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Muscle-resident mesenchymal progenitors sense and repair peripheral nerve injury via the GDNF-BDNF axis.

Fibro-adipogenic progenitors (FAPs) are muscle-resident mesenchymal progenitors that can contribute to muscle tissue homeostasis and regener … nactivation of Bdnf (Prrx1Cre; Bdnffl/fl) resulted in delayed nerve regeneration owing to defective remyelination, indicating that GDNF-sensing FAPs play an important role in the remyelination process during peripheral nerve regeneration. In aged mice, significantly reduced Bdnf expression in FAPs was observed upon nerve injury, suggesting the clinical relevanc …

Overview of emerging therapies for demyelinating diseases.

This paper provides an overview of autoimmune disorders of the central nervous system, specifically those caused by demyelination. We explore new research regarding potential therapeutic interventions, particularly those aimed at inducing remyelination. Remyelination is a detailed process, involving many cell types-oligodendrocyte precursor cells (OPCs), astrocytes, and microglia-and both the innate and adaptive immune systems. Our discussion of this process includes the differentiation potential of neural stem cells, the function of adult OPCs, and the impact of molecular mediators on myelin …

EBP50 is a key molecule for the Schwann cell-axon interaction in peripheral nerves.

Peripheral nerve injury disrupts the Schwann cell-axon interaction and the cellular communication between them. The peripheral nervous syste … he ablation of EBP50 in mice resulted in delayed nerve repair, recovery of behavioral function, and remyelination following nerve injury. EBP50 deficiency led to deficits in SC functions, including proliferation, migration, cytoskeleton dynamics, and axon interactions. The adeno-associated virus (AAV)-mediated local expression of EBP50 improved SCs migration, f …

Visual Evoked Potentials to Monitor Myelin Cuprizone-Induced Functional Changes.

The visual system is one of the most accessible routes to study the central nervous system under pathological conditions, such as in multipl … ze non-invasively, in vivo, the functional and structural changes associated with demyelination and remyelination in a preclinical model of MS. This approach contributes to the non-invasive study of possible effective treatments to promote remyelination in demyelinating pathologies.

Oligodendrocyte dysfunction and regeneration failure: A novel hypothesis of delayed encephalopathy after carbon monoxide poisoning.

Carbon monoxide (CO) poisoning usually causes brain lesions and delayed encephalopathy, also known as delayed neurological sequelae (DNS). D … ls can induce OPC expansion followed by OL differentiation, axonal contact and myelin regeneration (remyelination). Therefore, OL dysfunction and regeneration failure in the deep WM of the brain are the key pathophysiological mechanisms leading to delayed brain injury after CO poisoning. CO-induced toxicity may interfere with OL function and render OPCs unable …

TIP30 inhibits oligodendrocyte precursor cell differentiation via cytoplasmic sequestration of Olig1.

Differentiation of oligodendrocyte precursor cells (OPCs) is a prerequisite for both developmental myelination and adult remyelination in the central nervous system. The molecular mechanisms underlying OPC differentiation remain largely unknown. Here, we show that the thirty-kDa HIV-1 Tat interacting protein (TIP30) is a negative regulator in oligodendrocyte development. The TIP30(-/-) mice displayed an increased myelin protein level at postnatal day 14 and 21. By using a primary OPC culture system, we demonstrated that overexpression of TIP30 dramatically inhibited the stage progression of di…

Expression of interleukin-6 receptor alpha in normal and injured rat sciatic nerve.

Interleukin-6 (IL-6) is a pleiotropic cytokine synthesized by many different cells after appropriate stimulation. IL-6 binds first to the in … e period of Schwann cell proliferation. The expression of IL6-Ralpha continues during the period of remyelination, suggesting that IL6-Ralpha might be involved in both Schwann cell proliferation and remyelination of the rat sciatic nerve.

Congenital hypo- and hypermyelination neuropathy. Two cases.

Two young patients were referred recently to the authors for investigation of a peroneal atrophy syndrome. Since the first symptoms were observed in infancy, a congenital hypomyelination neuropathy was suspected, and superficial peroneal nerve biopsies were taken. Signs of severe and widespread demyelination/remyelination were observed. These features appeared morphologically similar to those observed in the globular or tomaculous neuropathies. The mechanism of the hypermyelination is discussed.

Reversibility of neurological deficits in vitamin B12 deficiency.

A female patient with subacute neurological deficits secondary to an hereditary vitamin B12 deficiency was repeatedly examined clinically and neurophysiologically. It is concluded that neurological normalization after treatment with vitamin B12 also occurs within the CNS. Such normalization takes place soon after initiating treatment and probably reflects other neuronal mechanisms that remyelination, i.e. recovery from conduction block in fast somatosensory pathways and/or improvement of synaptic transmission.

Protection From Demyelination by the Novel Adenosine Dual A2A/A2B Receptor Antagonist P626 in EAE and Cultured Oligodendrocyte Precursor Cells.

Multiple sclerosis (MS) is a chronic inflammatory disease characterised by myelin and axonal loss. Lack of remyelination is primarily attributed to the failure of oligodendrocyte progenitor cells (OPCs) to differentiate into mature oligodendrocytes. The neuromodulator adenosine can influence OPC differentiation, and by selectively stimulating A2A and A2B receptors (A2AR, A2BR), it inhibits OPC maturation. In the efforts of developing remyelinating and neuroprotective agents, this study evaluated the ability of a novel dual A2AR/A2BR antagonist, P626, in the experimental autoimmune encephalomye…

Exploring the Molecular Aspects of Glycosylation in MOG Antibody Disease (MOGAD).

Myelin Oligodendrocyte Glycoprotein-antibody disease (MOGAD) is an immune-mediated disorder that mainly targets the central nervous system o … . In the current scenario, there is an urgent need to develop therapeutic interventions that induce remyelination. Remyelination in terms of MOG glycosylation is hypothesized as a possible strategy to treat patients diagnosed with MOGAD. On the whole, the article aims to provide a clear insight into the disease and the structural aspects associated with it.

Occurrence of active demyelinating lesions in children with hereditary motor and sensory neuropathy (HMSN) type I.

In three children with dominant hereditary motor and sensory neuropathy type I, peripheral nerve biopsy showed the classical lesions of segmental demyelination with remyelination and onion bulb formations. In two cases, ultrastructural examination also demonstrated numerous characteristic features of active demyelination. The presence of active demyelinating lesions suggests an autoimmune attack superimposed on the course of a chronic genetic disease.

Spatiotemporal liposome-zwitterionic nano-hydrogel orchestrates immunomodulation and neurogenesis in spinal cord injury repair.

Following spinal cord injury (SCI), the sequential dysregulation of the inflammatory microenvironment coupled with insufficient endogenous n … nctional neurons and oligodendrocytes, enhancing neuronal signal transmission efficiency via axonal remyelination. In murine SCI models, this system significantly restored motor function through: acute immunomodulation by reducing neuroinflammation and reduces apoptosis, thereby preserving endogenous NSCs, whereas chronic neural remodeling by boosting neurogene …

GV1001: repurposing a telomerase-derived peptide for neurological therapeutics.

INTRODUCTION: Neurodegenerative and demyelinating diseases represent major unmet medical needs, with existing therapeutics demonstrating lim … ion, modulation of glial functional states away from tissue-damaging inflammation, and promotion of remyelination. Clinical translation through Phase 2 trials in Alzheimer's disease demonstrated statistically significant cognitive improvements consistent with neurotrophic benefit, with excellent safety profiles lacking amyloid-related imaging abnormalities. EX …

Будущее PET Imaging in Multical Sclerosis: Характеризация индивидуальных белых материалов.

Множественный склероз (MS) — многоплановое воспалительное, демиелинирующее и нейродегенеративное заболевание, характерное для повреждений с отличительными признаками в центральной нервной системе. Регулирование микроэкологических факторов, включая реконструирование внеклеточной матрицы (ВКМ) и активацию глиальных клеток, оказывает решающее воздействие на развитие повреждений и прогрессию заболеваний. Понимание биологических и патологических особенностей повреждений будет способствовать прогнозированию и индивидуализированному принятию решений о лечении. Позитронная эмиссионная томография (ПЕТ)

Совпадение в аннотации оригинала
Multiple sclerosis (MS) is a multifaceted inflammatory, demyelinating, and neurodegenerative disease typified by lesions with distinct hallm … ve MS, such as the availability of oligodendrocyte progenitor cells and ECM composition that affect remyelination and/or axon regeneration. This review explores the cellular and molecular ECM signatures and neuropathological processes of white matter MS lesions, discusses current and potential novel PET targets that may help characterise MS lesions in vivo, and …

Модуляция развернутой реакции белка с помощью C-терминального фрагмента MANF облегчает восстановление в моделях множественного склероза.

Воспаление в множестве склероза ведет к хронической активации механизма клеточного стресса, развернутой реакции белка (УПО), которая, как считается, усиливает нейроинфламмацию и предотвращает регенеративную реакцию тканей, например ремиилизацию. Модифицирующийся в рамках УПО белковый MANF продемонстрировал большие перспективы для смягчения хронической активации УПО и усиления регенерации тканей в различных моделях заболеваний, но не достигает CNS, когда он предоставляется в периферии. Мы использовали C-MANF, C-терминальный фрагмент MANF, и показали, что подкожное управление C-MANF способствова

Совпадение в аннотации оригинала
Inflammation in multiple sclerosis leads to chronic activation of a cellular stress mechanism, the unfolded protein response (UPR), which is thought to both exacerbate neuroinflammation and prevent regenerative tissue responses such as remyelination. The UPR-modulating protein MANF has shown great promise for attenuating chronic UPR activation and enhancing …

Effectiveness of Insolubilized Poly(vinyl alcohol)-Based Electrospun Fiber-Loaded Methylprednisolone by Enzyme-Catalyzed Cross-Linking in a Rat Spinal Cord Injury Model.

Spinal cord injury (SCI) has been implicated in neural loss and, consequently, motor/sensory impairment. Here, we propose an improved formation for fibrous mat fabrication from the derivatives of poly(vinyl alcohol) (PVA) and gelatin (Gela) through horseradish peroxidase-mediated cross-linking, providing a sustained release of methylprednisolone (MP) for SCI repair. After 28 days, the animals were evaluated in terms of remyelination and apoptosis and underwent behavioral tests. The mechanical properties, hydrophobicity, and degradation rate of PVAPh/GelaPh fibrous mats were significantly impro…

Galectin-3 alleviates demyelination by modulating microglial anti-inflammatory polarization through PPARγ-CD36 axis.

Demyelination is characterized by disruption of myelin sheath and disorders in myelin formation. Currently, there are no effective therapeutic treatments available. Microglia, especially anti-inflammatory phenotype microglia are critical for remyelination. Galectin-3 (Gal-3), which is known to modulate microglia activation, is correlated with myelination. In this study, we aimed to elucidate the roles of Gal-3 during myelin formation and explore the efficiency and mechanism of rGal-3 administration in remyelination. We enrolled Gal-3 knockout (Lgals3 KO) mice and demonstrated Lgals3 KO causes …

Постройте мышцы и защитите миелина.

Множественный склероз (MS) представляет собой хроническое и изнуряющее аутоиммунное заболевание центральной нервной системы (СНС), при котором иммунная реакция, основанная на CNS, разрушает миелин, что приводит к широкому спектру симптомов, включая онемение и покалывание, проблемы зрения, нарушение подвижности и т.д. Oligodendrocytes — это миелионирующие клетки в CNS, которые образуются из олигодендроголовых потомков (OPC) посредством дифференциации. Однако по целому ряду причин ОЗК не проводят различия с олигодендроцитами в РС, и в результате, стимулирование дифференциации ОЗК с олигодендроци

Совпадение в аннотации оригинала
Multiple sclerosis (MS) is a chronic and debilitating autoimmune disease of the central nervous system (CNS) in which a CNS-driven immune re … low-dose HMB is capable of stimulating the differentiation of cultured OPCs to oligodendrocytes for remyelination. Moreover, other causes of autoimmune demyelination are the decrease and/or suppression of Foxp3-expressing anti-autoimmune regulatory T cells (Tregs) and upregulation of autoimmune T-helper 1(Th1) and Th17 cells. Experimental autoimmune encephalomy …

Prostaglandin D2 synthase modulates macrophage activity and accumulation in injured peripheral nerves.

We have previously reported that prostaglandin D2 Synthase (L-PGDS) participates in peripheral nervous system (PNS) myelination during devel … on-cell autonomous mechanism, allowing myelin debris clearance and favoring axonal regeneration and remyelination. In addition, L-PGDS also appear to control macrophages accumulation in injured nerves, possibly by regulating the blood-nerve barrier permeability and SOX2 expression levels in Schwann cells. Collectively, our results suggest that L-PGDS has multip …