Home > Riviste > Journal of Neurosurgical Sciences > Fascicoli precedenti > Articles online first > Journal of Neurosurgical Sciences 2016 Nov 30





Rivista di Neurochirurgia

Indexed/Abstracted in: e-psyche, EMBASE, PubMed/MEDLINE, Neuroscience Citation Index, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 1,651



Journal of Neurosurgical Sciences 2016 Nov 30

lingua: Inglese

Stem cell therapy for sequestering neuroinflammation in traumatic brain injury: an update on exosome-targeting to the spleen

Marci G. CROWLEY, Michael G. LISKA, Cesar V. BORLONGAN

Center of Excellence for Aging and Brain Repair, Department of Neurosurgery and Brain Repair, University of South Florida Morsani College of Medicine, Tampa FL, USA


Traumatic brain injury (TBI), manifests with acute and chronic cell death pathways leading to initial impacted injury and subsequent neurodegeneration. In particular, the secondary cell death, plagued by a massive and lingering neuroinflammatory response, contributes significantly to worsening outcomes of the progressive TBI pathology. Fortunately, neuroinflammation also provides an opportunity for therapeutic interventions. Limited treatment options currently exist for the disease, but stem cell-based therapies offer promise in promoting neuroprotection and neuroregeneration by mitigating central neuroinflammation as well as modulating peripheral inflammation via the spleen. Indeed, peripherally administered stem cells preferentially migrate to the spleen when injected after a neurovascular injury, advancing the concept that stem cells are inflammation-homing “biologics” and afford their neuroprotection primarily by abrogating the systemic inflammatory response. Accumulating preclinical evidence has revealed new insights on the systemic inflammation as a pathological culprit, but also arguably as a therapeutic target for stem cell therapies as a treatment for TBI and relevant neurovascular diseases. Here, we provide an update on recent scientific evidence supporting the stem cells’ novel mechanism of sequestering the inflammation-mediated secondary cell death that closely accompanies the evolution of TBI pathology.

inizio pagina

Publication History

Per citare questo articolo

Corresponding author e-mail