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.Citations
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CRISPR-Cas12a (Cpf1): A Versatile Tool in the Plant Genome Editing Tool Box for Agricultural Advancement.
Anindya Bandyopadhyay,Nagesh Kancharla,Vivek S. Javalkote,Santanu Dasgupta,Thomas P. Brutnell +4 more
TL;DR: A comparative survey of CRISPR-Cas12a and Cas9 is provided, and a perspective on applications of CRisPR- Cas12 in agriculture is provided.
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miR-34a in Neurophysiology and Neuropathology.
TL;DR: The known and emerging roles of the miR-34a regulatory network in neurophysiology and neuropathology are discussed and modulated by factors that control its expression as well as its downstream target genes and signaling pathways.
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Dexmedetomidine Provides Protection Against Hippocampal Neuron Apoptosis and Cognitive Impairment in Mice with Alzheimer’s Disease by Mediating the miR-129/YAP1/JAG1 Axis
Weiying Sun,Jun Zhao,Chunzhi Li +2 more
TL;DR: The findings showed that Dex administration resulted in the enhancement of miR-129 expression with declined hippocampal neuron apoptosis and attenuated cognitive impairment in Aβ1–42-injected mice, suggesting the miR -129/YAP1/JAG1 axis could potentially be the mechanism by which Dex protects AD mice from cognitive impairment.
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MicroRNA-7: expression and function in brain physiological and pathological processes
TL;DR: In-depth studies on the role of miR-7 in brain physiology and pathology undoubtedly not only provide a light on the roles of miRNAs in brain development and diseases, but also are much helpful for ultimate development of therapeutic strategies against brain diseases.
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Resveratrol-Selenium Nanoparticles Alleviate Neuroinflammation and Neurotoxicity in a Rat Model of Alzheimer’s Disease by Regulating Sirt1/miRNA-134/GSK3β Expression
Omayma A.R. AboZaid,M. W. Sallam,Sawsan M El-Sonbaty,Samy Ali Hussein Aziza,Basma Emad,Esraa S. A. Ahmed +5 more
TL;DR: N nano-formulation of resveratrol with selenium maximized the therapeutic potential of RSV against Alzheimer’s disease not only by their antioxidant but also by anti-inflammatory effect improving the neurocognitive function and modulating the signaling pathways.
References
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Journal ArticleDOI
Ubiquitin carboxy-terminal hydrolase L1 binds to and stabilizes monoubiquitin in neuron
Hitoshi Osaka,Yu Lai Wang,Koji Takada,Shuichi Takizawa,Rieko Setsuie,Hang Li,Yae Sato,Kaori Nishikawa,Ying Jie Sun,Mikako Sakurai,Takayuki Harada,Yoko Hara,Ichiro Kimura,Shigeru Chiba,Kazuhiko Namikawa,Hiroshi Kiyama,Mami Noda,Shunsuke Aoki,Keiji Wada +18 more
TL;DR: It is found that UCH L1 associates and colocalizes with monoubiquitin and elongates ubiquitin half-life and insures ubiquitIn stability within neurons.
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Angiotensin-converting Enzyme Degrades Alzheimer Amyloid β-Peptide (Aβ); Retards Aβ Aggregation, Deposition, Fibril Formation; and Inhibits Cytotoxicity
TL;DR: The hypothesis that ACE may affect susceptibility to AD by degrading Aβ and preventing the accumulation of amyloid plaques in vivo is proposed.
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Overexpression of ABCA1 reduces amyloid deposition in the PDAPP mouse model of Alzheimer disease
Suzanne E. Wahrle,Hong Jiang,Maia Parsadanian,Jungsu Kim,Aimin Li,Amanda Knoten,Sanjay Jain,Veronica Hirsch-Reinshagen,Cheryl L. Wellington,Kelly R. Bales,Steven M. Paul,David M. Holtzman +11 more
TL;DR: The conclusions that increased ABCA1-mediated lipidation of apoE in the CNS can reduce amyloid burden and that increasingABCA1 function may have a therapeutic effect on AD are supported.
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Lack of ABCA1 considerably decreases brain ApoE level and increases amyloid deposition in APP23 mice.
TL;DR: It is demonstrated that the targeted disruption of ABCA1 increases amyloid deposition in APP23 mice, and the effect is manifested by an increased level of Aβ immunoreactivity, as well as thioflavine S-positive plaques in brain parenchyma, and thus may be considered a therapeutic target in AD.
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Amyloid β-Protein Is Degraded by Cellular Angiotensin-converting Enzyme (ACE) and Elevated by an ACE Inhibitor
TL;DR: It is shown that ACE can lower the levels of secreted Aβ in living cells and that this effect is blocked by inhibiting the protease's activity with an ACE inhibitor.