Recent advancements in stem cell and gene therapies for neurological disorders and intractable epilepsy

Naegele, Janice R.; Maisano, Xu; Yang, Jialei; Royston, Sara E.; Ribeiro, Efrain

doi:10.1016/j.neuropharm.2010.01.019

Cited by 49 publications

(29 citation statements)

References 160 publications

(186 reference statements)

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“…In addition, the plasticity of surviving neurons and the circuitry of a fraction of newly born dentate granule cells after the injury appear to be detrimental toward normalizing the hippocampal function after injury [24,27,33,34]. These issues have provided an impetus for replacing lost neurons through grafting of fresh hippocampal precursor cells obtained from the fetal brain or NSCs/neuronal progenitors expanded from diverse sources in animal models of hippocampal injury and TLE [25,[27][28][29][30]. Grafting of specific post-mitotic hippocampal precursor cells shortly after hippocampal injury or SE has significance, because such an approach has promise for replacing the lost neurons, as well as facilitating the reconstruction the disrupted hippocampal circuitry [14,24,25,35,36].…”

Section: Cell Therapy For Restraining Epileptogenesis Shortly After Amentioning

confidence: 99%

“…In this context, cell transplantation approach has promise in serving as an adept alternate therapy for TLE. This is because this strategy has shown the capability to curb epileptogenesis (the succession that modifies a normal brain region into an epileptic precinct) when employed soon after an IPI, and to contain SRS when utilized after the occurrence of TLE in pre-clinical studies [24][25][26][27][28][29][30]. Because the seizuregenerating zone and the associated cell loss are mainly localized to the hippocampus in most cases, TLE appears to be good candidate to treat it with the cell transplantation approach.…”

Section: Introductionmentioning

confidence: 99%

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Progress in Cell Grafting Therapy for Temporal Lobe Epilepsy

Shetty

2011

Neurotherapeutics

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Temporal lobe epilepsy (TLE), exemplified by complex partial seizures, is recognized in~30% of epileptic patients. Seizures in TLE are associated with cognitive dysfunction and are resistant to antiepileptic drug therapy iñ 35% of patients. Although surgical resection of the hippocampus bestows improved seizure regulation in most cases of intractable TLE, this choice can cause lasting cognitive deficiency and reliance on antiepileptic drugs. Thus, alternative therapies that are proficient in both containing the spontaneous recurrent seizures and reversing the cognitive dysfunction are needed. The cell transplantation approach is promising in serving as an adept alternate therapy for TLE, because this strategy has shown the capability to curtail epileptogenesis when used soon after an initial precipitating brain injury, and to restrain spontaneous recurrent seizures and improve cognitive function when utilized after the occurrence of TLE. Nonetheless, this treatment needs further advancement and rigorous evaluation in animal prototypes of chronic TLE before the conceivable clinical use. It is especially vital to gauge the efficacy of distinct donor cell types, such as the hippocampal precursor cells, γ-aminobutyric acid-ergic progenitors, and neural stem cells derived from diverse human sources (including the embryonic stem cells and induced pluripotent stem cells) for longstanding seizure suppression using continuous electroencephalographic recordings for prolonged periods. Additionally, the identification of the mechanisms underlying the graft-mediated seizure suppression and improved cognitive function, and the development of apt grafting strategies that enhance the anti-seizure and procognitive effects of grafts will be necessary. The goal of this review is to evaluate the progress made hitherto in this area and to discuss the prospect for cell-based therapy for TLE.

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Section: Cell Therapy For Restraining Epileptogenesis Shortly After Amentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Progress in Cell Grafting Therapy for Temporal Lobe Epilepsy

Shetty

2011

Neurotherapeutics

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“…iPSCs exhibit similar phenotype of ESC, and proliferate and differentiate into all cell types of the body as well as teratomas formation (103,104). Remyelination activity of iPSCs was assessed in mouse EAE models.…”

Section: Induced Pluripotent Stem Cellsmentioning

confidence: 99%

Stem Cell Therapy: A Promising Therapeutic Approach for Multiple Sclerosis

Pourabdolhossein

Hamidabadi

Bojnordi

et al. 2017

Multiple Sclerosis: Perspectives in Treatment and Pathogenesis

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Multiple sclerosis (MS) is an inflammatory disease of the central nervous system which is accompanied by demyelination of the nerves, axonal loss, and disability. Currently, no definitive treatment is recognized for MS. Stem-cell therapy for MS has shown promising results and has attracted attention as an alternative therapeutic option. Various stem cell sources such as mesenchymal, embryonic, and neural have been identified. This chapter gives an overview of the advances made in our understanding of these stem cells under two broad categories: exogenous and endogenous. Stem-cell therapy in MS and the substantial literature regarding their

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“…The hope is that stem cell transplantation will replace dysfunctional motor neurons or neural supporting cells (i.e., glia) and eventually restore neuromuscular function to premorbid levels [31]. Among the many stem cell types undergoing testing for neurological treatments [32, 33], the most common are fetal and adult neuronal stem cells, ES cells, induced pluripotent stem cells, and mesenchymal stem cells [34]. …”

Section: Stem Cell Therapy For Alsmentioning

confidence: 99%

Neuroprotection for Amyotrophic Lateral Sclerosis: Role of Stem Cells, Growth Factors, and Gene Therapy

2012

CNSAMC

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Various molecular mechanisms including apoptosis, inflammation, oxidative stress, and excitotoxicity have been implicated in the pathogenesis of amyotrophic lateral sclerosis (ALS), though the exact mechanisms have yet to be specified. Furthermore, the underlying restorative molecular mechanisms resulting in neuronal and/or non-neuronal regeneration have to be yet elucidated. Therapeutic agents targeting one or more of these mechanisms to combat either initiation or progression of the disease are under research. Novel treatments including stem cell therapy, growth factors, and gene therapy might prolong survival and delay progression of symptoms. Harnessing the regenerative potential of the central nervous system would be a novel approach for the treatment of motor neuron death resulting from ALS. Endogenous neural replacement, if augmented with administration of exogenous growth factors or with pharmaceuticals that increase the rate of neural progenitor formation, neural migration, and neural maturation could slow the rate of cell loss enough to result in clinical improvement. In this review, we discuss the impact of therapeutic treatment involving stem cell therapy, trophic factors, gene therapy, and combination therapy on disease onset and progression of ALS. In addition, we summarize human clinical trials of stem cell therapy, growth factor therapy, and gene therapy in individuals with ALS.

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Recent advancements in stem cell and gene therapies for neurological disorders and intractable epilepsy

Cited by 49 publications

References 160 publications

Progress in Cell Grafting Therapy for Temporal Lobe Epilepsy

Progress in Cell Grafting Therapy for Temporal Lobe Epilepsy

Stem Cell Therapy: A Promising Therapeutic Approach for Multiple Sclerosis

Neuroprotection for Amyotrophic Lateral Sclerosis: Role of Stem Cells, Growth Factors, and Gene Therapy

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