Extracellular Zn2+-Dependent Amyloid-β1–42 Neurotoxicity in Alzheimer’s Disease Pathogenesis

Sato, Yuichi; Takiguchi, Mako; Tamano, Haruna; Takeda, Atsüshi

doi:10.1007/s12011-020-02131-w

Cited by 10 publications

(5 citation statements)

References 105 publications

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“…It has been known for some time now that deregulation of the levels of metal ions stimulates the pathogeneses of neurodegenerative states, such as AD . Alterations in the levels of zinc (Zn) in particular is closely implicated in AD pathology, via multiple mechanisms such as promotion of amyloidogenesis and Aβ deposition, induction of dysfunction of synaptic signaling and plasticity, and activation of oxidative, neuroinflammatory, and apoptotic signaling (reviewed in , ).…”

Section: Neuroprotection Mediated By Emodin In Admentioning

confidence: 99%

Neuroprotective, Anti-Inflammatory and Antifibrillogenic Offerings by Emodin against Alzheimer’s Dementia: A Systematic Review

Saha,

Ahmad

2024

ACS Omega

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Background: Alzheimer's disease (AD) is among the major causes of dementia in the elderly and exerts tremendous clinical, psychological and socioeconomic constraints. Currently, there are no effective disease-modifying/retarding anti-AD agents. Emodin is a bioactive phytochemical with potent multimodal antiinflammatory, antioxidant, and antifibrillogenic properties. In particular, emodin may result in significant repression of the pathogenic mechanisms underlying AD. The purpose of this review is to accumulate and summarize all the primary research data evaluating the therapeutic actions of emodin in AD pathogenesis. Methodology: The search, selection, and retrieval of pertinent primary research articles were systematically performed using a methodically designed approach. A variety of keyword combinations were employed on online scholarly web-databases. Strict preset inclusion and exclusion criteria were used to select the retrieved studies. Data from the individual studies were summarized and compiled into different sections, based upon their findings. Results: Cellular and animal research indicates that emodin exerts robust multimodal neuroprotection in AD. While emodin effectively prevents tau and amyloid-beta (Aβ) oligomerization, it also mitigates their neurotoxicity by attenuating neuroinflammatory, oxidative, and bioenergetic defects. Evidences for emodin-mediated enhancements in memory, learning, and cognition were also found in the literature. Conclusion: Emodin is a potential anti-AD dietary supplement; however, further studies are warrantied to thoroughly understand its target players and mechanisms. Moreover, human clinical data on emodin-mediated amelioration of AD phenotype is largely lacking, and must be addressed in the future. Lastly, the safety of exogenously supplemented emodin must be thoroughly evaluated.

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Section: Neuroprotection Mediated By Emodin In Admentioning

confidence: 99%

Neuroprotective, Anti-Inflammatory and Antifibrillogenic Offerings by Emodin against Alzheimer’s Dementia: A Systematic Review

Saha,

Ahmad

2024

ACS Omega

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“…Consequently, these neurons are outlined as “gluzinergic” neurons ( 56 ). Zn will be discharged from presynaptic ends throughout conjugation transmission and enable to penetrate in postsynaptic stomata through specified gated channels holding N-methyl-D-aspartate (NMDA) ( 57 ). Zn exposure for 15 min at 300–600 μM to the nerve cells ends in animal neural death.…”

Section: Zinc Deficiency-triggered Defense Mechanismsmentioning

confidence: 99%

Mechanistic Impact of Zinc Deficiency in Human Development

et al. 2022

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Zinc (Zn) deficiency in humans is an emerging global health issue affecting approximately two billion people across the globe. The situation prevails due to the intake of Zn deficient grains and vegetables worldwide. Clinical identification of Zn deficiency in humans remains problematic because the symptoms do not appear until impair the vital organs, such as the gastrointestinal track, central nervous system, immune system, skeletal, and nervous system. Lower Zn body levels are also responsible for multiple physiological disorders, such as apoptosis, organs destruction, DNA injuries, and oxidative damage to the cellular components through reactive oxygen species (ROS). The oxidative damage causes chronic inflammation lead toward several chronic diseases, such as heart diseases, cancers, alcohol-related malady, muscular contraction, and neuro-pathogenesis. The present review focused on the physiological and growth-related changes in humans under Zn deficient conditions, mechanisms adopted by the human body under Zn deficiency for the proper functioning of the body systems, and the importance of nutritional and nutraceutical approaches to overcome Zn deficiency in humans and concluded that the biofortified food is the best source of Zn as compared to the chemical supplementation to avoid their negative impacts on human.

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“…An increasing body of evidence has shown that the basal level of extracellular zinc in hippocampus is typically in the low nanomolar range, and that the increase in zinc content aggravates the neurotoxicity of amyloid protein[ 40 ]. Zinc was shown to increase the expression of amyloid precursor protein in a mouse model of AD, which in turn increased amyloid synthesis.…”

Section: Ad and Micronutrientsmentioning

confidence: 99%

Role of micronutrients in Alzheimer's disease: Review of available evidence

Hong-xin¹,

Qian²,

Wu³

et al. 2022

WJCC

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Alzheimer's disease (AD) is one of the most common age-related neurodegenerative disorders that have been studied for more than 100 years. Although an increased level of amyloid precursor protein is considered a key contributor to the development of AD, the exact pathogenic mechanism remains known. Multiple factors are related to AD, such as genetic factors, aging, lifestyle, and nutrients. Both epidemiological and clinical evidence has shown that the levels of micronutrients, such as copper, zinc, and iron, are closely related to the development of AD. In this review, we summarize the roles of eight micronutrients, including copper, zinc, iron, selenium, silicon, manganese, arsenic, and vitamin D in AD based on recently published studies.

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Extracellular Zn2+-Dependent Amyloid-β1–42 Neurotoxicity in Alzheimer’s Disease Pathogenesis

Cited by 10 publications

References 105 publications

Neuroprotective, Anti-Inflammatory and Antifibrillogenic Offerings by Emodin against Alzheimer’s Dementia: A Systematic Review

Neuroprotective, Anti-Inflammatory and Antifibrillogenic Offerings by Emodin against Alzheimer’s Dementia: A Systematic Review

Mechanistic Impact of Zinc Deficiency in Human Development

Role of micronutrients in Alzheimer's disease: Review of available evidence

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