The role of microRNA-34 family in Alzheimer’s disease: A potential molecular link between neurodegeneration and metabolic disorders

Bazrgar, Maryam; Khodabakhsh, Pariya; Prudencio, Mercedes; Mohagheghi, Fatemeh; Ahmadiani, Abolhassan

doi:10.1016/j.phrs.2021.105805

Cited by 28 publications

(12 citation statements)

References 223 publications

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“…Recent studies have reported AD development to be a comorbidity with other pathologies, including type 2 diabetes, obesity, and cardiovascular disease . There is also an increased risk of metabolic syndrome, which has been observed in both human population-based surveys and AD-related mice models. , Patients with AD demonstrate a deregulation in insulin signaling, leading to the identification of AD as type 3 diabetes . A nationwide epidemiological study indicated the prevalence of diabetes was 12% among AD cases, and AD patients had an increased (1.14 times) risk of having diabetes compared to healthy subjects .…”

Section: Introductionmentioning

confidence: 99%

Helicobacter pylori and Alzheimer’s Disease-Related Metabolic Dysfunction: Activation of TLR4/Myd88 Inflammation Pathway from p53 Perspective and a Case Study of Low-Dose Radiation Intervention

Zhao

Shen

Zhou

et al. 2022

ACS Chem. Neurosci.

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Gut dysbiosis is observed in Alzheimer's disease (AD) and is frequently associated with AD-induced metabolic dysfunction. However, the extent and specific underlying molecular mechanisms triggered by alterations of gut microbiota composition and function mediating ADinduced metabolic dysfunction in AD remain incompletely uncovered. Here, we indicate that Helicobacter pylori (H. pylori) is abundant in AD patients with relative metabolic dysfunction. Fecal microbiota transplantation from the AD patients promoted metabolic dysfunction in mice and increased gut permeability. H. pylori increased gut permeability through activation of the TLR4/Myd88 inflammation pathway in a p53-dependent manner, leading to metabolic dysfunction. Moreover, p53 deficiency reduced bile acid concentration, leading to an increased abundance of H. pylori colonization. Overall, these data identify H. pylori as a key promoter of ADinduced metabolic dysfunction.

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Section: Introductionmentioning

confidence: 99%

Helicobacter pylori and Alzheimer’s Disease-Related Metabolic Dysfunction: Activation of TLR4/Myd88 Inflammation Pathway from p53 Perspective and a Case Study of Low-Dose Radiation Intervention

Zhao

Shen

Zhou

et al. 2022

ACS Chem. Neurosci.

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“…In clinical applications, the miR-34 family is often used for cancer treatment (Hermeking 2010 ). However, as a key miRNA regulating programmed cell death, the miR-34 family’s function in neurodegenerative illnesses should not be overlooked (Bazrgar et al 2021 ). Pro-inflammatory, immune-mediated mechanisms are undeniably important in the pathogenesis and progression of neurodegenerative disease.…”

Section: The Role Of Endogenous Mirnasmentioning

confidence: 99%

The role of microRNAs in neurodegenerative diseases: a review

Lei

Sun

2022

Cell Biol Toxicol

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MicroRNAs (miRNAs) are non-coding RNAs which are essential post-transcriptional gene regulators in various neuronal degenerative diseases and playact a key role in these physiological progresses. Neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, multiple sclerosis, and, stroke, are seriously threats to the life and health of all human health and life kind. Recently, various studies have reported that some various miRNAs can regulate the development of neurodegenerative diseases as well as act as biomarkers to predict these neuronal diseases conditions. Endogenic miRNAs such as miR-9, the miR-29 family, miR-15, and the miR-34 family are generally dysregulated in animal and cell models. They are involved in regulating the physiological and biochemical processes in the nervous system by targeting regulating different molecular targets and influencing a variety of pathways. Additionally, exogenous miRNAs derived from homologous plants and defined as botanmin, such as miR2911 and miR168, can be taken up and transferred by other species to be and then act analogously to endogenic miRNAs to regulate the physiological and biochemical processes. This review summarizes the mechanism and principle of miRNAs in the treatment of some neurodegenerative diseases, as well as discusses several types of miRNAs which were the most commonly reported in diseases. These miRNAs could serve as a study provided some potential biomarkers in neurodegenerative diseases might be an ideal and/or therapeutic targets for neurodegenerative diseases. Finally, the role accounted of the prospective exogenous miRNAs involved in mammalian diseases is described. Graphical abstract 1. Listing a large number of neural-related miRNAs and sorting out their pathways. 2. Classify and sort miRNAs according to their mechanism of action. 3. Demonstrating the effects of up-regulation or down-regulation of each miRNAs on the nervous system.

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“…The expression changes in miRNAs may cause diseases. The miR-34c has been found upregulated in AD, with intracellular Aβ aggregation and tau hyperphosphorylation in different regions of the brain, together contributing to cognitive deficits (Bazrgar et al, 2021 ). A recent study shows that the upregulated miR-34c participates in the pathogenesis of AD via ROS/JNK/P53 pathway and the inhibition of miR-34c can improve memory decline in AD models (Shi et al, 2020 ).…”

Section: Alzheimer’s Diseasementioning

confidence: 99%

Deconvoluting the Complexity of Reactive Oxygen Species (ROS) in Neurodegenerative Diseases

et al. 2022

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Neurodegenerative diseases (NDs) are becoming a serious public health concern as the world’s population continues to age, demanding the discovery of more effective therapies. Excessive formation of reactive oxygen species (ROS) can result in oxidative stress (OS), which can be regarded as one of the common causes of neurodegenerative diseases (NDs). Thus, in this review, we focus on summarizing the consequences of ROS NDs, while taking the four prevalent NDs as examples, including Alzheimer’s disease (AD), Parkinson’s disease (PD), Amyotrophic lateral sclerosis (ALS), and Huntington’s disease (HD), to illustrate the key signaling pathways and relevant drugs. Together, these findings may shed new light on a field in which ROS-related pathways play a key role; thereby setting the groundwork for the future therapeutic development of neurodegenerative diseases.

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The role of microRNA-34 family in Alzheimer’s disease: A potential molecular link between neurodegeneration and metabolic disorders

Cited by 28 publications

References 223 publications

Helicobacter pylori and Alzheimer’s Disease-Related Metabolic Dysfunction: Activation of TLR4/Myd88 Inflammation Pathway from p53 Perspective and a Case Study of Low-Dose Radiation Intervention

Helicobacter pylori and Alzheimer’s Disease-Related Metabolic Dysfunction: Activation of TLR4/Myd88 Inflammation Pathway from p53 Perspective and a Case Study of Low-Dose Radiation Intervention

The role of microRNAs in neurodegenerative diseases: a review

Deconvoluting the Complexity of Reactive Oxygen Species (ROS) in Neurodegenerative Diseases

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