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  1. Article: Human amnionic progenitor cell secretome mitigates the consequence of traumatic optic neuropathy in a mouse model.

    McCartan, Robyn / Gratkowski, Arissa / Browning, Mackenzie / Hahn-Townsend, Coral / Ferguson, Scott / Morin, Alexander / Bachmeier, Corbin / Pearson, Andrew / Brown, Larry / Mullan, Michael / Crawford, Fiona / Tzekov, Radouil / Mouzon, Benoit

    Molecular therapy. Methods & clinical development

    2023  Volume 29, Page(s) 303–318

    Abstract: Traumatic optic neuropathy (TON) is a condition in which acute injury to the optic nerve from direct or indirect trauma results in vision loss. The most common cause of TON is indirect injury to the optic nerve caused by concussive forces that are ... ...

    Abstract Traumatic optic neuropathy (TON) is a condition in which acute injury to the optic nerve from direct or indirect trauma results in vision loss. The most common cause of TON is indirect injury to the optic nerve caused by concussive forces that are transmitted to the optic nerve. TON occurs in up to 5% of closed-head trauma patients and there is currently no known effective treatment. One potential treatment option for TON is ST266, a cell-free biological solution containing the secretome of amnion-derived multipotent progenitor (AMP) cells. We investigated the efficacy of intranasal ST266 in a mouse model of TON induced by blunt head trauma. Injured mice treated with a 10-day regimen of ST266 showed an improvement in spatial memory and learning, a significant preservation of retinal ganglion cells, and a decrease in neuropathological markers in the optic nerve, optic tract, and dorsal lateral geniculate nucleus. ST266 treatment effectively downregulated the NLRP3 inflammasome-mediated neuroinflammation pathway after blunt trauma. Overall, treatment with ST266 was shown to improve functional and pathological outcomes in a mouse model of TON, warranting future exploration of ST266 as a cell-free therapeutic candidate for testing in all optic neuropathies.
    Language English
    Publishing date 2023-04-18
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2872938-9
    ISSN 2329-0501 ; 2329-0501
    ISSN (online) 2329-0501
    ISSN 2329-0501
    DOI 10.1016/j.omtm.2023.04.002
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 7107: Show issues Location:
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    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  2. Article ; Online: Influence of traumatic brain injury on extracellular tau elimination at the blood-brain barrier.

    Eisenbaum, Maxwell / Pearson, Andrew / Gratkowski, Arissa / Mouzon, Benoit / Mullan, Michael / Crawford, Fiona / Ojo, Joseph / Bachmeier, Corbin

    Fluids and barriers of the CNS

    2021  Volume 18, Issue 1, Page(s) 48

    Abstract: Repetitive head trauma has been associated with the accumulation of tau species in the brain. Our prior work showed brain vascular mural cells contribute to tau processing in the brain, and that these cells progressively degenerate following repetitive ... ...

    Abstract Repetitive head trauma has been associated with the accumulation of tau species in the brain. Our prior work showed brain vascular mural cells contribute to tau processing in the brain, and that these cells progressively degenerate following repetitive mild traumatic brain injury (r-mTBI). The current studies investigated the role of the cerebrovasculature in the elimination of extracellular tau from the brain, and the influence of r-mTBI on these processes. Following intracranial injection of biotin-labeled tau, the levels of exogenous labeled tau residing in the brain were elevated in a mouse model of r-mTBI at 12 months post-injury compared to r-sham mice, indicating reduced tau elimination from the brain following head trauma. This may be the result of decreased caveolin-1 mediated tau efflux at the blood-brain barrier (BBB), as the caveolin inhibitor, methyl-β-cyclodextrin, significantly reduced tau uptake in isolated cerebrovessels and significantly decreased the basolateral-to-apical transit of tau across an in vitro model of the BBB. Moreover, we found that the upstream regulator of endothelial caveolin-1, Mfsd2a, was elevated in r-mTBI cerebrovessels compared to r-sham, which coincided with a decreased expression of cerebrovascular caveolin-1 in the chronic phase following r-mTBI (> 3 months post-injury). Lastly, angiopoietin-1, a mural cell-derived protein governing endothelial Mfsd2a expression, was secreted from r-mTBI cerebrovessels to a greater extent than r-sham animals. Altogether, in the chronic phase post-injury, release of angiopoietin-1 from degenerating mural cells downregulates caveolin-1 expression in brain endothelia, resulting in decreased tau elimination across the BBB, which may describe the accumulation of tau species in the brain following head trauma.
    MeSH term(s) Animals ; Blood-Brain Barrier/metabolism ; Brain Injuries, Traumatic/metabolism ; Disease Models, Animal ; Female ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; tau Proteins/metabolism
    Chemical Substances tau Proteins
    Language English
    Publishing date 2021-10-26
    Publishing country England
    Document type Journal Article
    ZDB-ID 2595406-4
    ISSN 2045-8118 ; 2045-8118
    ISSN (online) 2045-8118
    ISSN 2045-8118
    DOI 10.1186/s12987-021-00283-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Impact of gulf war toxic exposures after mild traumatic brain injury.

    Ferguson, Scott / McCartan, Robyn / Browning, Mackenzie / Hahn-Townsend, Coral / Gratkowski, Arissa / Morin, Alexander / Abdullah, Laila / Ait-Ghezala, Ghania / Ojo, Joseph / Sullivan, Kimberly / Mullan, Michael / Crawford, Fiona / Mouzon, Benoit

    Acta neuropathologica communications

    2022  Volume 10, Issue 1, Page(s) 147

    Abstract: Chemical and pharmaceutical exposures have been associated with the development of Gulf War Illness (GWI), but how these factors interact with the pathophysiology of traumatic brain injury (TBI) remains an area of study that has received little attention ...

    Abstract Chemical and pharmaceutical exposures have been associated with the development of Gulf War Illness (GWI), but how these factors interact with the pathophysiology of traumatic brain injury (TBI) remains an area of study that has received little attention thus far. We studied the effects of pyridostigmine bromide (an anti-nerve agent) and permethrin (a pesticide) exposure in a mouse model of repetitive mild TBI (r-mTBI), with 5 impacts over a 9-day period, followed by Gulf War (GW) toxicant exposure for 10 days beginning 30 days after the last head injury. We then assessed the chronic behavioral and pathological sequelae 5 months after GW agent exposure. We observed that r-mTBI and GWI cumulatively affect the spatial memory of mice in the Barnes maze and result in a shift of search strategies employed by r-mTBI/GW exposed mice. GW exposure also produced anxiety-like behavior in sham animals, but r-mTBI produced disinhibition in both the vehicle and GW treated mice. Pathologically, GW exposure worsened r-mTBI dependent axonal degeneration and neuroinflammation, increased oligodendrocyte cell counts, and increased r-mTBI dependent phosphorylated tau, which was found to colocalize with oligodendrocytes in the corpus callosum. These results suggest that GW exposures may worsen TBI-related deficits. Veterans with a history of both GW chemical exposures as well as TBI may be at higher risk for worse symptoms and outcomes. Subsequent exposure to various toxic substances can influence the chronic nature of mTBI and should be considered as an etiological factor influencing mTBI recovery.
    MeSH term(s) Mice ; Animals ; Gulf War ; Brain Concussion/complications ; Pyridostigmine Bromide/toxicity ; Permethrin/toxicity ; Disease Models, Animal ; Brain Injuries, Traumatic ; Pesticides ; Pharmaceutical Preparations
    Chemical Substances Pyridostigmine Bromide (KVI301NA53) ; Permethrin (509F88P9SZ) ; Pesticides ; Pharmaceutical Preparations
    Language English
    Publishing date 2022-10-18
    Publishing country England
    Document type Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2715589-4
    ISSN 2051-5960 ; 2051-5960
    ISSN (online) 2051-5960
    ISSN 2051-5960
    DOI 10.1186/s40478-022-01449-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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