Downregulation of miR-33 Has Protective Effect Against Aβ₂₅₋₃₅-Induced Injury in SH-SH-SY5Y Cells

Wang, Xiaoping; Li, Xiaojia; Huang, Bin; Yang, Lili; Chen, Kai; Zhao, Dongdong; Luo, Xiaohua; Ying-ji, Wang

doi:10.12659/msm.921026

Cited by 8 publications

(11 citation statements)

References 27 publications

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“…Recently, the potential of blocking miR-592 in order to lower oxidative stress injury in astrocytes was reported and it was suggested to be mediated by dyslexia-associated protein KIAA0319 and (Kelch-like ECH-associating protein 1) nuclear factor erythroid 2 related factor 2-antioxidant response element (Keap1/Nrf2/ARE) signaling pathway. 179 Wang et al 180 detected upregulation of miR-33 expression in SH-SY5Y cells after treatment with Aβ 25–35 . Downregulation of miR-33 suppressed inflammation, oxidative stress, and cell apoptosis, while also improving synaptic plasticity.…”

Section: Potential Epigenetic Therapy For Admentioning

confidence: 99%

“…Downregulation of miR-33 suppressed inflammation, oxidative stress, and cell apoptosis, while also improving synaptic plasticity. 180 The protective effect of miR-33 downregulation was achieved by suppressing Akt/mammalian target of rapamycin (mTOR) signaling pathway activation. 180 Intra-hippocampal injection of miR-342-3p antagomir in 3xTg-AD mice confirmed the association between miR-342-3p and AD, suggesting that miR-342-3p inhibition can improve cognitive deficits.…”

Section: Potential Epigenetic Therapy For Admentioning

confidence: 99%

“… 180 The protective effect of miR-33 downregulation was achieved by suppressing Akt/mammalian target of rapamycin (mTOR) signaling pathway activation. 180 Intra-hippocampal injection of miR-342-3p antagomir in 3xTg-AD mice confirmed the association between miR-342-3p and AD, suggesting that miR-342-3p inhibition can improve cognitive deficits. 181 Downregulation of miR-342-3p also attenuated the hippocampal Aβ-plaque burden revealing the important effect of miR-342-3p on Aβ metabolism pathways in AD and suggesting its therapeutical potential.…”

Section: Potential Epigenetic Therapy For Admentioning

confidence: 99%

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Personalizing the Care and Treatment of Alzheimer’s Disease: An Overview

Štrac¹,

Konjevod²,

Šagud³

et al. 2021

PGPM

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Alzheimer’s disease (AD) is a progressive, complex, and multifactorial neurodegenerative disorder, still without effective and stable therapeutic strategies. Currently, available medications for AD are based on symptomatic therapy, which include acetylcholinesterase (AChE) inhibitors and N-methyl-D-aspartate (NMDA) receptor antagonist. Additionally, medications such as antipsychotic drugs, antidepressants, sedative, and hypnotic agents, and mood stabilizers are used for the management of behavioral and psychological symptoms of dementia (BPSD). Clinical research has been extensively investigated treatments focusing on the hallmark pathology of AD, including the amyloid deposition, tau hyperphosphorylation, neuroinflammation, and vascular changes; however, so far without success, as all new potential drugs failed to show significant clinical benefit. The underlying heterogeneous etiology and diverse symptoms of AD suggest that a precision medicine strategy is required, which would take into account the complex genetic, epigenetic, and environmental landscape of each AD patient. The article provides a comprehensive overview of the literature on AD, the current and potential therapy of both cognitive symptoms as well as BPSD, with a special focus on gut microbiota and epigenetic modifications as new emerging drug targets. Their specific patterns could represent the basis for novel individually tailored approaches aimed to optimize precision medicine strategies for AD prevention and treatment. However, the successful application of precision medicine to AD demands a further extensive research of underlying pathological processes, as well as clinical and biological complexity of this multifactorial neurodegenerative disorder.

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Section: Potential Epigenetic Therapy For Admentioning

confidence: 99%

Section: Potential Epigenetic Therapy For Admentioning

confidence: 99%

Section: Potential Epigenetic Therapy For Admentioning

confidence: 99%

See 1 more Smart Citation

Personalizing the Care and Treatment of Alzheimer’s Disease: An Overview

Štrac¹,

Konjevod²,

Šagud³

et al. 2021

PGPM

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“…The role of miR-33 has also been implicated in the neurodegenerative processes. Studies have demonstrated that the knockdown of miR-33 improved synaptic plasticity, reduced inflammation, oxidative stress, and cell apoptosis (Wang et al, 2020). The direct intracerebral delivery of a miR-33 antisense oligonucleotide into mouse brain was shown to be an effective strategy for increasing brain ABCA1 expression/activity, which can have beneficial effects on various neurodegenerative and cardiovascular diseases (Jan et al, 2015).…”

Section: Mir-33mentioning

confidence: 99%

A Review of miRNAs as Biomarkers and Effect of Dietary Modulation in Obesity Associated Cognitive Decline and Neurodegenerative Disorders

Perdoncin

Konrad

Wyner

et al. 2021

Front. Mol. Neurosci.

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There has been a progressive increase in the prevalence of obesity and its comorbidities such as type 2 diabetes and cardiovascular diseases worldwide. Recent studies have suggested that the crosstalk between adipose tissue and central nervous system (CNS), through cellular mediators and signaling pathways, may causally link obesity with cognitive decline and give rise to neurodegenerative disorders. Several mechanisms have been proposed in obesity, including inflammation, oxidative stress, insulin resistance, altered lipid and cholesterol homeostasis, which may result in neuroinflammation, altered brain insulin signaling, amyloid-beta (Aβ) deposition and neuronal cell death. Since obesity is associated with functional and morphological alterations in the adipose tissues, the resulting peripheral immune response augments the development and progression of cognitive decline and increases susceptibility of neurodegenerative disorders, such as Alzheimer’s Disease (AD) and Parkinson’s Disease (PD). Studies have also elucidated an important role of high fat diet in the exacerbation of these clinical conditions. However, the underlying factors that propel and sustain this obesity associated cognitive decline and neurodegeneration, remains highly elusive. Moreover, the mechanisms linking these phenomena are not well-understood. The cumulative line of evidence have demonstrated an important role of microRNAs (miRNAs), a class of small non-coding RNAs that regulate gene expression and transcriptional changes, as biomarkers of pathophysiological conditions. Despite the lack of utility in current clinical practices, miRNAs have been shown to be highly specific and sensitive to the clinical condition being studied. Based on these observations, this review aims to assess the role of several miRNAs and aim to elucidate underlying mechanisms that link obesity with cognitive decline and neurodegenerative disorders. Furthermore, this review will also provide evidence for the effect of dietary modulation which can potentially ameliorate cognitive decline and neurodegenerative diseases associated with obesity.

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“…Through targeting of multiple factors involved in GABAergic signaling, miR‐33 has been shown to directly regulate state‐dependent memory (Jovasevic et al, 2015). Additionally, multiple groups have shown that miR‐33 can promote amyloid‐beta accumulation, indicating that inhibition of miR‐33 may protect against memory loss in patients with Alzheimer’s disease (Kim et al, 2015; Wang et al, 2020).…”

Section: Introductionmentioning

confidence: 99%

miR‐33 in cardiometabolic diseases: lessons learned from novel animal models and approaches

et al. 2021

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miRNAs have emerged as critical regulators of nearly all biologic processes and important therapeutic targets for numerous diseases. However, despite the tremendous progress that has been made in this field, many misconceptions remain among much of the broader scientific community about the manner in which miRNAs function. In this review, we focus on miR‐33, one of the most extensively studied miRNAs, as an example, to highlight many of the advances that have been made in the miRNA field and the hurdles that must be cleared to promote the development of miRNA‐based therapies. We discuss how the generation of novel animal models and newly developed experimental techniques helped to elucidate the specialized roles of miR‐33 within different tissues and begin to define the specific mechanisms by which miR‐33 contributes to cardiometabolic diseases including obesity and atherosclerosis. This review will summarize what is known about miR‐33 and highlight common obstacles in the miRNA field and then describe recent advances and approaches that have allowed researchers to provide a more complete picture of the specific functions of this miRNA.

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Downregulation of miR-33 Has Protective Effect Against Aβ₂₅₋₃₅-Induced Injury in SH-SH-SY5Y Cells

Cited by 8 publications

References 27 publications

Personalizing the Care and Treatment of Alzheimer’s Disease: An Overview

Personalizing the Care and Treatment of Alzheimer’s Disease: An Overview

A Review of miRNAs as Biomarkers and Effect of Dietary Modulation in Obesity Associated Cognitive Decline and Neurodegenerative Disorders

miR‐33 in cardiometabolic diseases: lessons learned from novel animal models and approaches

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