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Alzheimer's disease neuropathology is exacerbated following traumatic brain injury. Neuroprotection by co-administration of nanowired mesenchymal stem cells and cerebrolysin with monoclonal antibodies to amyloid beta peptide
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Rekke forfattare: 142021 (engelsk)Inngår i: Progress in Brain Research, ISSN 0079-6123, E-ISSN 1875-7855, Vol. 265, s. 1-97Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Military personnel are prone to traumatic brain injury (TBI) that is one of the risk factors in developing Alzheimer's disease (AD) at a later stage. TBI induces breakdown of the blood-brain barrier (BBB) to serum proteins into the brain and leads to extravasation of plasma amyloid beta peptide (ΑβP) into the brain fluid compartments causing AD brain pathology. Thus, there is a need to expand our knowledge on the role of TBI in AD. In addition, exploration of the novel roles of nanomedicine in AD and TBI for neuroprotection is the need of the hour. Since stem cells and neurotrophic factors play important roles in TBI and in AD, it is likely that nanodelivery of these agents exert superior neuroprotection in TBI induced exacerbation of AD brain pathology. In this review, these aspects are examined in details based on our own investigations in the light of current scientific literature in the field. Our observations show that TBI exacerbates AD brain pathology and TiO2 nanowired delivery of mesenchymal stem cells together with cerebrolysin—a balanced composition of several neurotrophic factors and active peptide fragments, and monoclonal antibodies to amyloid beta protein thwarted the development of neuropathology following TBI in AD, not reported earlier.

sted, utgiver, år, opplag, sider
2021. Vol. 265, s. 1-97
Emneord [en]
Alzheimer's disease, Traumatic brain injury, Brain pathology, Mesenchymal stem cells, Cerebrolysin, Nanowired delivery, Nanomedicine
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Identifikatorer
URN: urn:nbn:se:su:diva-202665DOI: 10.1016/bs.pbr.2021.04.008ISI: 000750009700002PubMedID: 34560919OAI: oai:DiVA.org:su-202665DiVA, id: diva2:1644375
Tilgjengelig fra: 2022-03-14 Laget: 2022-03-14 Sist oppdatert: 2022-03-14bibliografisk kontrollert

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