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Neurovascular unit permeability in neuroinflammatory diseases:a common pathologic and therapeutic target?

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Neural Regeneration Research 2023年第8期18卷 1715-1716页

Deleterious inflammatory cell invasion has been implicated in neurological diseases,partly manifesting as a leaky blood-central nervous system ba rrier(BCNSB)(Huang et al.,2021).Uncovering the perturbations of the neurovascular unit(NvU)may reveal the role of detrimental proinflammatory cells and signaling molecules in disrupting the central nervous system immuneprivileged environment.

关键词： invasion inflammatory diseases

Going straight for the gut:gut-brain axis pathology and treatment of Parkinson's disease

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Neural Regeneration Research 2024年第10期19卷 2111-2112页

作者： Dominique Ebedes Cesar V.Borlongan University of South Florida Morsani College of Medicine TampaFLUSA Center of Excellence for Aging and Brain Repair Department of Neurosurgery and Brain RepairUniversity of South Florida Morsani College of MedicineTampaFLUSA

This perspective focuses on the recent literature regarding the role of the gut-brain axis(GBA) in fecal microbiota transplantation(FMT) and stem cell therapy(SCT) in Parkinson's disease(PD).PD is the second most common neurodegenerative disease in the United States,yet therapies remain limited.Current research suggests that the GBA may play a role in the pathogenesis of PD.GBAbased FMT as well as SCT offer promising new avenues for PD treatment.Pro bing the interactions between FMT and SCT with the GBA may reveal novel therapeutics for PD.

关键词： straight pathology pathogenesis

Traumatic brain injury treatment using a rodent model of homelessness

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Neural Regeneration Research 2024年第9期19卷 1873-1874页

作者： Molly Monsour Cesar V.Borlongan University of South Florida Morsani College of Medicine TampaFLUSA Center of Excellence for Aging and Brain Repair Department of Neurosurgery and Brain RepairUniversity of South Florida Morsani College of MedicineTampaFLUSA

Introduction:Traumatic brain injury(TBI)is a common diagnosis among veterans secondary to combat experiences.TBI is also rampant among those experiencing homelessness,possibly due to veterans making up 12.3%of the homeless population(Tsai and Rosenheck,2015),or due to the high risk of violence or trauma among those experiencing homelessness.TBI is up to 10×more prevalent among those experiencing homelessness(Stubbs et al.,2020;Dell et al.,2021).

关键词： diagnosis TBI less

Drug-and cell-based therapies for targeting neuroinflammation in traumatic brain injury

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Neural Regeneration Research 2016年第10期11卷 1575-1576页

作者： Sussannah Kaelber Paolina Pantcheva Cesar V.Borlongan Center of Excellence for Aging and Brain Repair Department of Neurosurgery and Brain Repair University of South Florida College of Medicine

TBI pathology： Traumatic brain injury （TBI） is caused by an external force to the head, resulting in trauma to the brain. Approximately 1.7 million Americans suffer from TBI every year. Out of the 1.7 million suffering from TBI, an estimated 52,000 injuries result in death, leaving a mass amount of peo- ple with symptoms that could last a few days, a few years, or their entire life （Faul et al., 2010）. TBI can be classified as mild, moderate and severe. Depending on the classification and the extent of the injury, TBI can cause both physical symptoms and cognitive disorders （Lozano et al., 2015）.

关键词： TBI cell Drug-and cell-based therapies for targeting neuroinflammation in traumatic brain injury

Stroke gets in your eyes: stroke-induced retinal ischemia and the potential of stem cell therapy

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Neural Regeneration Research 2020年第6期15卷 1014-1018页

作者： Chase Kingsbury Matt Heyck Brooke Bonsack Jea-Young Lee Cesar V.Borlongan Center of Excellence for Aging and Brain Repair University of South Florida College of Medicine

Stroke persists as a global health and economic crisis,yet only two interventions to reduce stroke-induced brain injury exist.In the clinic,many patients who experience an ischemic stroke often further suffer from retinal ischemia,which can inhibit their ability to make a functional recovery and may diminish their overall quality of life.Despite this,no treatments for retinal ischemia have been developed.In both cases,ischemia-induced mitochondrial dysfunction initiates a cell loss cascade and inhibits endogenous brain repair.Stem cells have the ability to transfer healthy and functional mitochondria not only ischemic neurons,but also to similarly endangered retinal cells,replacing their defective mitochondria and thereby reducing cell death.In this review,we encapsulate and assess the relationship between cerebral and retinal ischemia,recent preclinical advancements made using in vitro and in vivo retinal ischemia models,the role of mitochondrial dysfunction in retinal ischemia pathology,and the therapeutic potential of stem cell-mediated mitochondrial transfer.Furthermore,we discuss the pitfalls in classic rodent functional assessments and the potential advantages of laser Doppler as a metric of stroke progression.The studies evaluated in this review highlight stem cell-derived mitochondrial transfer as a novel therapeutic approach to both retinal ischemia and stroke.Furthermore,we posit the immense correlation between cerebral and retinal ischemia as an underserved area of study,warranting exploration with the aim of these treating injuries together.

关键词： laser Doppler MCAO mesenchymal stem cells mitochondrial network mitochondrial transfer ophthalmic artery optic nerve oxygen-glucose deprivation regenerative medicine retinal ganglion cells visual impairment

Neuroprotective and neuroregenerative potential of pharmacologically-induced hypothermia with D-alanine D-leucine enkephalin in brain injury

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Neural Regeneration Research 2018年第12期13卷 2029-2037页

作者： M.Grant Liska Marci G.Crowley Julian P.Tuazon Cesar V.Borlongan Center of Excellence for Aging and Brain Repair University of South Florida College of Medicine

Neurovascular disorders, such as traumatic brain injury and stroke, persist as leading causes of death and disability - thus, the search for novel therapeutic approaches for these disorders continues. Many hurdles have hindered the translation of effective therapies for traumatic brain injury and stroke primarily because of the inherent complexity of neuropathologies and an inability of current treatment approaches to adapt to the unique cell death pathways that accompany the disorder symptoms. Indeed, developing potent treatments for brain injury that incorporate dynamic and multiple disorder-engaging therapeutic targets are likely to produce more effective outcomes than traditional drugs. The therapeutic use of hypothermia presents a promising option which may fit these criteria. While regulated temperature reduction has displayed great promise in preclinical studies of brain injury, clinical trials have been far less consistent and associated with adverse effects, especially when hypothermia is pursued via systemic cooling. Accordingly, devising better methods of inducing hypothermia may facilitate the entry of this treatment modality into the clinic. The use of the delta opioid peptide D-alanine D-leucine enkephalin（DADLE） to pharmacologically induce temperature reduction may offer a potent alternative, as DADLE displays both the ability to cause temperature reduction and to confer a broad profile of other neuroprotective and neuroregenerative processes. This review explores the prospect of DADLE-mediated hypothermia to treat neurovascular brain injuries, emphasizing the translational steps necessary for its clinical translation.

关键词： stroke traumatic brian injury neurodegeneration temperature management regenerative medicine delta opioids metabolic suppression cerebrovascular disease neurovascular disease

Translational lab-to-clinic hurdles in stem cell therapy

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Chinese Neurosurgical Journal 2016年第4期2卷 229-232页

作者： Sydney Corey Trenton Lippert 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 12901 Bruce B.Downs Blvd Tampa FL 33612 USA

Several experimental therapeutics have been demonstrated to be safe and effective in animal models of neurological disorders, but have failed when they reached the clinic. Postulated factors that affected the poor clinical outcomes include the lack of proper treatment controls and clinically relevant animal models. This failure of lab-to-clinic translation has plagued many neuroprotective drugs for stroke. With this in mind, the stem cell therapy field has cautiously approached translating stem cell products for clinical application, in that a negative clinical trial may hinder the entire regenerative medicine therapeutics. Here, we discuss the many translational challenges associated with stem cell therapy in the setting of stroke.

关键词： Physical therapy Cerebral ischemia Neurogenesis Cell transplantation

Utilizing pharmacotherapy and mesenchymal stem cell therapy to reduce inflammation following traumatic brain injury

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Neural Regeneration Research 2016年第9期11卷 1379-1384页

作者： Sherwin Mashkouri Marci G.Crowley Michael G.Liska Sydney Corey Cesar V.Borlongan Department of Neurosurgery and Brain Repair University of South Florida Morsani College of Medicine

The pathologic process of chronic phase traumatic brain injury is associated with spreading inflamma- tion, cell death, and neural dysfunction. It is thought that sequestration of inflammatory mediators can facilitate recovery and promote an environment that fosters cellular regeneration. Studies have targeted post-traumatic brain injury inflammation with the use of pharmacotherapy and cell therapy. These thera- peutic options are aimed at reducing the edematous and neurodegenerative inflammation that have been associated with compromising the integrity of the blood-brain barrier. Although studies have yielded posi- tive results from anti-inflammatory pharmacotherapy and cell therapy individually, emerging research has begun to target inflammation using combination therapy. The joint use of anti-inflammatory drugs along- side stem cell transplantation may provide better clinical outcomes for traumatic brain injury patients. Despite the promising results in this field of research, it is important to note that most of the studies men- tioned in this review have completed their studies using animal models. Translation of this research into a clinical setting will require additional laboratory experiments and larger predinical trials.

关键词： stem cells drugs neuroinflammation trauma neuroprotection regeneration

The role of DJ-1 in the oxidative stress cell death cascade after stroke

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Neural Regeneration Research 2014年第15期9卷 1430-1433页

作者： Paolina Pantcheva Maya Elias Kelsey Duncan Cesar V.Borlongan Naoki Tajiri Yuji Kaneko Department of Neurosurgery and Brain Repair University of South FloridaTampaFLUSA

Oxidative stress is closely associated with secondary cell death in many disorders of the central nervous system including stroke, Parkinson＇s disease, Alzheimer＇s disease. Among many aber-rant oxidative stress-associated proteins, DJ-1 has been associated with the oxidative stress cell death cascade primarily in Parkinson＇s disease. Although principally expressed in the cytoplasm and nucleus, DJ-1 can be secreted into the serum under pathological condition. Recently, a close pathological association between DJ-I and oxidative stress in stroke has been implicated. To this end, we and others have demonstrated the important role of mitochondria in neuroprotection for stroke by demonstrating that the translocation of DJ-1 in the mitochondria could potentially mitigate mitochondrial injury. Here, we discuss our recent findings testing the hypothesis that DJ- 1 not only functions as a form of intracellular protection from oxidative stress, but that it also utilizes paracrine and/or autocrine cues in order to accomplish extracellular signaling between neighboring neuronal cells, resulting in neuroprotection. This article highlights recent evidence supporting the status of DJ-1 as key anti-oxidative stress therapeutic target for stroke.

关键词： cerebral ischemia neuroprotection mitochondria translocation extracellular signaling