination exerts more protective influence than their individual application, against excitotoxicity in age related changes.
Highlights
Aging is a time-dependent functional decline, leading to the cell’s incapacity to withstand external and internal challenges
We examine the neuroprotective effect of Neurokinin B (NKB) and with E2 against Aβ (25 - 35) toxicity on the activity of superoxide dismutase and monoamine oxidase in the brain of aging female rats
We observed an increase in body weight and brain weight in 12 and 24-month-old control rats when compared to 3-month young rats (Result stated in the Table 1) but weight decreased significantly with E2 treatment when compared with respective controls
Summary
Aging is a time-dependent functional decline, leading to the cell’s incapacity to withstand external and internal challenges. There is a physiological decline and an increase in the prevalence of diseases [1]. It is the consequence of two independent biological processes: the loss of functionality, and the loss of resistance or adaptability to stress. Increase in reactive oxygen species (ROS) production and imbalance in antioxidant defense and repair mechanism leads to cell death during aging and age related neurological disorders [2]. E2 modulates multiple functions of the brain, via activation of ERa and ERb including development, cognition and memory [8], highlighting its protective effects against neuronal damage [9]
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