Neuroprotective effects of mesenchymal stem cell transplantation in animal model of cerebellar degeneration

Edalatmanesh, Mohammad Amin; Bahrami, Ahmad Reza; Hosseini, Ebrahim; Hosseini, Mahmoud; Khatamsaz, Saeed

doi:10.1179/1743132811y.0000000036

Cited by 27 publications

(16 citation statements)

References 40 publications

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“…When injected into the same location as a forced quinolinic acid (QA)‐induced cerebellar lesion site, the negative impacts of QA on rotarod learning and beam walking speed were ameliorated. Also, hMSC transplantation protected against Purkinje cell loss [17]. Similarly, in a rat model of ischemic stroke, hUC‐MSC transplantation provided a significant increase in neurobehavioral function (neurobehavioral tests included consciousness, gait, limb tone, and pain reflex), and a significant decrease in the final infarct volume relative to the control group [13].…”

Section: Stem Cell Therapymentioning

confidence: 99%

Concise Review: Stem Cell Therapies for Neuropathic Pain

Fortino

Pelaez

Cheung

2013

Stem Cells Translational Medicine

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Neuropathic pain is a chronic condition that is heterogeneous in nature and has different causes. Different from and more burdensome than nociceptive pain, neuropathic pain more severely affects people's quality of life. Understanding the various mechanisms of the onset and progression of neuropathic pain is important in the development of an effective treatment. Research is being done to replace current pharmacological treatments with cellular therapies that will have longer lasting effects. Stem cells present an exciting potential therapy for neuropathic pain. In this review, we describe the neuroprotective effects of stem cells along with special emphasis on the current translational research using stem cells to treat neuropathic pain.

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Section: Stem Cell Therapymentioning

confidence: 99%

Concise Review: Stem Cell Therapies for Neuropathic Pain

Fortino

Pelaez

Cheung

2013

Stem Cells Translational Medicine

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“…With 2 μ g/mL of CM-DiI, MSCs were labeled and transplanted into the right cerebellar hemisphere (folia VI). After 6 weeks, DiI-labeled MSCs were found surviving and migrating in a deep layer of the cerebellar cortex [20]. Lee et al transplanted adipose-derived stem cells (ASCs) labeled with Vybrant DiO and costained with specific antibodies including those against BDNF, calbindin, γ -amino butyric acid (GABA), and glutamic acid decarboxylase (GAD).…”

Section: Stem Cell Trackingmentioning

confidence: 99%

In Vivo Assessment of Stem Cells for Treating Neurodegenerative Disease: Current Approaches and Future Prospects

Song

2017

Stem Cells International

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In recent years, stem cell-related therapies have been widely applied for treating neurodegenerative disease. Despite their potential, stem cell tracking and imaging techniques for the evaluation of in vivo proof-of-concept (PoC) therapies have not been sufficiently represented in the research area. This review summarizes the recent approaches that have been used for tracking and imaging engrafted stem cells in vivo. Furthermore, we introduce tissue clearing technology that can be applied to develop three-dimensional in vivo experiments. Monitoring stem cell survival and migration and graft-host relationships is a useful strategy to evaluate the therapeutic efficacy of regenerative medicine approaches in neurodegenerative disease.

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“…An increasing number of studies have proven the efficacy of stem cell therapy for animal models of a variety of diseases, including cerebellar ataxia [42-44]; however, stem cell therapy still has not been shown to be a proven therapy in humans and is not recommended at this time.…”

Section: Stem Cell Therapymentioning

confidence: 99%

Autosomal dominant cerebellar ataxia type III: a review of the phenotypic and genotypic characteristics

Fujioka

Sundal

Wszołek

2013

Orphanet J Rare Dis

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Autosomal Dominant Cerebellar Ataxia (ADCA) Type III is a type of spinocerebellar ataxia (SCA) classically characterized by pure cerebellar ataxia and occasionally by non-cerebellar signs such as pyramidal signs, ophthalmoplegia, and tremor. The onset of symptoms typically occurs in adulthood; however, a minority of patients develop clinical features in adolescence. The incidence of ADCA Type III is unknown. ADCA Type III consists of six subtypes, SCA5, SCA6, SCA11, SCA26, SCA30, and SCA31. The subtype SCA6 is the most common. These subtypes are associated with four causative genes and two loci. The severity of symptoms and age of onset can vary between each SCA subtype and even between families with the same subtype. SCA5 and SCA11 are caused by specific gene mutations such as missense, inframe deletions, and frameshift insertions or deletions. SCA6 is caused by trinucleotide CAG repeat expansions encoding large uninterrupted glutamine tracts. SCA31 is caused by repeat expansions that fall outside of the protein-coding region of the disease gene. Currently, there are no specific gene mutations associated with SCA26 or SCA30, though there is a confirmed locus for each subtype. This disease is mainly diagnosed via genetic testing; however, differential diagnoses include pure cerebellar ataxia and non-cerebellar features in addition to ataxia. Although not fatal, ADCA Type III may cause dysphagia and falls, which reduce the quality of life of the patients and may in turn shorten the lifespan. The therapy for ADCA Type III is supportive and includes occupational and speech modalities. There is no cure for ADCA Type III, but a number of recent studies have highlighted novel therapies, which bring hope for future curative treatments.

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Neuroprotective effects of mesenchymal stem cell transplantation in animal model of cerebellar degeneration

Cited by 27 publications

References 40 publications

Concise Review: Stem Cell Therapies for Neuropathic Pain

Concise Review: Stem Cell Therapies for Neuropathic Pain

In Vivo Assessment of Stem Cells for Treating Neurodegenerative Disease: Current Approaches and Future Prospects

Autosomal dominant cerebellar ataxia type III: a review of the phenotypic and genotypic characteristics

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