CoChat
Sign Up
Cited by 25

The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.

Small Extracellular Vesicles’ miRNAs: Biomarkers and Therapeutics for Neurodegenerative Diseases

Lim, Wei Qing, Michelle Luk, Kie Hoon, Lee, Kah Yee, Nurul, Nasuha, Loh, Sin Jade, Yeow, Zhen Xiong, Wong, Qi Xuan, Daniel Looi, Qi Hao, Chong, Pan Pan, How, Chee Wun, Hamzah, Sharina, Foo, Jhi Biau·2023·Pharmaceutics
DOI 10.3390/pharmaceutics15041216PMC PMC10143523
Open this paper in CoChat — free account

Abstract

Neurodegenerative diseases are critical in the healthcare system as patients suffer from progressive diseases despite currently available drug management. Indeed, the growing ageing population will burden the country’s healthcare system and the caretakers. Thus, there is a need for new management that could stop or reverse the progression of neurodegenerative diseases. Stem cells possess a remarkable regenerative potential that has long been investigated to resolve these issues. Some breakthroughs have been achieved thus far to replace the damaged brain cells; however, the procedure’s invasiveness has prompted scientists to investigate using stem-cell small extracellular vesicles (sEVs) as a non-invasive cell-free therapy to address the limitations of cell therapy. With the advancement of technology to understand the molecular changes of neurodegenerative diseases, efforts have been made to enrich stem cells’ sEVs with miRNAs to increase the therapeutic efficacy of the sEVs. In this article, the pathophysiology of various neurodegenerative diseases is highlighted. The role of miRNAs from sEVs as biomarkers and treatments is also discussed. Lastly, the applications and delivery of stem cells and their miRNA-enriched sEVs for treating neurodegenerative diseases are emphasised and reviewed.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.3390/pharmaceutics15041216

Cites

11 of 11 references verified0 citation errors · 0 not checkable

Statistics

Figures

Figure 1 Pathophysiology of Alzheimer’s and Parkinson’s disease. Generally, the formation of amyloid-β plaques and neurofibrillary tangles results in neuron loss and degeneration. This triggers an uncontrolled immune response resulting in BBB leakage and neuroinflammation (created with BioRender.com) (accessed on 3 January 2023).
Figure 1 Pathophysiology of Alzheimer’s and Parkinson’s disease. Generally, the formation of amyloid-β plaques and neurofibrillary tangles results in neuron loss and degeneration. This triggers an uncontrolled immune response resulting in BBB leakage and neuroinflammation (created with BioRender.com) (accessed on 3 January 2023).CC BY · PubMed Central
Figure 2 Pathophysiology of Huntington’s disease. In the early stage, the aggregates delay axonal transport, resulting in a failed delivery of GABA(A), which inhibits the synaptic excitability of the subthalamic nucleus. As a result, the compensatory mechanism of the thalamus leads to hyperkinesia. In the late stage, the trafficking of NMDA receptors in striatal neurons is affected and may cause an imbalance between synaptic and extrasynaptic NMDA receptors. This leads to excitotoxicity either due to increased glutamate or impaired uptake and clearance. Ultimately, bradykinesia is observed (created with BioRender.com) (accessed on 5 January 2023).
Figure 2 Pathophysiology of Huntington’s disease. In the early stage, the aggregates delay axonal transport, resulting in a failed delivery of GABA(A), which inhibits the synaptic excitability of the subthalamic nucleus. As a result, the compensatory mechanism of the thalamus leads to hyperkinesia. In the late stage, the trafficking of NMDA receptors in striatal neurons is affected and may cause an imbalance between synaptic and extrasynaptic NMDA receptors. This leads to excitotoxicity either due to increased glutamate or impaired uptake and clearance. Ultimately, bradykinesia is observed (created with BioRender.com) (accessed on 5 January 2023).CC BY · PubMed Central
Figure 3 Pathophysiology of amyotrophic lateral sclerosis. The dying forward hypothesis states that ALS results in anterograde corticomotor neuron degeneration. In the dying back hypothesis, mutations in the TDP-43, c9orf72, and FUS genes form intracellular neuronal aggregates. The independent degeneration hypothesis argues that upper and lower motor neuron degeneration occurs independently (created with BioRender.com) (accessed on 8 January 2023).
Figure 3 Pathophysiology of amyotrophic lateral sclerosis. The dying forward hypothesis states that ALS results in anterograde corticomotor neuron degeneration. In the dying back hypothesis, mutations in the TDP-43, c9orf72, and FUS genes form intracellular neuronal aggregates. The independent degeneration hypothesis argues that upper and lower motor neuron degeneration occurs independently (created with BioRender.com) (accessed on 8 January 2023).CC BY · PubMed Central
Figure 4 The ability of sEVs’ miRNAs to cross the blood-brain barrier presents an opportunity to correct endogenous miRNAs’ levels through miRNAs/anti-miRNAs treatment (created with BioRender.com) (accessed on 13 January 2023).
Figure 4 The ability of sEVs’ miRNAs to cross the blood-brain barrier presents an opportunity to correct endogenous miRNAs’ levels through miRNAs/anti-miRNAs treatment (created with BioRender.com) (accessed on 13 January 2023).CC BY · PubMed Central
Figure 5 miRNA-enriched sEVs can be transmitted to target cells via three methods which are fusion, endocytosis, and receptor–ligand interactions (created with BioRender.com) (accessed on 13 January 2023).
Figure 5 miRNA-enriched sEVs can be transmitted to target cells via three methods which are fusion, endocytosis, and receptor–ligand interactions (created with BioRender.com) (accessed on 13 January 2023).CC BY · PubMed Central
Figure 6 Advantages and disadvantages of miRNA-enriched small extracellular vesicles.
Figure 6 Advantages and disadvantages of miRNA-enriched small extracellular vesicles.CC BY · PubMed Central

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

1 retracted

Research works printed but not linked: 143

  1. Rekatsina, 2020, Pathophysiology and Therapeutic Perspectives of Oxidative Stress and Neurodegenerative Diseases: A Narrative Review, Adv. Ther., 37, 113, 10.1007/s12325-019-01148-5 · DOI
  2. Fayazi, 2021, Stem Cell-Derived Exosomes: A New Strategy of Neurodegenerative Disease Treatment, Mol. Neurobiol., 58, 3494, 10.1007/s12035-021-02324-x · DOI
  3. Parambi, 2022, Gene Therapy Approach with an Emphasis on Growth Factors: Theoretical and Clinical Outcomes in Neurodegenerative Diseases, Mol. Neurobiol., 59, 191, 10.1007/s12035-021-02555-y · DOI
  4. Muddapu, 2020, Neurodegenerative Diseases–Is Metabolic Deficiency the Root Cause?, Front. Neurosci., 14, 213, 10.3389/fnins.2020.00213 · DOI
  5. Whalen, K. (2014). Pharmacology, Lippincott Williams & Wilkins.
  6. Ogbodo, 2022, Alzheimer’s Disease: Pathogenesis and Therapeutic Interventions, Curr. Aging Sci., 15, 2, 10.2174/1874609814666210302085232 · DOI
  7. Kim, 2021, Efficacy and tolerability of aripiprazole versus D2 antagonists in the early course of schizophrenia: A systematic review and meta-analysis, Npj Schizophr., 7, 29, 10.1038/s41537-021-00158-z · DOI
  8. Ferrini, 2021, Persistency of Mesenchymal Stromal/Stem Cells in Lungs, Front. Cell Dev. Biol., 9, 1825, 10.3389/fcell.2021.709225 · DOI
  9. Wang, 2015, Excess Integrins Cause Lung Entrapment of Mesenchymal Stem Cells, Stem Cells, 33, 3315, 10.1002/stem.2087 · DOI
  10. Witwer, 2018, Minimal information for studies of extracellular vesicles 2018 (MISEV2018): A position statement of the International Society for Extracellular Vesicles and update of the MISEV2014 guidelines, J. Extracell. Vesicles, 7, 1535750, 10.1080/20013078.2018.1535750 · DOI · Paper page
  11. Abdelaal, N.E., and Abdelhai, M.F. (2021). Role of Exosomes in Biological Communication Systems, Springer.
  12. Beatriz, 2021, Exosomes: Innocent Bystanders or Critical Culprits in Neurodegenerative Diseases, Front. Cell Dev. Biol., 9, 635104, 10.3389/fcell.2021.635104 · DOI
  13. Takahashi, 2023, Extracellular vesicle-based therapeutics: Extracellular vesicles as therapeutic targets and agents, Pharmacol. Ther., 242, 108352, 10.1016/j.pharmthera.2023.108352 · DOI
  14. Sarvar, 2016, Mesenchymal stem cell-derived exosomes: New opportunity in cell-free therapy, Adv. Pharm. Bull., 6, 293, 10.15171/apb.2016.041 · DOI
  15. Yang, 2019, MiR-124 Enriched Exosomes Promoted the M2 Polarization of Microglia and Enhanced Hippocampus Neurogenesis After Traumatic Brain Injury by Inhibiting TLR4 Pathway, Neurochem. Res., 44, 811, 10.1007/s11064-018-02714-z · DOI · Paper page
  16. Salarpour, 2022, The application of exosomes and Exosome-nanoparticle in treating brain disorders, J. Mol. Liq., 350, 118549, 10.1016/j.molliq.2022.118549 · DOI
  17. Alzheimer, 1906, Uber einen eigenartigen schweren Erkrankungsprozess der Hirninde, Neurol. Cent., 25, 1134
  18. Inga, Z. (2015). Alzheimer’s Disease, IntechOpen. Chapter 10.
  19. Chow, 2014, CDK5 activator protein p25 preferentially binds and activates GSK3β, Proc. Natl. Acad. Sci. USA, 111, E4887, 10.1073/pnas.1402627111 · DOI
  20. Bourdenx, 2017, Protein aggregation and neurodegeneration in prototypical neurodegenerative diseases: Examples of amyloidopathies, tauopathies and synucleinopathies, Prog. Neurobiol., 155, 171, 10.1016/j.pneurobio.2015.07.003 · DOI
  21. Singh, A., Kukreti, R., Saso, L., and Kukreti, S. (2019). Oxidative Stress: A Key Modulator in Neurodegenerative Diseases. Molecules, 24. · DOI
  22. Neniskyte, 2017, Errant gardeners: Glial-cell-dependent synaptic pruning and neurodevelopmental disorders, Nat. Rev. Neurosci., 18, 658, 10.1038/nrn.2017.110 · DOI
  23. Actor, J.K., and Smith, K.C. (2019). Translational Inflammation, Academic Press. · DOI
  24. Zuroff, 2017, Clearance of cerebral Aβ in Alzheimer’s disease: Reassessing the role of microglia and monocytes, Cell. Mol. Life Sci., 74, 2167, 10.1007/s00018-017-2463-7 · DOI
  25. Wang, 2015, TREM2 lipid sensing sustains the microglial response in an Alzheimer’s disease model, Cell, 160, 1061, 10.1016/j.cell.2015.01.049 · DOI · Paper page
  26. Khan, 2019, Awareness and current knowledge of Parkinson’s disease: A neurodegenerative disorder, Int. J. Neurosci., 129, 55, 10.1080/00207454.2018.1486837 · DOI
  27. Parashos, S.A., and Wichmann, R. (2020). Navigating Life with Parkinson’s Disease, Oxford University Press. [2nd ed.].
  28. Bellucci, 2020, Nuclear Factor-κB Dysregulation and α-Synuclein Pathology: Critical Interplay in the Pathogenesis of Parkinson’s Disease, Front. Aging Neurosci., 12, 68, 10.3389/fnagi.2020.00068 · DOI
  29. Ma, 2018, C-terminal truncation exacerbates the aggregation and cytotoxicity of α-Synuclein: A vicious cycle in Parkinson’s disease, Biochim. Biophys. Acta (BBA) Mol. Basis Dis., 1864, 3714, 10.1016/j.bbadis.2018.10.003 · DOI
  30. Sato, 2011, Authentically phosphorylated α-synuclein at Ser129 accelerates neurodegeneration in a rat model of familial Parkinson’s disease, J. Neurosci., 31, 16884, 10.1523/JNEUROSCI.3967-11.2011 · DOI
  31. Park, 2011, Elevated levels of α-synuclein oligomer in the cerebrospinal fluid of drug-naïve patients with Parkinson’s disease, J. Clin. Neurol., 7, 215, 10.3988/jcn.2011.7.4.215 · DOI
  32. Jones, R. (2010). The roles of PINK1 and Parkin in Parkinson’s disease. PLoS Biol., 8. · DOI
  33. Behl, 2022, Exploring the Role of Ubiquitin–Proteasome System in Parkinson’s Disease, Mol. Neurobiol., 59, 4257, 10.1007/s12035-022-02851-1 · DOI
  34. Liu, 2022, Deubiquitinating enzymes (DUBs): Decipher underlying basis of neurodegenerative diseases, Mol. Psychiatry, 27, 259, 10.1038/s41380-021-01233-8 · DOI
  35. Zhang, 2022, MANF Inhibits α-Synuclein Accumulation through Activation of Autophagic Pathways, Oxid. Med. Cell. Longev., 2022, 7925686
  36. Wilkaniec, 2021, Exogenous Alpha-Synuclein Evoked Parkin Downregulation Promotes Mitochondrial Dysfunction in Neuronal Cells. Implications for Parkinson’s Disease Pathology, Front. Aging Neurosci., 13, 591475, 10.3389/fnagi.2021.591475 · DOI
  37. Stoker, T.B., and Greenland, J.C. (2018). Parkinson’s Disease: Pathogenesis and Clinical Aspects, Codon Publications. · DOI
  38. Stoker, 2022, Huntington’s disease: Diagnosis and management, Pract. Neurol., 22, 32, 10.1136/practneurol-2021-003074 · DOI
  39. Licitra, 2017, Huntington’s Disease: Mechanisms of Pathogenesis and Therapeutic Strategies, Cold Spring Harb. Perspect. Med., 7, a024240, 10.1101/cshperspect.a024240 · DOI
  40. Kostrzewa, R.M. (2021). Handbook of Neurotoxicity, Springer International Publishing. · DOI
  41. Carmo, 2018, Mitochondrial Dysfunction in Huntington’s Disease, Adv. Exp. Med. Biol., 1049, 59, 10.1007/978-3-319-71779-1_3 · DOI
  42. Paul, 2014, Cystathionine γ-lyase deficiency mediates neurodegeneration in Huntington’s disease, Nature, 509, 96, 10.1038/nature13136 · DOI
  43. Catanesi, M., d’Angelo, M., Tupone, M.G., Benedetti, E., Giordano, A., Castelli, V., and Cimini, A. (2020). MicroRNAs Dysregulation and Mitochondrial Dysfunction in Neurodegenerative Diseases. Int. J. Mol. Sci., 21. · DOI
  44. Buren, C. (2017). Global Neuroprotection of Huntingtin in Culture and Alterations of Cortico-Striatal Connections in Huntington’s Disease Culture and Mouse Models. [Ph.D. Thesis, University of British Columbia].
  45. Raymond, 2011, Pathophysiology of Huntington’s disease: Time-dependent alterations in synaptic and receptor function, Neuroscience, 198, 252, 10.1016/j.neuroscience.2011.08.052 · DOI
  46. Watanabe, 2022, Impaired neuromuscular transmission in facial muscles of amyotrophic lateral sclerosis: A single-fiber electromyography study, Neurol. Clin. Neurosci., 10, 78, 10.1111/ncn3.12580 · DOI
  47. Satarker, S., Bojja, S.L., Gurram, P.C., Mudgal, J., Arora, D., and Nampoothiri, M. (2022). Astrocytic Glutamatergic Transmission and Its Implications in Neurodegenerative Disorders. Cells, 11. · DOI
  48. Didonna, 2019, The role of neurofilament aggregation in neurodegeneration: Lessons from rare inherited neurological disorders, Mol. Neurodegener., 14, 19, 10.1186/s13024-019-0318-4 · DOI
  49. Van den Bos, M.A.J., Geevasinga, N., Higashihara, M., Menon, P., and Vucic, S. (2019). Pathophysiology and Diagnosis of ALS: Insights from Advances in Neurophysiological Techniques. Int. J. Mol. Sci., 20. · DOI
  50. He, 2021, Diagnostic and Therapeutic Potential of Exosomal MicroRNAs for Neurodegenerative Diseases, Neural Plast., 2021, 8884642, 10.1155/2021/8884642 · DOI
  51. Matsumoto, 2017, Transmission of α-synuclein-containing erythrocyte-derived extracellular vesicles across the blood-brain barrier via adsorptive mediated transcytosis: Another mechanism for initiation and progression of Parkinson’s disease?, Acta Neuropathol. Commun., 5, 71, 10.1186/s40478-017-0470-4 · DOI · Paper page
  52. Manna, I., De Benedittis, S., Quattrone, A., Maisano, D., Iaccino, E., and Quattrone, A. (2020). Exosomal miRNAs as Potential Diagnostic Biomarkers in Alzheimer’s Disease. Pharmaceuticals, 13. · DOI
  53. Mathew, B., Mansuri, M.S., Williams, K.R., and Nairn, A.C. (2021). Exosomes as Emerging Biomarker Tools in Neurodegenerative and Neuropsychiatric Disorders-A Proteomics Perspective. Brain Sci., 11. · DOI
  54. Cheng, 2014, Exosomes provide a protective and enriched source of miRNA for biomarker profiling compared to intracellular and cell-free blood, J. Extracell. Vesicles, 3, 23743, 10.3402/jev.v3.23743 · DOI · Paper page
  55. Fenoglio, 2019, Exosome Determinants of Physiological Aging and Age-Related Neurodegenerative Diseases, Front. Aging Neurosci., 11, 232, 10.3389/fnagi.2019.00232 · DOI · Paper page
  56. Kumar, 2016, Are circulating microRNAs peripheral biomarkers for Alzheimer’s disease?, Biochim. Biophys. Acta, 1862, 1617, 10.1016/j.bbadis.2016.06.001 · DOI
  57. Thomi, 2019, Exosomes derived from umbilical cord mesenchymal stem cells reduce microglia-mediated neuroinflammation in perinatal brain injury, Stem Cell Res. Ther., 10, 105, 10.1186/s13287-019-1207-z · DOI
  58. Foo, J.B., Looi, Q.H., How, C.W., Lee, S.H., Al-Masawa, M.E., Chong, P.P., and Law, J.X. (2021). Mesenchymal Stem Cell-Derived Exosomes and MicroRNAs in Cartilage Regeneration: Biogenesis, Efficacy, miRNA Enrichment and Delivery. Pharmaceuticals, 14. · DOI
  59. Markoutsa, 2022, Extracellular vesicles derived from inflammatory-educated stem cells reverse brain inflammation-implication of miRNAs, Mol. Ther., 30, 816, 10.1016/j.ymthe.2021.08.008 · DOI
  60. Chen, 2021, Exosomal Proteins and miRNAs as Mediators of Amyotrophic Lateral Sclerosis, Front. Cell Dev. Biol., 9, 718803, 10.3389/fcell.2021.718803 · DOI
  61. Yang, 2017, Exosome Mediated Delivery of miR-124 Promotes Neurogenesis after Ischemia, Mol. Ther. Nucleic Acids, 7, 278, 10.1016/j.omtn.2017.04.010 · DOI · Paper page
  62. Cheng, 2009, MiR-124 Regulates Adult Neurogenesis in the Subventricular Zone Stem Cell Niche, Nat. Neurosci., 12, 399, 10.1038/nn.2294 · DOI · Paper page
  63. Yu, 2011, MicroRNA miR-133b is essential for functional recovery after spinal cord injury in adult zebrafish, Eur. J. Neurosci., 33, 1587, 10.1111/j.1460-9568.2011.07643.x · DOI
  64. Xin, 2017, MicroRNA cluster miR-17–92 Cluster in Exosomes Enhance Neuroplasticity and Functional Recovery After Stroke in Rats, Stroke, 48, 747, 10.1161/STROKEAHA.116.015204 · DOI
  65. Zuo, 2019, MicroRNA-132 attenuates cerebral injury by protecting blood-brain-barrier in MCAO mice, Exp. Neurol., 316, 12, 10.1016/j.expneurol.2019.03.017 · DOI
  66. Ma, 2014, MiR-181a Regulates Blood-Tumor Barrier Permeability by Targeting Krüppel-Like Factor 6, J. Cereb. Blood Flow Metab., 34, 1826, 10.1038/jcbfm.2014.152 · DOI
  67. Yu, 2019, Exosomes derived from microRNA-199a-overexpressing mesenchymal stem cells inhibit glioma progression by down-regulating AGAP2, Aging, 11, 5300, 10.18632/aging.102092 · DOI
  68. Li, 2019, MiR-199a Inhibits Tumor Growth and Attenuates Chemoresistance by Targeting K-RAS via AKT and ERK Signalings, Front. Oncol., 9, 1071, 10.3389/fonc.2019.01071 · DOI
  69. Wang, 2021, Challenges in the development and establishment of exosome-based drug delivery systems, J. Control. Release, 329, 894, 10.1016/j.jconrel.2020.10.020 · DOI
  70. Wang, 2014, The role of miR-146a in dorsal root ganglia neurons of experimental diabetic peripheral neuropathy, Neuroscience, 259, 155, 10.1016/j.neuroscience.2013.11.057 · DOI
  71. Wang, 2020, The Role of Exosomal microRNAs and Oxidative Stress in Neurodegenerative Diseases, Oxid. Med. Cell. Longev., 2020, 3232869, 10.1155/2020/3232869 · DOI
  72. Yu, 2021, The role of exosomal microRNAs in central nervous system diseases, Mol. Cell. Biochem., 476, 2111, 10.1007/s11010-021-04053-0 · DOI
  73. Bolukbasi, 2012, miR-1289 and “Zipcode”-like Sequence Enrich mRNAs in Microvesicles, Mol. Ther. Nucleic Acids, 1, e10, 10.1038/mtna.2011.2 · DOI
  74. Hooper, C., Sainz-Fuertes, R., Lynham, S., Hye, A., Killick, R., Warley, A., Bolondi, C., Pocock, J., and Lovestone, S. (2012). Wnt3a induces exosome secretion from primary cultured rat microglia. BMC Neurosci., 13. · DOI
  75. Trindade, 2021, Diagnostic and therapeutic potential of exosomes in Alzheimer’s disease, J. Neurochem., 156, 162, 10.1111/jnc.15112 · DOI
  76. Cui, 2017, Exosomes derived from hypoxia-preconditioned mesenchymal stromal cells ameliorate cognitive decline by rescuing synaptic dysfunction and regulating inflammatory responses in APP/PS1 mice, FASEB J., 32, 654, 10.1096/fj.201700600R · DOI · Paper page
  77. Cai, 2018, Exosomes: A novel therapeutic target for Alzheimer’s disease?, Neural Regen. Res., 13, 930, 10.4103/1673-5374.232490 · DOI
  78. Katsuda, 2013, Human adipose tissue-derived mesenchymal stem cells secrete functional neprilysin-bound exosomes, Sci. Rep., 3, 1197, 10.1038/srep01197 · DOI
  79. Shen, 2018, MiR-125b-5p is involved in oxygen and glucose deprivation injury in PC-12 cells via CBS/H(2)S pathway, Nitric Oxide, 78, 11, 10.1016/j.niox.2018.05.004 · DOI
  80. Sharples, 2008, Inhibition of gamma-secretase causes increased secretion of amyloid precursor protein C-terminal fragments in association with exosomes, FASEB J., 22, 1469, 10.1096/fj.07-9357com · DOI
  81. Yuyama, 2014, Decreased amyloid-β pathologies by intracerebral loading of glycosphingolipid-enriched exosomes in Alzheimer model mice, J. Biol. Chem., 289, 24488, 10.1074/jbc.M114.577213 · DOI
  82. Falker, 2016, Exosomal cellular prion protein drives fibrillization of amyloid beta and counteracts amyloid beta-mediated neurotoxicity, J. Neurochem., 137, 88, 10.1111/jnc.13514 · DOI
  83. Xin, 2012, Exosome-mediated transfer of miR-133b from multipotent mesenchymal stromal cells to neural cells contributes to neurite outgrowth, Stem Cells, 30, 1556, 10.1002/stem.1129 · DOI
  84. Ba, 2015, Schisandrin B shows neuroprotective effect in 6-OHDA-induced Parkinson’s disease via inhibiting the negative modulation of miR-34a on Nrf2 pathway, Biomed. Pharm., 75, 165, 10.1016/j.biopha.2015.07.034 · DOI
  85. Narbute, 2019, Intranasal Administration of Extracellular Vesicles Derived from Human Teeth Stem Cells Improves Motor Symptoms and Normalizes Tyrosine Hydroxylase Expression in the Substantia Nigra and Striatum of the 6-Hydroxydopamine-Treated Rats, Stem Cells Transl. Med., 8, 490, 10.1002/sctm.18-0162 · DOI · Paper page
  86. Mao, 2015, Secreted miR-34a in astrocytic shedding vesicles enhanced the vulnerability of dopaminergic neurons to neurotoxins by targeting Bcl-2, Protein Cell, 6, 529, 10.1007/s13238-015-0168-y · DOI · Paper page
  87. Chen, 2019, Activation of the miR-34a-Mediated SIRT1/mTOR Signaling Pathway by Urolithin A Attenuates D-Galactose-Induced Brain Aging in Mice, Neurotherapeutics, 16, 1269, 10.1007/s13311-019-00753-0 · DOI
  88. Jiang, 2019, Serum secreted miR-137-containing exosomes affects oxidative stress of neurons by regulating OXR1 in Parkinson’s disease, Brain Res., 1722, 146331, 10.1016/j.brainres.2019.146331 · DOI
  89. Oh, 2017, The Cleavage Effect of Mesenchymal Stem Cell and Its Derived Matrix Metalloproteinase-2 on Extracellular α-Synuclein Aggregates in Parkinsonian Models, Stem Cells Transl. Med., 6, 949, 10.5966/sctm.2016-0111 · DOI
  90. Lee, 2021, Exosomes as a potential messenger unit during heterochronic parabiosis for amelioration of Huntington’s disease, Neurobiol. Dis., 155, 105374, 10.1016/j.nbd.2021.105374 · DOI
  91. Lee, 2016, Exosomes from adipose-derived stem cells ameliorate phenotype of Huntington’s disease in vitro model, Eur. J. Neurosci., 44, 2114, 10.1111/ejn.13275 · DOI · Paper page
  92. Jeon, 2016, Human-to-mouse prion-like propagation of mutant huntingtin protein, Acta Neuropathol., 132, 577, 10.1007/s00401-016-1582-9 · DOI
  93. Das, 2013, MicroRNA-124 targets CCNA2 and regulates cell cycle in STHdh(Q111)/Hdh(Q111) cells, Biochem. Biophys. Res. Commun., 437, 217, 10.1016/j.bbrc.2013.06.041 · DOI
  94. Lee, 2017, Exosome-Based Delivery of miR-124 in a Huntington’s Disease Model, J. Mov. Disord., 10, 45, 10.14802/jmd.16054 · DOI · Paper page
  95. Ananbeh, H., Vodicka, P., and Kupcova Skalnikova, H. (2021). Emerging Roles of Exosomes in Huntington’s Disease. Int. J. Mol. Sci., 22. · DOI
  96. Rizzuti, 2018, MicroRNA expression analysis identifies a subset of downregulated miRNAs in ALS motor neuron progenitors, Sci. Rep., 8, 10105, 10.1038/s41598-018-28366-1 · DOI
  97. Pusic, 2014, IFNγ-stimulated dendritic cell exosomes as a potential therapeutic for remyelination, J. Neuroimmunol., 266, 12, 10.1016/j.jneuroim.2013.10.014 · DOI
  98. Derkus, 2017, A new approach in stem cell research—Exosomes: Their mechanism of action via cellular pathways, Cell Biol. Int., 41, 466, 10.1002/cbin.10742 · DOI
  99. Lugli, G., Cohen, A.M., Bennett, D.A., Shah, R.C., Fields, C.J., Hernandez, A.G., and Smalheiser, N.R. (2015). Plasma Exosomal miRNAs in Persons with and without Alzheimer Disease: Altered Expression and Prospects for Biomarkers. PLoS ONE, 10. · DOI · Paper page
  100. Barbagallo, 2020, Specific Signatures of Serum miRNAs as Potential Biomarkers to Discriminate Clinically Similar Neurodegenerative and Vascular-Related Diseases, Cell. Mol. Neurobiol., 40, 531, 10.1007/s10571-019-00751-y · DOI
  101. Yang, 2018, The Serum Exosome Derived MicroRNA−135a, −193b, and −384 Were Potential Alzheimer’s Disease Biomarkers, Biomed. Environ. Sci., 31, 87
  102. Liu, 2014, MicroRNA-193b is a regulator of amyloid precursor protein in the blood and cerebrospinal fluid derived exosomal microRNA-193b is a biomarker of Alzheimer’s disease, Mol. Med. Rep., 10, 2395, 10.3892/mmr.2014.2484 · DOI · Paper page
  103. Riancho, 2017, MicroRNA Profile in Patients with Alzheimer’s Disease: Analysis of miR-9–5p and miR-598 in Raw and Exosome Enriched Cerebrospinal Fluid Samples, J. Alzheimer’s Dis., 57, 483, 10.3233/JAD-161179 · DOI · Paper page
  104. Yao, 2018, Circulating exosomal miRNAs as diagnostic biomarkers in Parkinson’s disease, Eur. Rev. Med. Pharmacol. Sci., 22, 5278
  105. Gui, 2015, Altered microRNA profiles in cerebrospinal fluid exosome in Parkinson disease and Alzheimer disease, Oncotarget, 6, 37043, 10.18632/oncotarget.6158 · DOI · Paper page
  106. Xu, 2018, Comparison of the extraction and determination of serum exosome and miRNA in serum and the detection of miR-27a-3p in serum exosome of ALS patients, Intractable Rare Dis. Res., 7, 13, 10.5582/irdr.2017.01091 · DOI
  107. Freischmidt, 2013, Systemic dysregulation of TDP-43 binding microRNAs in amyotrophic lateral sclerosis, Acta Neuropathol. Commun., 1, 42, 10.1186/2051-5960-1-42 · DOI
  108. Toh, 2018, MSC exosome works through a protein-based mechanism of action, Biochem. Soc. Trans., 46, 843, 10.1042/BST20180079 · DOI
  109. Albanese, M., Chen, Y.A., Hüls, C., Gärtner, K., Tagawa, T., Mejias-Perez, E., Keppler, O.T., Göbel, C., Zeidler, R., and Shein, M. (2021). MicroRNAs are minor constituents of extracellular vesicles that are rarely delivered to target cells. PLoS Genet., 17. · DOI
  110. Chevillet, 2014, Quantitative and stoichiometric analysis of the microRNA content of exosomes, Proc. Natl. Acad. Sci. USA, 111, 14888, 10.1073/pnas.1408301111 · DOI
  111. Song, 2017, Exosomal miR-146a Contributes to the Enhanced Therapeutic Efficacy of Interleukin-1β-Primed Mesenchymal Stem Cells Against Sepsis, Stem Cells, 35, 1208, 10.1002/stem.2564 · DOI
  112. Tejeda-Mora, H., Leon, L.G., Demmers, J., Baan, C.C., Reinders, M.E.J., Bleck, B., Lombardo, E., Merino, A., and Hoogduijn, M.J. (2021). Proteomic Analysis of Mesenchymal Stromal Cell-Derived Extracellular Vesicles and Reconstructed Membrane Particles. Int. J. Mol. Sci., 22. · DOI
  113. Akbari, 2020, Free and hydrogel encapsulated exosome-based therapies in regenerative medicine, Life Sci., 249, 117447, 10.1016/j.lfs.2020.117447 · DOI
  114. Cui, 2019, RVG-modified exosomes derived from mesenchymal stem cells rescue memory deficits by regulating inflammatory responses in a mouse model of Alzheimer’s disease, Immun. Ageing, 16, 10, 10.1186/s12979-019-0150-2 · DOI
  115. Haney, 2015, Exosomes as drug delivery vehicles for Parkinson’s disease therapy, J. Control. Release, 207, 18, 10.1016/j.jconrel.2015.03.033 · DOI · Paper page
  116. Liu, 2017, Integration of stem cell-derived exosomes with in situ hydrogel glue as a promising tissue patch for articular cartilage regeneration, Nanoscale, 9, 4430, 10.1039/C7NR00352H · DOI
  117. Tejedor, 2017, The Effect of Stereotactic Injections on Demyelination and Remyelination: A Study in the Cuprizone Model, J. Mol. Neurosci., 61, 479, 10.1007/s12031-017-0888-y · DOI
  118. Neffendorf, 2015, Stereotactic radiotherapy for wet age-related macular degeneration: Current perspectives, Clin. Ophthalmol., 9, 1829
  119. Kim, 2015, Stereotactic brain injection of human umbilical cord blood mesenchymal stem cells in patients with Alzheimer’s disease dementia: A phase 1 clinical trial, Alzheimers Dement., 1, 95, 10.1016/j.trci.2015.06.007 · DOI
  120. Bors, 2018, Evaluation of intranasal delivery route of drug administration for brain targeting, Brain Res. Bull., 143, 155, 10.1016/j.brainresbull.2018.10.009 · DOI
  121. Matsumoto, 2017, Accelerated growth of B16BL6 tumor in mice through efficient uptake of their own exosomes by B16BL6 cells, Cancer Sci., 108, 1803, 10.1111/cas.13310 · DOI
  122. Kodali, M., Castro, O.W., Kim, D.K., Thomas, A., Shuai, B., Attaluri, S., Upadhya, R., Gitai, D., Madhu, L.N., and Prockop, D.J. (2019). Intranasally Administered Human MSC-Derived Extracellular Vesicles Pervasively Incorporate into Neurons and Microglia in both Intact and Status Epilepticus Injured Forebrain. Int. J. Mol. Sci., 21. · DOI
  123. Wu, 2008, From nose to brain: Understanding transport capacity and transport rate of drugs, Expert Opin. Drug Deliv., 5, 1159, 10.1517/17425247.5.10.1159 · DOI
  124. Wei, 2021, Mesenchymal Stem Cell–Derived Exosomes: A Promising Biological Tool in Nanomedicine, Front. Pharmacol., 11, 590470, 10.3389/fphar.2020.590470 · DOI
  125. Shi, 2020, Exosomes from oral tissue stem cells: Biological effects and applications, Cell Biosci., 10, 108, 10.1186/s13578-020-00471-7 · DOI
  126. Munir, J., Yoon, J.K., and Ryu, S. (2020). Therapeutic miRNA-Enriched Extracellular Vesicles: Current Approaches and Future Prospects. Cells, 9. · DOI
  127. Luarte, 2016, Potential Therapies by Stem Cell-Derived Exosomes in CNS Diseases: Focusing on the Neurogenic Niche, Stem Cells Int., 2016, 5736059, 10.1155/2016/5736059 · DOI
  128. Jeske, 2020, Human Pluripotent Stem Cell-Derived Extracellular Vesicles: Characteristics and Applications, Tissue Eng. Part B Rev., 26, 129, 10.1089/ten.teb.2019.0252 · DOI
  129. Araldi, R.P., D’Amelio, F., Vigerelli, H., de Melo, T.C., and Kerkis, I. (2020). Stem Cell-Derived Exosomes as Therapeutic Approach for Neurodegenerative Disorders: From Biology to Biotechnology. Cells, 9. · DOI
  130. Joo, H.S., Suh, J.H., Lee, H.J., Bang, E.S., and Lee, J.M. (2020). Current Knowledge and Future Perspectives on Mesenchymal Stem Cell-Derived Exosomes as a New Therapeutic Agent. Int. J. Mol. Sci., 21. · DOI
  131. Rezaie, 2018, Exosomes and their Application in Biomedical Field: Difficulties and Advantages, Mol. Neurobiol., 55, 3372, 10.1007/s12035-017-0582-7 · DOI
  132. Vinaiphat, 2019, Clinical implications of extracellular vesicles in neurodegenerative diseases, Expert Rev. Mol. Diagn., 19, 813, 10.1080/14737159.2019.1657407 · DOI · Paper page
  133. 2016, Exosomes as a potential novel therapeutic tools against neurodegenerative diseases, Pharmacol. Res., 113, 816, 10.1016/j.phrs.2016.02.002 · DOI
  134. Kalavrizioti, 2006, RNA-mediated therapeutics: From gene inactivation to clinical application, Curr. Top. Med. Chem., 6, 1737, 10.2174/156802606778194253 · DOI
  135. Qiu, L., Tan, E.K., and Zeng, L. (2015). microRNA: Medical Evidence: From Molecular Biology to Clinical Practice, Springer.
  136. Li, 2014, Therapeutic targeting of microRNAs: Current status and future challenges, Nat. Rev. Drug Discov., 13, 622, 10.1038/nrd4359 · DOI
  137. Choo, 2018, M1 macrophage-derived nanovesicles potentiate the anticancer efficacy of immune checkpoint inhibitors, ACS Nano, 12, 8977, 10.1021/acsnano.8b02446 · DOI
  138. Pulliam, 2020, Using neuronal extracellular vesicles and machine learning to predict cognitive deficits in HIV, J. Neurovirol., 26, 880, 10.1007/s13365-020-00877-6 · DOI
  139. Yee, 2015, Stem Cell Therapy for Neurodegenerative Diseases, Hanyang Med. Rev., 35, 229, 10.7599/hmr.2015.35.4.229 · DOI
  140. Smyth, 2015, Biodistribution and delivery efficiency of unmodified tumor-derived exosomes, J. Control. Release, 199, 145, 10.1016/j.jconrel.2014.12.013 · DOI
  141. Takakura, 2020, Therapeutic application of small extracellular vesicles (sEVs): Pharmaceutical and pharmacokinetic challenges, Biol. Pharm. Bull., 43, 576, 10.1248/bpb.b19-00831 · DOI
  142. Maciotta, 2013, The involvement of microRNAs in neurodegenerative diseases, Front. Cell. Neurosci., 7, 265, 10.3389/fncel.2013.00265 · DOI
  143. Junn, 2012, MicroRNAs in neurodegenerative diseases and their therapeutic potential, Pharmacol. Ther., 133, 142, 10.1016/j.pharmthera.2011.10.002 · DOI · Paper page

Cited by

Sorted by citations

See all 25

Metadata

Authors
Lim, W. Q., Michelle Luk, K. H., Lee, K. Y., Nurul, N., Loh, S. J., Yeow, Z. X., Wong, Q. X., Daniel Looi, Q. H., Chong, P. P., How, C. W., Hamzah, S., & Foo, J. B.
Affiliations
  • School of Pharmacy, Faculty of Health and Medical Sciences, Taylor’s University, Subang Jaya 47500, Selangor, Malaysia
  • My CytoHealth Sdn. Bhd., Lab 6, DMC Level 2, Hive 5, Taman Teknologi MRANTI, Bukit Jalil, Kuala Lumpur 57000, Malaysia
  • National Orthopaedic Centre of Excellence for Research and Learning (NOCERAL), Department of Orthopaedic Surgery, Faculty of Medicine, Universiti Malaya, Kuala Lumpur 50603, Malaysia
  • School of Pharmacy, Monash University Malaysia, Bandar Sunway, Subang Jaya 47500, Selangor, Malaysia
ORCID
Venue
Pharmaceutics
Publisher
MDPI AG
Published
2023-04-11
Volume
15
Issue
4
Pages
1216
ISSN
1999-4923
DOI
10.3390/pharmaceutics15041216
PMC
PMC10143523
Cited by
25
References
11
Language
en
Licence
creativecommons.org/licenses/by/4.0/ (vor)
Funders
My CytoHealth Sdn. Bhd

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review