Abstract

Propose. This study aimed to evaluate the protective role of young coconut juice (YCJ) against the pathological changes in Alzheimer's disease (AD) in orchidectomized (orx) rats. Methods and Results. Animals were divided into 7 groups including: baseline normal control group, sham control, orx rat group, orx rat group injected with 2.5 μg/kg b.w. estradiol benzoate (EB) 3 days a week for 10 weeks, and the orx rat groups treated orally with 10, 20, and 40 ml/kg b.w. of YCJ for 10 weeks. At the end of treatment period, animals were sacrificed and the brain of each rat was removed, fixed in 10% neutral formalin, and stained by specific antibodies against NF200, parvalbumin (PV), β-amyloid (Aβ), and estrogen receptors (ERα and ERβ). The results showed that the number of NF200- and PV-reactive neurons in the hippocampus and cerebral cortex was significantly reduced in orx rats. However, it restored to normal in orx rats injected with EB or those administrated with YCJ in a dose-related manner. Neurons containing β-amyloid (Aβ), a hallmark of Alzheimer's disease (AD), were found to be increased in the orx rats; however; they were reduced by EB injection or YCJ administration. These results suggested the binding of the YCJ active ingredient(s) with estrogen receptors (ERs) in the brain as indicated by the detection of ERα and ERβ in neurons since a significant correlation was detected between NF200-/PV-reactive neurons vs ERα-/ERβ-reactive neurons.Conclusion. It could be concluded that YCJ is effective as EB in reducing AD pathology, probably by being selective estrogen receptor modulators.

Highlights

  • With advancing age, a significant decrease in sex steroid hormones is occurred in men and women leading to the development of Alzheimer’s disease (AD) [1, 2]

  • Positive reaction was observed in the triangular cell bodies and prominently in the dendrites and axon. e PV-reactive neurons were found in Cornu ammonis 1 (CA1), CA2, and CA3 of hippocampus and in all tested areas of the cerebral cortex

  • E positive reaction was observed prominently in the cell bodies and axons, but lightly in the dendrites (Figure 1(b)). Both estrogen receptor-α (ERα)-reactive (Figure 1(c)) and estrogen receptor-β (ERβ)-reactive (Figure 1(d)) neurons were observed, predominantly in layers III and V of the cerebral cortex, and the reaction was in the cell bodies, dendrites, and axons. e amyloid β (Aβ)-reactive neurons (Figure 1(e)) were detected in layers III and V of the cerebral cortex with more intensity in layer IV and in CA3. e reaction was observed in the cytoplasm and partially present in the basal dendrites of pyramidal cells, but not in the nucleus

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Summary

Introduction

A significant decrease in sex steroid hormones is occurred in men and women leading to the development of Alzheimer’s disease (AD) [1, 2]. It was reported that the level of testosterone in the brain is inversely correlated with the brain levels of β-amyloid 1-42 (Aβ), which is well known as one of the AD hallmark pathologies [3]. E Aβ plaques are increased in andropausal human brains [5, 6] and in the brains of aging male mice [7]. E increased risk for AD in women as initiated by brain modifications during the menopause transition (MT) and the estrogen deficiency is well documented [11]. It was found that estrogen supplement plays an important role in the protection of AD in male mice by significantly lowering Aβ levels in the Cornu ammonis 1 (CA1) area of the hippocampus [7]

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