In Vivo Expression of Reprogramming Factor OCT4 Ameliorates Myelination Deficits and Induces Striatal Neuroprotection in Huntington’s Disease

Yu, Ji Hea; Nam, Bae Geun; Kim, Min Gi; Pyo, Soonil; Seo, Jung Hwa; Cho, Sung Rae

doi:10.3390/genes12050712

Cited by 4 publications

(4 citation statements)

References 82 publications

(101 reference statements)

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“…Such results reveal undeniable defect of the microstructure of brain tissues. DTI was used as a biomarker of myelination to evaluate the effect of a reprogramming factor injection in R6/2 mice ( Yu et al, 2021 ). Continuous Time Random Walk (CTRW) model on the same mice showed decreased Dαβ and α parameters, highlighting increased tortuosity and axonal density of corpus callosum ( Gatto et al, 2019 ).…”

Section: Mri and Mrs Findings In Genetic Mouse Models Of Hdmentioning

confidence: 99%

The contribution of preclinical magnetic resonance imaging and spectroscopy to Huntington’s disease

Pérot,

Brouillet,

Flament

2024

Front. Aging Neurosci.

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Huntington’s disease is an inherited disorder characterized by psychiatric, cognitive, and motor symptoms due to degeneration of medium spiny neurons in the striatum. A prodromal phase precedes the onset, lasting decades. Current biomarkers include clinical score and striatal atrophy using Magnetic Resonance Imaging (MRI). These markers lack sensitivity for subtle cellular changes during the prodromal phase. MRI and MR spectroscopy offer different contrasts for assessing metabolic, microstructural, functional, or vascular alterations in the disease. They have been used in patients and mouse models. Mouse models can be of great interest to study a specific mechanism of the degenerative process, allow better understanding of the pathogenesis from the prodromal to the symptomatic phase, and to evaluate therapeutic efficacy. Mouse models can be divided into three different constructions: transgenic mice expressing exon-1 of human huntingtin (HTT), mice with an artificial chromosome expressing full-length human HTT, and knock-in mouse models with CAG expansion inserted in the murine htt gene. Several studies have used MRI/S to characterized these models. However, the multiplicity of modalities and mouse models available complicates the understanding of this rich corpus. The present review aims at giving an overview of results obtained using MRI/S for each mouse model of HD, to provide a useful resource for the conception of neuroimaging studies using mouse models of HD. Finally, despite difficulties in translating preclinical protocols to clinical applications, many biomarkers identified in preclinical models have already been evaluated in patients. This review also aims to cover this aspect to demonstrate the importance of MRI/S for studying HD.

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Section: Mri and Mrs Findings In Genetic Mouse Models Of Hdmentioning

confidence: 99%

The contribution of preclinical magnetic resonance imaging and spectroscopy to Huntington’s disease

Pérot,

Brouillet,

Flament

2024

Front. Aging Neurosci.

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“…In a 2021 study by Yu et al, the reprogramming effects of Oct4 were investigated using R6/2 mice, a Huntington's disease model [22]. Two weeks after Oct4 injection, an increase in Nestin+ cells, a marker of neural stem cells, was observed.…”

Section: Disease or Injured Animal Modelsmentioning

confidence: 99%

“…These induced neurons were identified as calretinin+ and Neun+ neurons, and they were detected for up to 36 weeks. Moreover, these induced neurons displayed electrophysiological functionality and integrated into local circuits, allowing them to receive inputs from presynaptic neurons [22]. Regarding the cell of origin, Zhang C. L.'s group suggested astrocytes as the source.…”

Section: Healthy Animal Modelsmentioning

confidence: 99%

In Vivo Reprogramming Using Yamanaka Factors in the CNS: A Scoping Review

Cho,

Lee,

Seo

et al. 2024

Cells

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Central nervous system diseases, particularly neurodegenerative disorders, pose significant challenges in medicine. These conditions, characterized by progressive neuronal loss, have remained largely incurable, exacting a heavy toll on individuals and society. In recent years, in vivo reprogramming using Yamanaka factors has emerged as a promising approach for central nervous system regeneration. This technique involves introducing transcription factors, such as Oct4, Sox2, Klf4, and c-Myc, into adult cells to induce their conversion into neurons. This review summarizes the current state of in vivo reprogramming research in the central nervous system, focusing on the use of Yamanaka factors. In vivo reprogramming using Yamanaka factors has shown promising results in several animal models of central nervous system diseases. Studies have demonstrated that this approach can promote the generation of new neurons, improve functional outcomes, and reduce scar formation. However, there are still several challenges that need to be addressed before this approach can be translated into clinical practice. These challenges include optimizing the efficiency of reprogramming, understanding the cell of origin for each transcription factor, and developing methods for reprogramming in non-subventricular zone areas. Further research is needed to overcome the remaining challenges, but this approach has the potential to revolutionize the way we treat central nervous system disorders.

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“…Studies have demonstrated that more functionally induced neurons and oligodendrocytes can be obtained by in vivo reprogramming ( Farhangi et al, 2019 ; Wu et al, 2020 ; Zhou et al, 2020 ). In vivo reprogramming has been attempted in neurological diseases, such as Parkinson’s disease ( Theodorou et al, 2015 ; Niu et al, 2018 ) and Huntington’s disease ( Wu et al, 2020 ; Yu et al, 2021 ). Experiments have shown that reactive glial cells can be converted into functional neurons using a single TF NeuroD1 fate in vivo in brain injury and AD models ( Guo et al, 2014 ).…”

Section: Potential To Cure For Alzheimer’s Disease Using In...mentioning

confidence: 99%

Cellular Reprogramming and Its Potential Application in Alzheimer’s Disease

Zhou

Zhu

et al. 2022

Front. Neurosci.

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Alzheimer’s disease (AD) has become the most common age-related dementia in the world and is currently incurable. Although many efforts have been made, the underlying mechanisms of AD remain unclear. Extracellular amyloid-beta deposition, intracellular tau hyperphosphorylation, neuronal death, glial cell activation, white matter damage, blood–brain barrier disruption, and other mechanisms all take part in this complicated disease, making it difficult to find an effective therapy. In the study of therapeutic methods, how to restore functional neurons and integrate myelin becomes the main point. In recent years, with the improvement and maturity of induced pluripotent stem cell technology and direct cell reprogramming technology, it has become possible to induce non-neuronal cells, such as fibroblasts or glial cells, directly into neuronal cells in vitro and in vivo. Remarkably, the induced neurons are functional and capable of entering the local neural net. These encouraging results provide a potential new approach for AD therapy. In this review, we summarized the characteristics of AD, the reprogramming technique, and the current research on the application of cellular reprogramming in AD. The existing problems regarding cellular reprogramming and its therapeutic potential for AD were also reviewed.

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In Vivo Expression of Reprogramming Factor OCT4 Ameliorates Myelination Deficits and Induces Striatal Neuroprotection in Huntington’s Disease

Cited by 4 publications

References 82 publications

The contribution of preclinical magnetic resonance imaging and spectroscopy to Huntington’s disease

The contribution of preclinical magnetic resonance imaging and spectroscopy to Huntington’s disease

In Vivo Reprogramming Using Yamanaka Factors in the CNS: A Scoping Review

Cellular Reprogramming and Its Potential Application in Alzheimer’s Disease

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