Patients who are bedridden often suffer from muscular atrophy due to reduced daily activities and can become depressed. However, patients who undergo physical therapy sometimes demonstrate positive benefits including a reduction of stressful and depressed behavior. Regenerative medicine has seen improvements in two stem cell-based therapies for central nervous system disorders. One therapy is through the transfer of exogenous stem cells. The other therapy is a more natural method and focuses on the increasing endogenous neurogenesis and restoring the neurological impairments. This study overviews how immobilization-induced disuse atrophy affects neurogenesis in rats, specifically hypothesizing that immobilization diminishes circulating trophic factor levels, like vascular endothelial growth factors or brain-derived neurotrophic factor, which in turn limits neurogenesis. This hypothesis requires the classification of the stem cell microenvironment by probing growth factors in addition to other stress-related proteins that correlate with exercise-induced neurogenesis. There is research examining the effects of increased exercise on neurogenesis while limiting exercise, which better demonstrates the pathological states of immobile stroke patients, remains relatively unexplored. To examine the effects of immobilization on neurogenesis quantitative measurements of movements, 5-bromo-2deoxyuridine labeling of proliferative cells, biochemical assays of serum, cerebrospinal fluid and neurological levels of trophic factors, growth factors, and stress-related proteins will indicate levels of neurogenesis. In further research, studies are needed to show how in vivo stimulation, or lack thereof, affects stem cell microenvironments to advance treatment procedures for strengthening neurogenesis in bedridden patients. This paper is a review article. Referred literature in this paper has been listed in the references section. The datasets supporting the conclusions of this article are available online by searching various databases, including PubMed. Some original points in this article come from the laboratory practice in our research center and the authors' experiences.

Stroke continues to maintain its status as one of the top causes of mortality within the United States. Currently, the only Food and Drug Administration (FDA)-approved drug in place for stroke patients, tissue plasminogen activator (tPA), has a rigid therapeutic window, closing at approximately 4.5 h after stroke onset. Due to this short time frame and other restrictions, such as any condition that increases a patient's risk for hemorrhaging, it has been predicted that <5% of ischemic stroke patients benefit from tPA. Given that rehabilitation therapy remains the only other option for stroke victims, there is a clear unmet clinical need for treatment available for the remaining 95%. While still considered an experimental treatment, the utilization of stem cell therapies for stroke holds consistent promise. Copious preclinical studies report the capacity for transplanted stem cells to rescue the brain parenchyma surrounding the stroke-induced infarct core. At present, the exact mechanisms in which stem cells contribute a robust therapeutic benefit remains unclear. Following stem cell administration, researchers have observed cell replacement, an increase in growth factors, and a reduction in inflammation. With a deeper understanding of the precise mechanism of stem cells, these therapies can be optimized in the clinic to afford the greatest therapeutic benefit. Recent studies have depicted a unique method of endogenous stem cell activation as a result of stem cell therapy. In both traumatic brain injury and stroke models, transplanted mesenchymal stromal cells (MSCs) facilitated a pathway between the neurogenic niches of the brain and the damaged area through extracellular matrix remodeling. The biobridge pioneered by the MSCs was utilized by the endogenous stem cells, and these cells were able to travel to the damaged areas distal to the neurogenic niches, a feat unachievable without prior remodeling. These studies broaden our understanding of stem cell interactions within the injured brain and help to guide both researchers and clinicians in developing an effective stem cell treatment for stroke. This paper is a review article. Referred literature in this paper has been listed in the references section. The datasets supporting the conclusions of this article are available online by searching various databases, including PubMed. Some original points in this article come from the laboratory practice in our research center and the authors' experiences.

Every year, approximately 1.4 million US citizens visit emergency rooms for traumatic brain injuries. Formerly known as an acute injury, chronic neurodegenerative symptoms such as compromised motor skills, decreased cognitive abilities, and emotional and behavioral changes have caused the scientific community to consider chronic aspects of the disorder. The injury causing impact prompts multiple cell death processes, starting with neuronal necrosis, and progressing to various secondary cell death mechanisms. Secondary cell death mechanisms, including excitotoxicity, oxidative stress, mitochondrial dysfunction, blood–brain barrier disruption, and inflammation accompany chronic traumatic brain injury (TBI) and often contribute to long-term disabilities. One hallmark of both acute and chronic TBI is neuroinflammation. In acute stages, neuroinflammation is beneficial and stimulates an anti-inflammatory response to the damage. Conversely, in chronic TBI, excessive inflammation stimulates the aforementioned secondary cell death. Converting inflammatory cells from pro-inflammatory to anti-inflammatory may expand the therapeutic window for treating TBI, as inflammation plays a role in all stages of the injury. By expanding current research on the role of inflammation in TBI, treatment options and clinical outcomes for afflicted individuals may improve. This paper is a review article. Referred literature in this paper has been listed in the references section. The data sets supporting the conclusions of this article are available online by searching various databases, including PubMed. Some original points in this article come from the laboratory practice in our research center and the authors' experiences.

Traumatic brain injury (TBI) is now characterized as a progressive, degenerative disease and continues to stand as a prevalent cause of death and disability. The pathophysiology of TBI is complex, with a variety of secondary cell death pathways occurring which may persist chronically following the initial cerebral insult. Current therapeutic options for TBI are minimal, with surgical intervention or rehabilitation therapy existing as the only viable treatments. Considering the success of stem-cell therapies in various other neurological diseases, their use has been proposed as a potential potent therapy for patients suffering TBI. Moreover, stem cells are highly amenable to adjunctive use with other therapies, providing an opportunity to overcome the inherent limitations of using a single therapeutic agent. Our research has verified this additive potential by demonstrating the efficacy of co-delivering human umbilical cord blood (hUCB) cells with granulocyte-colony stimulating factor (G-CSF) in a murine model of TBI, providing encouraging results which support the potential of this approach to treat patients suffering from TBI. These findings justify ongoing research toward uncovering the mechanisms which underlie the functional improvements exhibited by hUCB + G-CSF combination therapy, thereby facilitating its safe and effect transition into the clinic. This paper is a review article. Referred literature in this paper has been listed in the reference section. The datasets supporting the conclusions of this article are available online by searching various databases, including PubMed. Some original points in this article come from the laboratory practice in our research center and the authors' experiences.

Cell death and neurogenesis have been examined after stroke in the subventricular zone of the adult mammalian brain. New research focuses on the use of drugs to improve the viability of neural progenitor cells in rats after stroke. The aim of the drugs is to lengthen the timeframe for stroke therapy by targeting the endogenous repair mechanism that follows injury. In this paper, we look at the broad state of stroke therapy to assess the effectiveness of endogenous neurogenesis-enhancing drugs on stroke. This paper is a review article. Referred literature in this paper has been listed in the reference section. The data sets supporting the conclusions of this article are available online by searching various databases, including PubMed. Some original points in this article come from the laboratory practice in our research center and the authors' experiences.

Epilepsy is considered a chronic neurological disorder and is accompanied by persistent and diverse disturbances in electrical brain activity. While antiepileptic pharmaceuticals are still the predominant treatment for epilepsy, the advent of numerous surgical interventions has further improved outcomes for patients. Despite these advancements, a subpopulation continues to experience intractable seizures which are resistant to current conventional and nonconventional therapeutic options. In this review, we begin with an introduction to the clinical presentation of epilepsy before discussing the clinically relevant laboratory models of epilepsy. Finally, we explore the implications of regenerative medicine – including cell therapy, neuroprotective agents, and electrical stimulation – for epilepsy, supplemented with our laboratory's data. This paper is a review article. Referred literature in this paper has been listed in the references section. The datasets supporting the conclusions of this article are available online by searching various databases, including PubMed. Some original points in this article come from the laboratory practice in our research center and the authors' experiences.

This mini-review highlights the innovative observation that transplanted human neural stem cells can bring about endogenous brain repair through the stimulation of multiple regenerative processes in the neurogenic area (i.e., subventricular zone [SVZ]) in an animal model of Parkinson's disease (PD). In addition, we convey that identifying anti-inflammatory cytokines, therapeutic proteomes, and neurotrophic factors within the SVZ may be essential to induce brain repair and behavioral recovery. This work opens up a new area of research for further understanding the pathology and treatment of PD. This paper is a review article. Referred literature in this paper has been listed in the references section. The datasets supporting the conclusions of this article are available online by searching various databases, including PubMed. Some original points in this article come from the laboratory practice in our research center and the authors' experiences.

Induced pluripotent stem (iPS) cells have attracted attention in recent years as a model of human genetic diseases. Starting from the diseased somatic cells isolated from an affected patient, iPS cells can be created and subsequently differentiated into various cell types that can be used to gain a better understanding of the disease at a cellular and molecular level. There are limitations of iPS cell generation, however, due to low efficiency, high costs, and lengthy protocols. The use of amniotic fluid stem cells (AFS) presents a worthy alternative as a stem cell source for modeling of human genetic diseases. Prenatal identification of chromosomal or Mendelian diseases may require the collection of amniotic fluid which is not only useful for the sake of diagnosis but also from this, AFS cells can be isolated and cultured. Since AFS cells show some characteristics of pluripotency, having the capacity to differentiate into various cell types derived from all three germ layers in vitro, they are a well-suited model for investigations regarding alterations in the molecular biology of a cell due to a specific genetic disease. This readily accessible source of stem cells can replace the necessity for generating iPS cells. Here, we expand on the applicability and importance of AFS cells as a model for discovery in the field of human genetic disease research. This paper is a review article. Referred literature in this paper has been listed in the references section. The data sets supporting the conclusions of this article are available online by searching various databases, including PubMed. Some original points in this article come from the laboratory practice in our research center and the authors' experiences.

The ability of stem cells to differentiate into various lineages has made them powerful tools of regenerative medicine and applicable to multiple human diseases. Of particular interest, amniotic fluid-derived stem cells (AFSC) have been characterized to express both adult and embryonic cell markers, indicating them as cells within an intermediate stage between embryonic and adult phenotype. AFSC can differentiate into cells of all three germ layers, including hepatic, myogenic, osteogenic, and neurogenic cell types. Furthermore, AFSC have minimal replicative senescence, retaining the ability to divide effectively for over 250 doublings. These facts indicate that amniotic fluid may exist as a promising donor source of stem cells for the treatment of multiple clinically relevant conditions. Of particular interest is the convenience of harvesting stem cells from the amniotic fluid stem for the treatment of newborns, as well as for banking or cryopreserving purposes to be used at a later date. Importantly, the promise of amniotic fluid as a source of stem cells merits ongoing research into their potential therapeutic applications. This paper is a review article. Referred literature in this paper has been listed in the references section. The datasets supporting the conclusions of this article are available online by searching various databases, including PubMed. Some original points in this article come from the laboratory practice in our research center and the authors' experiences.

Whole-brain irradiation (WBI) is commonly used to treat primary tumors of the central nervous systems tumors as well as brain metastases. While this technique has increased survival among brain tumor patients, the side effects of including a decline in cognitive abilities that are generally progressive. In an effort to combat WBI side effects, researchers explored the treatment of colony stimulating factor-1 receptor (CSF-1R) inhibitor. Data show that when a CSF-1R inhibitor is administered with fractionated WBI treatment, there is a decline in the number of resident and peripheral mononuclear phagocytes, a decrease in dendritic spine loss and a reduction in functional and memory deficits. CSFR-1R inhibitors have displayed promising results as an effective counter-treatment for WBI-induced deficits. Further research is required to optimize treatment strategies, establish a treatment timeline and gain a better understanding of the long-term side effects of targeting CSF-1R as a treatment strategy for WBI symptoms. This paper is a review article. Referred literature in this paper has been listed in the references section. The datasets supporting the conclusions of this article are available online by searching various databases, including PubMed. Some original points in this article come from the laboratory practice in our research center and the authors' experiences.