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Assessing Neuronal and Astrocyte Derived Exosomes From Individuals With Mild Traumatic Brain Injury for Markers of Neurodegeneration and Cytotoxic Activity

Winston, Charisse N., Romero, Haylie K., Ellisman, Maya, Nauss, Sophie, Julovich, David A., Conger, Tori, Hall, James R., Campana, Wendy, O’Bryant, Sid E., Nievergelt, Caroline M., Baker, Dewleen G., Risbrough, Victoria B., Rissman, Robert A.·2019·Frontiers in Neuroscience
DOI 10.3389/fnins.2019.01005PMC PMC6797846
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FIGURE 1 Fluorescent activated cell sorting (FACS) enrichment of plasma NDEs from service members with and without mTBI during deployment. Schematic cartoon of FACS enrichment via the formation of a bead-antibody-exosome (BAE) – FITC complex (A). Representative FACS plot for non-exosome, negative control (red) and BAE – FITC complexes exosomes (green) isolated from control subject, 12207 (age: 22) and mTBI subject, 11541 (age: 21) and enriched against anti-human CD171 biotin (L1CAM) or anti-GLAST antibody (B). Total number of FITC+ events were not significantly different between the two populations (C; 114719 ± 3712 FITC+ events vs. 116121 ± 4969 FITC+ events). Plasma NDE and ADE concentrations of exosome marker, CD81 were not statistically different between the two populations as measured by standard ELISA (D).
FIGURE 1 Fluorescent activated cell sorting (FACS) enrichment of plasma NDEs from service members with and without mTBI during deployment. Schematic cartoon of FACS enrichment via the formation of a bead-antibody-exosome (BAE) – FITC complex (A). Representative FACS plot for non-exosome, negative control (red) and BAE – FITC complexes exosomes (green) isolated from control subject, 12207 (age: 22) and mTBI subject, 11541 (age: 21) and enriched against anti-human CD171 biotin (L1CAM) or anti-GLAST antibody (B). Total number of FITC+ events were not significantly different between the two populations (C; 114719 ± 3712 FITC+ events vs. 116121 ± 4969 FITC+ events). Plasma NDE and ADE concentrations of exosome marker, CD81 were not statistically different between the two populations as measured by standard ELISA (D).CC BY · PubMed Central
FIGURE 2 Human plasma NDE and ADE levels Aβ1–42 and NRGN differentiate young mTBI individuals from individuals with no TBI history. Plasma NDE and ADE (A) concentrations of Aβ42 were significantly higher, whereas plasma NDE and ADE (B) concentrations of NRGN were significantly lower in young individuals with mTBI (n = 17) compared to age-matched controls (n = 20). Plasma NDE and ADE concentrations of P-T181-tau (C), and P-S396-tau (D) were not significantly different between the two groups. Non-parametric t-test, ∗P < 0.05 vs. control.
FIGURE 2 Human plasma NDE and ADE levels Aβ1–42 and NRGN differentiate young mTBI individuals from individuals with no TBI history. Plasma NDE and ADE (A) concentrations of Aβ42 were significantly higher, whereas plasma NDE and ADE (B) concentrations of NRGN were significantly lower in young individuals with mTBI (n = 17) compared to age-matched controls (n = 20). Plasma NDE and ADE concentrations of P-T181-tau (C), and P-S396-tau (D) were not significantly different between the two groups. Non-parametric t-test, ∗P < 0.05 vs. control.CC BY · PubMed Central
FIGURE 3 Plasma NDE levels of Aβ40, total tau, and NFL are not significantly different between individuals with and without mTBI. Plasma NDE levels of Aβ40 (A), NFL (B), and total tau (C), were not significantly different between the two populations while plasma ADE Aβ40 (A), NFL (B), and total tau (C) were not detectable by the Simoa Assay.
FIGURE 3 Plasma NDE levels of Aβ40, total tau, and NFL are not significantly different between individuals with and without mTBI. Plasma NDE levels of Aβ40 (A), NFL (B), and total tau (C), were not significantly different between the two populations while plasma ADE Aβ40 (A), NFL (B), and total tau (C) were not detectable by the Simoa Assay.CC BY · PubMed Central
FIGURE 4 Plasma NDE cargo from individuals with mTBI compromise membrane integrity and are toxic to neuron-like cells in vitro. Differentiated PC12 cells and SH-SY5Y cells were incubated with 100 ng/ml of NDE and ADE for 48 h. Representative photomicrographs indicate exosome-induced cytotoxicity. Signs of cytotoxicity include dendritic blebbing (indicated by arrows), suppressed neurite outgrowth and cell death in NGF + PC12 cells (A). Compared to controls (100% viability), there was a threefold increase in exosome-induced cytotoxicity (LDH release) in wells that were treated with NDEs derived from service members with mTBI (B), ∗P < 0.05 vs. control, dashed horizontal line represents 100% viability. SH-SY5Y cells were treated with NDE and ADE preparations from control and mTBI service members and AD patients. A similar level of cytotoxicity was observed in cultured SH-SY5Y. A threefold increase in exosome-induced cytotoxicity (LDH release) was observed in wells that were treated with NDEs derived from mTBI samples and a fourfold increase exosome-induced cytotoxicity in wells that were treated with NDEs derived from AD samples as compared to NDEs derived from control samples (C). Non-parametric t-test; ∗P < 0.05 vs. control, dashed horizontal line represents 100% viability.
FIGURE 4 Plasma NDE cargo from individuals with mTBI compromise membrane integrity and are toxic to neuron-like cells in vitro. Differentiated PC12 cells and SH-SY5Y cells were incubated with 100 ng/ml of NDE and ADE for 48 h. Representative photomicrographs indicate exosome-induced cytotoxicity. Signs of cytotoxicity include dendritic blebbing (indicated by arrows), suppressed neurite outgrowth and cell death in NGF + PC12 cells (A). Compared to controls (100% viability), there was a threefold increase in exosome-induced cytotoxicity (LDH release) in wells that were treated with NDEs derived from service members with mTBI (B), ∗P < 0.05 vs. control, dashed horizontal line represents 100% viability. SH-SY5Y cells were treated with NDE and ADE preparations from control and mTBI service members and AD patients. A similar level of cytotoxicity was observed in cultured SH-SY5Y. A threefold increase in exosome-induced cytotoxicity (LDH release) was observed in wells that were treated with NDEs derived from mTBI samples and a fourfold increase exosome-induced cytotoxicity in wells that were treated with NDEs derived from AD samples as compared to NDEs derived from control samples (C). Non-parametric t-test; ∗P < 0.05 vs. control, dashed horizontal line represents 100% viability.CC BY · PubMed Central

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Research works printed but not linked: 62

  1. Agoston, 2017, Biofluid biomarkers of traumatic brain injury., Brain Inj., 31, 1195, 10.1080/02699052.2017.1357836 · DOI
  2. Baker, 2012, Predictors of risk and resilience for posttraumatic stress disorder among ground combat marines: methods of the Marine Resiliency Study., Prev. Chronic Dis., 9
  3. Binder, 1986, Persisting symptoms after mild head injury: a review of the postconcussive syndrome., J. Clin. Exp. Neuropsychol., 8, 323, 10.1080/01688638608401325 · DOI
  4. Blake, 1995, The development of a clinician-administered PTSD Scale., J. Trauma Stress, 8, 75, 10.1002/jts.2490080106 · DOI · Paper page
  5. Bogoslovsky, 2017, Increases of plasma levels of glial fibrillary acidic protein, tau, and amyloid β up to 90 days after traumatic brain injury., J. Neurotrauma, 34, 66, 10.1089/neu.2015.4333 · DOI
  6. Budnik, 2016, Extracellular vesicles round off communication in the nervous system., Nat. Rev, Neurosci., 17, 160, 10.1038/nrn.2015.29 · DOI · Paper page
  7. Chauhan, 2014, Chronic neurodegenerative consequences of traumatic brain injury., Restor. Neurol. Neurosci., 32, 337
  8. DeKosky, 1998, Secondary injury after head trauma: subacute and long-term mechanisms., Semin. Clin, Neuropsychiatry, 3, 176
  9. Eme, 2017, Neurobehavioral outcomes of mild traumatic brain injury: a mini review., Brain Sci., 7, 10.3390/brainsci7050046 · DOI
  10. Gill, 2018, Higher exosomal tau, amyloid-beta 42 and IL-10 are associated with mild TBIs and chronic symptoms in military personnel., Brain Inj., 32, 1277, 10.1080/02699052.2018.1471738 · DOI
  11. Glenn, 2017, Fear learning alterations after traumatic brain injury and their role in development of posttraumatic stress symptoms., Depress. Anxiety, 34, 723, 10.1002/da.22642 · DOI
  12. Goetzl, High complement levels in astrocyte-derived exosomes of Alzheimer disease., Ann. Neurol., 83, 544, 10.1002/ana.25172 · DOI
  13. Goetzl, Diagnostic potential of neural exosome cargo as biomarkers. for acute brain injury., Ann. Clin, Transl. Neurol., 5, 4, 10.1002/acn3.499 · DOI
  14. Goetzl, 2019, Altered levels of plasma neuron-derived exosomes and their cargo proteins characterize acute and chronic mild traumatic brain injury., FASEB J., 33, 5082, 10.1096/fj.201802319R · DOI
  15. Goetzl, Decreased synaptic proteins in neuronal exosomes of frontotemporal dementia, and Alzheimer’s disease., FASEB J., 30, 4141, 10.1096/fj.201600816r · DOI · Paper page
  16. Goetzl, Cargo proteins of plasma astrocyte-derived exosomes in Alzheimer’s disease., FASEB J., 30, 3853, 10.1096/fj.201600756r · DOI · Paper page
  17. Greene, 1976, Establishment of a noradrenergic clonal line of rat adrenal pheochromocytoma cells which respond to nerve growth factor., Proc. Natl. Acad. Sci. U.S.A., 73, 2424, 10.1073/pnas.73.7.2424 · DOI
  18. Hamberger, 2003, Redistribution of neurofilaments and accumulation of beta-amyloid protein after brain injury by rotational acceleration of the head., J. Neurotrauma, 20, 169, 10.1089/08977150360547080 · DOI · Paper page
  19. Helmick, 2006, Defense and Veterans Brain Injury Center Working Group on the Acute Management of mild Traumatic Brain Injury in Military Operational Settings: Clinical Practice Guideline and Recommendations.
  20. Hessvik, 2018, Current knowledge on exosome biogenesis and release., Cell Mol. Life Sci., 75, 193, 10.1007/s00018-017-2595-9 · DOI · Paper page
  21. Holm, 2005, Summary of the WHO collaborating centre for neurotrauma task force on mild traumatic brain injury., J. Rehabil. Med., 37, 137, 10.1080/16501970510027321 · DOI
  22. Hyder, 2007, The impact of traumatic brain injuries: a global perspective., NeuroRehabilitation, 22, 341, 10.3233/NRE-2007-22502 · DOI · Paper page
  23. Kalani, 2014, Exosomes: mediators of neurodegeneration, neuroprotection and therapeutics., Mol. Neurobiol., 49, 590, 10.1007/s12035-013-8544-1 · DOI
  24. Karr, 2014, The neuropsychological outcomes of concussion: a systematic review of meta-analyses on the cognitive sequelae of mild traumatic brain injury., Neuropsychology, 28, 321, 10.1037/neu0000037 · DOI
  25. Karve, 2016, The contribution of astrocytes and microglia to traumatic brain injury., Br. J. Pharmacol., 173, 692, 10.1111/bph.13125 · DOI
  26. Kawata, 2018, A preliminary report on brain-derived extracellular vesicle as novel blood biomarkers for sport-related concussions., Front. Neurol., 9, 10.3389/fneur.2018.00239 · DOI
  27. Kim, 2015, Antagonizing neuronal toll-like receptor 2 prevents synucleinopathy by activating autophagy., Cell Rep., 13, 771, 10.1016/j.celrep.2015.09.044 · DOI · Paper page
  28. Kim, 2018, The current state of biomarkers of mild traumatic brain injury., JCI Insight, 3, 10.1172/jci.insight.97105 · DOI
  29. Kulbe, 2016, Current status of fluid biomarkers in mild traumatic brain injury., Exp. Neurol, 275, 334, 10.1016/j.expneurol.2015.05.004 · DOI
  30. Langlois, 2006, The epidemiology and impact of traumatic brain injury: a brief overview., J. Head Trauma Rehabil., 21, 375, 10.1097/00001199-200609000-00001 · DOI
  31. LeBlanc, 2006, Comparison of functional outcome following acute care in young, middle-aged and elderly patients with traumatic brain injury., Brain Inj., 20, 779, 10.1080/02699050600831835 · DOI
  32. Lee, 2014, Magnetoencephalography in the diagnosis of concussion., Prog. Neurol. Surg., 28, 94, 10.1159/000358768 · DOI
  33. Liddelow, 2017, Reactive astrocytes: production, function, and therapeutic potential., Immunity, 46, 957, 10.1016/j.immuni.2017.06.006 · DOI · Paper page
  34. Lin, 2018, Levels of plasma neurofilament light chain and cognitive function in patients with Alzheimer or Parkinson disease., Sci. Rep., 8, 10.1038/s41598-018-35766-w · DOI · Paper page
  35. Marion, 2011, Proceedings of the military mTBI Diagnostics Workshop, St. Pete Beach., J Neurotrauma, 28, 517, 10.1089/neu.2010.1638 · DOI
  36. McKee, 2009, Chronic traumatic encephalopathy in athletes: progressive tauopathy after repetitive head injury., J. Neuropathol. Exp. Neurol., 68, 709, 10.1097/NEN.0b013e3181a9d503 · DOI · Paper page
  37. McKee, 2013, The spectrum of disease in chronic traumatic encephalopathy., Brain, 136, 43, 10.1093/brain/aws307 · DOI · Paper page
  38. Montgomery, 1994, Astrocytes: form, functions, and roles in disease., Vet. Pathol., 31, 145, 10.1177/030098589403100201 · DOI
  39. Moore, 2017, Effects of military service and deployment on clinical symptomatology: The role of trauma exposure and social support., J. Psychiatr. Res., 95, 121, 10.1016/j.jpsychires.2017.08.013 · DOI
  40. 2003, Report to Congress on Mild Traumatic Brain Injury in the United States: Steps to Prevent a Serious Public Health Problem.
  41. Ngolab, 2017, Brain-derived exosomes from dementia with Lewy bodies propagate α-synuclein pathology., Acta Neuropathol. Commun., 5, 10.1186/s40478-017-0445-5 · DOI · Paper page
  42. O’Neil, 2014, Factors associated with mild traumatic brain injury in veterans and military personnel: a systematic review., J. Int. Neuropsychol. Soc., 20, 249, 10.1017/S1355617714000204 · DOI
  43. Ponsford, 2011, Long-term outcomes after uncomplicated mild traumatic brain injury: a comparison with trauma controls., J. Neurotrauma, 28, 937, 10.1089/neu.2010.1516 · DOI
  44. Povlishock, 2005, Update of neuropathology and neurological recovery after traumatic brain injury., J. Head Trauma Rehabil., 20, 76, 10.1097/00001199-200501000-00008 · DOI
  45. Putz, 2008, Nedd4 family-interacting protein 1 (Ndfip1) is required for the exosomal secretion of Nedd4 family proteins., J. Biol. Chem., 283, 32621, 10.1074/jbc.M804120200 · DOI
  46. Rajendran, 2006, Alzheimer’s disease beta-amyloid peptides are released in association with exosomes., Proc. Natl. Acad. Sci. U.S.A., 103, 11172, 10.1073/pnas.0603838103 · DOI · Paper page
  47. Reilly, 2017, Novel human neuronal tau model exhibiting neurofibrillary tangles and transcellular propagation., Neurobiol. Dis, 106, 222, 10.1016/j.nbd.2017.06.005 · DOI
  48. Salat, 2017, Neuroimaging of deployment-associated traumatic brain injury (TBI) with a focus on mild TBI (mTBI) since 2009., Brain Inj., 31, 1204, 10.1080/02699052.2017.1327672 · DOI
  49. Shahim, 2018, Neurofilament light and tau as blood biomarkers for sports-related concussion., Neurology, 90, e1780, 10.1212/WNL.0000000000005518 · DOI
  50. Shahim, 2017, Serum neurofilament light as a biomarker for mild traumatic brain injury in contact sports., Neurology, 88, 1788, 10.1212/WNL.0000000000003912 · DOI
  51. Shin, 2017, Structural imaging of mild traumatic brain injury may not be enough: overview of functional and metabolic imaging of mild traumatic brain injury., Brain Imaging Behav., 11, 591, 10.1007/s11682-017-9684-0 · DOI
  52. Stern, 2016, Preliminary study of plasma exosomal tau as a potential biomarker for chronic traumatic encephalopathy., J. Alzheimers Dis, 51, 1099, 10.3233/JAD-151028 · DOI · Paper page
  53. Tartaglia, 2014, Chronic traumatic encephalopathy and other neurodegenerative proteinopathies., Front. Hum. Neurosci., 8, 10.3389/fnhum.2014.00030 · DOI
  54. Tsitsopoulos, 2013, Amyloid-beta peptides and tau protein as biomarkers in cerebrospinal and interstitial fluid following traumatic brain injury: a review of experimental and clinical studies., Front. Neurol., 4, 10.3389/fneur.2013.00079 · DOI
  55. Vogt, 2013, Deployment risk and resilience inventory-2 (DRRI-2): an updated tool for assessing psychosocial risk and resilience factors among service members and veterans., J. Trauma Stress, 26, 710, 10.1002/jts.21868 · DOI
  56. von Holst, 2004, Mandate of the WHO collaborating centre task force on mild traumatic brain injury., J. Rehabil. Med., 36, 8, 10.1080/16501960410023633 · DOI
  57. Wakida, 2018, Phagocytic response of astrocytes to damaged neighboring cells., PLoS One, 13, 10.1371/journal.pone.0196153 · DOI
  58. Winston, 2018, Neuronal exosome-derived human tau is toxic to recipient mouse neurons in vivo., J. Alzheimers Dis, 67, 541, 10.3233/JAD-180776 · DOI
  59. Winston, 2016, Prediction of conversion from mild cognitive impairment to dementia with neuronally derived blood exosome protein profile., Alzheimers Dement, 3, 63, 10.1016/j.dadm.2016.04.001 · DOI
  60. Winston, 2019, Complement protein levels in plasma astrocyte-derived exosomes are abnormal in conversion from mild cognitive impairment to Alzheimer’s disease dementia., Alzheimers Dement, 11, 61, 10.1016/j.dadm.2018.11.002 · DOI
  61. Xiong, 2018, Current understanding of neuroinflammation after traumatic brain injury and cell-based therapeutic opportunities., Chin. J, Traumatol., 21, 137, 10.1016/j.cjtee.2018.02.003 · DOI
  62. Yurgil, 2014, Association between traumatic brain injury and risk of posttraumatic stress disorder in active-duty Marines., JAMA Psychiatry, 71, 149, 10.1001/jamapsychiatry.2013.3080 · DOI

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Authors
Winston, C. N., Romero, H. K., Ellisman, M., Nauss, S., Julovich, D. A., Conger, T., Hall, J. R., Campana, W., O’Bryant, S. E., Nievergelt, C. M., Baker, D. G., Risbrough, V. B., & Rissman, R. A.
Venue
Frontiers in Neuroscience
Publisher
Frontiers Media SA
Published
2019-10-02
Volume
13
ISSN
1662-453X
DOI
10.3389/fnins.2019.01005
PMC
PMC6797846
Cited by
105
References
8
Licence
creativecommons.org/licenses/by/4.0/ (vor)
Funders
  • National Institute on Aging (AG057459, AG057469, AG051848, AG18440, AG005131)
  • Veterans Affairs San Diego Healthcare System (BX004312, BX003040)

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CoChat. (2026). Citation check: Assessing Neuronal and Astrocyte Derived Exosomes From Individuals With Mild Traumatic Brain Injury for Markers of Neurodegeneration and Cytotoxic Activity. https://app.cochat.ai/papers/10.3389/fnins.2019.01005
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Winston, C. N., Romero, H. K., Ellisman, M., Nauss, S., Julovich, D. A., Conger, T., Hall, J. R., Campana, W., O’Bryant, S. E., Nievergelt, C. M., Baker, D. G., Risbrough, V. B., & Rissman, R. A. (2019). Assessing Neuronal and Astrocyte Derived Exosomes From Individuals With Mild Traumatic Brain Injury for Markers of Neurodegeneration and Cytotoxic Activity. Frontiers in Neuroscience. https://doi.org/10.3389/fnins.2019.01005