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      Catalpol Mitigates Alzheimer's Disease Progression by Promoting the Expression of Neural Stem Cell Exosomes Released miR-138-5p

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          Abstract

          Alzheimer’s disease (Alzheimer’s disease, AD) is a neurodegenerative disease characterized by senile plaque deposition and neurofibrillary tangles. The pathogenesis of AD is complicated and the drugs used to treat AD are single-targeted drugs, which can only improve or alleviate the symptoms of patients, but cannot delay or prevent the progress of the disease. Because of its ability to act on multiple targets, multiple systems, multiple links, and multiple pathways, Chinese herbal compound prescriptions have shown unique advantages in the research and treatment of AD. Our previous study has demonstrated the protect role of the Chinese medicine Rehmannia in AD. However, the underlying mechanism remains unclear. In the present study, both in vitro and vivo experiments were employed, and we found Catalpol (Ca), the main extract of Rehmannia, could mitigate AD progression both in vitro and in vivo by promoting miR-138-5p level in neural stem cell secreted exosomes

          Supplementary Information

          The online version contains supplementary material available at 10.1007/s12640-022-00626-z.

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          Exosomes: composition, biogenesis and function

          Clotilde Théry, Laurence Zitvogel, Sebastian Amigorena (2002)
          Article 0 comments Cited 1100 times – based on 0 reviews     Review now
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            Comprehensive Review on Alzheimer’s Disease: Causes and Treatment

            Zeinab Breijyeh, Rafik Karaman (2020)
            Alzheimer’s disease (AD) is a disorder that causes degeneration of the cells in the brain and it is the main cause of dementia, which is characterized by a decline in thinking and independence in personal daily activities. AD is considered a multifactorial disease: two main hypotheses were proposed as a cause for AD, cholinergic and amyloid hypotheses. Additionally, several risk factors such as increasing age, genetic factors, head injuries, vascular diseases, infections, and environmental factors play a role in the disease. Currently, there are only two classes of approved drugs to treat AD, including inhibitors to cholinesterase enzyme and antagonists to N-methyl d-aspartate (NMDA), which are effective only in treating the symptoms of AD, but do not cure or prevent the disease. Nowadays, the research is focusing on understanding AD pathology by targeting several mechanisms, such as abnormal tau protein metabolism, β-amyloid, inflammatory response, and cholinergic and free radical damage, aiming to develop successful treatments that are capable of stopping or modifying the course of AD. This review discusses currently available drugs and future theories for the development of new therapies for AD, such as disease-modifying therapeutics (DMT), chaperones, and natural compounds.
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              Alzheimer’s disease: pathogenesis, diagnostics, and therapeutics

              Sneham Tiwari, Venkata Atluri, Ajeet Kaushik … (2019)
              Abstract Currently, 47 million people live with dementia globally, and it is estimated to increase more than threefold (~131 million) by 2050. Alzheimer’s disease (AD) is one of the major causative factors to induce progressive dementia. AD is a neurodegenerative disease, and its pathogenesis has been attributed to extracellular aggregates of amyloid β (Aβ) plaques and intracellular neurofibrillary tangles made of hyperphosphorylated τ-protein in cortical and limbic areas of the human brain. It is characterized by memory loss and progressive neurocognitive dysfunction. The anomalous processing of APP by β-secretases and γ-secretases leads to production of Aβ40 and Aβ42 monomers, which further oligomerize and aggregate into senile plaques. The disease also intensifies through infectious agents like HIV. Additionally, during disease pathogenesis, the presence of high concentrations of Aβ peptides in central nervous system initiates microglial infiltration. Upon coming into vicinity of Aβ, microglia get activated, endocytose Aβ, and contribute toward their clearance via TREM2 surface receptors, simultaneously triggering innate immunoresponse against the aggregation. In addition to a detailed report on causative factors leading to AD, the present review also discusses the current state of the art in AD therapeutics and diagnostics, including labeling and imaging techniques employed as contrast agents for better visualization and sensing of the plaques. The review also points to an urgent need for nanotechnology as an efficient therapeutic strategy to increase the bioavailability of drugs in the central nervous system.
              Article 0 comments Cited 349 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Shengxi Meng: mengsx163@163.com
                Journal
                Journal ID (nlm-ta): Neurotox Res
                Journal ID (iso-abbrev): Neurotox Res
                Title: Neurotoxicity Research
                Publisher: Springer US (New York )
                ISSN (Print): 1029-8428
                ISSN (Electronic): 1476-3524
                Publication date (Electronic): 3 January 2023
                Publication date PMC-release: 3 January 2023
                Publication date (Print): 2023
                Volume: 41
                Issue: 1
                Pages: 41-56
                Affiliations
                [1 ]GRID grid.16821.3c, ISNI 0000 0004 0368 8293, Department of Traditional Chinese Medicine, , Shanghai Sixth People’s Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, ; Xuhui District, No.600 Yi Shan Road, Shanghai, 200233 China
                [2 ]GRID grid.412068.9, ISNI 0000 0004 1759 8782, Second  Clinical  Medicine  College, , Heilongjiang University of Chinese Medicine, ; Harbin, 150040 China
                Article
                Publisher ID: 626
                DOI: 10.1007/s12640-022-00626-z
                PMC ID: 9944361
                PubMed ID: 36595161
                SO-VID: 50baa00c-cfed-4584-8a3f-e36ce50adec1
                Copyright © © The Author(s) 2022
                License:

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

                History
                Date received : 13 May 2022
                Date revision received : 11 August 2022
                Date accepted : 16 December 2022
                Funding
                Funded by: the Project of Shanghai Science and Technology Commission
                Award ID: 19401970600
                Award Recipient :
                Categories
                Subject: Research Article
                Custom metadata
                issue-copyright-statement © Springer Science+Business Media, LLC, part of Springer Nature 2023

                ScienceOpen disciplines: Neurosciences
                Keywords: alzheimer’s disease,catalpol,neural stem cell,exosomes,mir-138-5p
                Data availability:
                ScienceOpen disciplines: Neurosciences
                Keywords: alzheimer’s disease, catalpol, neural stem cell, exosomes, mir-138-5p

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