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Potential microRNA-related targets in clearance pathways of amyloid-β: novel therapeutic approach for the treatment of Alzheimer's disease.

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TLDR
An overview on microRNAs that are involved in the Aβ cascade and their inhibitory impact on their target mRNAs whose products participate in Aβ clearance is discussed.

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Metformin in Alzheimer's disease: An overview of potential mechanisms, preclinical and clinical findings.

TL;DR: In this article , the authors summarize the relevant scientific literature on the effects of metformin on various aspects of Alzheimer's disease pathophysiology, such as amyloid-β (Aβ) production and clearance, tau phosphorylation, and neuroinflammation.
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Pharmacotranscriptomics of peptide drugs with neuroprotective properties.

TL;DR: The importance of noncoding RNAs in the regulation of these processes is shown and the prospects of research for determining the main mechanisms of peptide regulation are discussed, which is necessary for the further development of drugs with targeted neuroprotective effects.
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miR-143-3p Inhibits Aberrant Tau Phosphorylation and Amyloidogenic Processing of APP by Directly Targeting DAPK1 in Alzheimer’s Disease

TL;DR: The results suggest that miR-143-3p might play critical roles in regulating both aberrant tau phosphorylation and amyloidogenic processing of APP by targeting DAPK1 and thus offer a potential novel therapeutic strategy for AD.
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NEUBOrg: Artificially Induced Pluripotent Stem Cell-Derived Brain Organoid to Model and Study Genetics of Alzheimer's Disease Progression.

TL;DR: In this article, the authors have successfully developed and validated artificially induced whole brain organoid platform (NEUBOrg) using their previously validated machine learning platform, DeepNEU (v6.1). Using NEUBorg platform, they have generated aiWBO simulations of AD and provided a novel approach to test genetic risk factors associated with AD progression and pathogenesis.
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Neuroprotective Effects of Peptides in the Brain: Transcriptome Approach.

TL;DR: The results of studies on the ischemia-induced changes in the activity of genes and peptide-mediated alterations in the transcriptome profiles in experimental ischemian damage are presented and the basic principles of peptide regulation in the ischemical-induced damage are formulated.
References
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The Amyloid Hypothesis of Alzheimer's Disease: Progress and Problems on the Road to Therapeutics

TL;DR: It has been more than 10 years since it was first proposed that the neurodegeneration in Alzheimer's disease (AD) may be caused by deposition of amyloid β-peptide in plaques in brain tissue and the rest of the disease process is proposed to result from an imbalance between Aβ production and Aβ clearance.
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AMPK and mTOR regulate autophagy through direct phosphorylation of Ulk1

TL;DR: A molecular mechanism for regulation of the mammalian autophagy-initiating kinase Ulk1, a homologue of yeast ATG1, is demonstrated and a signalling mechanism for UlK1 regulation and autophagic induction in response to nutrient signalling is revealed.
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Amyloid plaque core protein in Alzheimer disease and Down syndrome

TL;DR: The shared 4-kDa subunit indicates a common origin for the amyloids of the plaque core and of the congophilic angiopathy of Alzheimer disease and Down syndrome.
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A paravascular pathway facilitates CSF flow through the brain parenchyma and the clearance of interstitial solutes, including amyloid β.

TL;DR: An anatomically distinct clearing system in the brain that serves a lymphatic-like function is described and may have relevance for understanding or treating neurodegenerative diseases that involve the mis-accumulation of soluble proteins, such as amyloid β in Alzheimer's disease.
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