Enhanced re-myelination in transthyretin null mice following cuprizone mediated demyelination

Pagnin, Maurice; Dekiwadia, Chaitali; Petratos, Steven; Richardson, Samantha J.

doi:10.1016/j.neulet.2021.136287

Cited by 4 publications

(2 citation statements)

References 38 publications

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“…We highlighted that such hypothyroidism, applied during demyelination, enabled a functional recovery of nerve conduction ( 21 ) ( Figure 1 ). Similarly, TTR null mice also displayed an increase in oligodendrogenesis during development ( 65 ) as well as a thicker myelin sheath in the corpus callosum following cuprizone withdrawal ( 66 ). Thus, SVZ-derived OPCs constitute an endogenous source of glial progenitors capable of functionally repairing a demyelinated lesion localized in the corpus callosum, close to the lateral ventricles as it has been also demonstrated by other works ( 51 , 52 ).…”

Section: Thyroid Hormone Action In the Svzmentioning

confidence: 99%

Thyroid hormone action in adult neurogliogenic niches: the known and unknown

Valcárcel-Hernández,

Mayerl,

Guadaño-Ferraz

et al. 2024

Front. Endocrinol.

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Over the last decades, thyroid hormones (THs) signaling has been established as a key signaling cue for the proper maintenance of brain functions in adult mammals, including humans. One of the most fascinating roles of THs in the mature mammalian brain is their ability to regulate adult neurogliogenic processes. In this respect, THs control the generation of new neuronal and glial progenitors from neural stem cells (NSCs) as well as their final differentiation and maturation programs. In this review, we summarize current knowledge on the cellular organization of adult rodent neurogliogenic niches encompassing well-established niches in the subventricular zone (SVZ) lining the lateral ventricles, the hippocampal subgranular zone (SGZ), and the hypothalamus, but also less characterized niches in the striatum and the cerebral cortex. We then discuss critical questions regarding how THs availability is regulated in the respective niches in rodents and larger mammals as well as how modulating THs availability in those niches interferes with lineage decision and progression at the molecular, cellular, and functional levels. Based on those alterations, we explore the novel therapeutic avenues aiming at harnessing THs regulatory influences on neurogliogenic output to stimulate repair processes by influencing the generation of either new neurons (i.e. Alzheimer’s, Parkinson’s diseases), oligodendrocytes (multiple sclerosis) or both (stroke). Finally, we point out future challenges, which will shape research in this exciting field in the upcoming years.

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Section: Thyroid Hormone Action In the Svzmentioning

confidence: 99%

Thyroid hormone action in adult neurogliogenic niches: the known and unknown

Valcárcel-Hernández,

Mayerl,

Guadaño-Ferraz

et al. 2024

Front. Endocrinol.

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“…Toxin models have greatly facilitated the investigation of pathways involved in oligodendroglial proliferation, recruitment, differentiation and remyelination. Promising mechanisms that are under investigation in clinical trials for remyelination in MS that have emerged from investigation of remyelination in focal and systemic toxin models include LINGO-1 antagonism ( Mi et al, 2009 ), Nogo-A antagonism ( Ineichen et al, 2017 ), RXR agonism ( Huang et al, 2011 ; Natrajan et al, 2015 ), muscarinic receptor antagonism ( Mei et al, 2014 ; Chen et al, 2017 ), semaphorin 3A ( Piaton et al, 2011 ; Syed et al, 2011 ), sex hormone estrogen and testosterone supplementation ( Patel et al, 2013 ), estrogen receptor modulators ( Sicotte et al, 2007 ; Gonzalez et al, 2016 ; Rankin et al, 2019 ; Voskuhl et al, 2019 ), thyroid hormone ( Bai et al, 2016 ; Hartley et al, 2019 ; Rosato-Siri et al, 2021 ; Pagnin et al, 2022 ) and metabolism modulation ( Berghoff et al, 2017 ; Neumann et al, 2019 ).…”

Section: Toxin-mediated Demyelination Modelsmentioning

confidence: 99%

Remyelination in animal models of multiple sclerosis: finding the elusive grail of regeneration

Packer,

Fresenko,

Harrington

2023

Front. Mol. Neurosci.

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Remyelination biology and the therapeutic potential of restoring myelin sheaths to prevent neurodegeneration and disability in multiple sclerosis (MS) has made considerable gains over the past decade with many regeneration strategies undergoing tested in MS clinical trials. Animal models used to investigate oligodendroglial responses and regeneration of myelin vary considerably in the mechanism of demyelination, involvement of inflammatory cells, neurodegeneration and capacity for remyelination. The investigation of remyelination in the context of aging and an inflammatory environment are of considerable interest for the potential translation to progressive multiple sclerosis. Here we review how remyelination is assessed in mouse models of demyelination, differences and advantages of these models, therapeutic strategies that have emerged and current pro-remyelination clinical trials.

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