MiR-146a promotes remyelination in a cuprizone model of demyelinating injury.

The death of mature oligodendrocytes (OLs) which are the sole myelinating cells of the central nervous system (CNS), leads to demyelination and functional deficits. Currently, there is lack of effective remyelination therapies for patients with demyelinating diseases. MicroRNAs (miRNAs) mediate OL function.

Thymosin beta4 promotes oligodendrogenesis in the demyelinating central nervous system.

Multiple sclerosis (MS) is a demyelinating disease of the central nervous system (CNS). No effective remyelination therapies are in use. We hypothesized that thymosin beta4 (Tβ4) is an effective remyelination treatment by promoting differentiation of oligodendrocyte progenitor cells (OPCs), and that the epidermal growth factor receptor (EGFR) signaling pathway contributes to this process.

Untargeted Plasma Metabolomics Identifies Endogenous Metabolite with Drug-like Properties in Chronic Animal Model of Multiple Sclerosis.

We performed untargeted metabolomics in plasma of B6 mice with experimental autoimmune encephalitis (EAE) at the chronic phase of the disease in search of an altered metabolic pathway(s). Of 324 metabolites measured, 100 metabolites that mapped to various pathways (mainly lipids) linked to mitochondrial function, inflammation, and membrane stability were observed to be significantly altered between EAE and control (p < 0.05, false discovery rate <0.

Fingolimod treatment promotes proliferation and differentiation of oligodendrocyte progenitor cells in mice with experimental autoimmune encephalomyelitis.

Multiple sclerosis (MS) is a major demyelinating disease of the central nervous system (CNS) leading to functional deficits. The remyelination process is mediated by oligodendrocyte progenitor cells (OPCs). In this study, we tested the hypothesis that Fingolimod, a sphingosine 1-phosphate (S1P) receptor modulator, stimulates OPC differentiation into mature oligodendrocytes, in addition to its well-known anti-inflammatory effect.

Perfusion and Diffusion Abnormalities of Multiple Sclerosis Lesions and Relevance of Classified Lesions to Disease Status.

Objective: Hemodynamic abnormality and disruption of white matter (WM) integrity are significant components in the pathophysiology of multiple sclerosis (MS) lesions. However, the roles of stratified lesions with distinct degrees of hemodynamic and structural injury in disease states remain to be explored. We tested the hypothesis that hemodynamic and structural impairment, as assessed by cerebral blood volume (CBV) and fractional anisotropy (FA), respectively, characterizes the extent of tissue injury, and the load of lesion with substantial tissue destruction would reflect the disease status and therefore, would be related to clinical disability.

Longitudinal Follow-up of a Cohort of Patients with Incidental Abnormal Magnetic Resonance Imaging Findings at Presentation and Their Risk of Developing Multiple Sclerosis.

Background: Magnetic resonance imaging (MRI) is widely used in clinical practice, and "abnormal brain MRI" findings often prompt assessment for multiple sclerosis (MS), even when there are no symptoms suggestive of the disease. Despite several studies involving individuals with "radiologically isolated syndrome" (RIS), little is known about what factors might predict future development of MS. The objective of this study was to longitudinally evaluate clinical and MRI characteristics of people who presented to an MS clinic because of incidental abnormal MRI findings but did not have typical symptoms of MS, in order to assess risk factors for developing MS.

Muscle-specific kinase-antibody-positive myasthenia gravis after autologous bone marrow transplantation.

A 44-year-old man presented with oculobulbar weakness approximately 5 years after autologous bone marrow transplantation (BMT). His workup led to the diagnosis of muscle-specific kinase-antibody-related myasthenia gravis (MG). There has been only one case report of muscle-specific kinase-antibody-positive MG after BMT, which was allogeneic.

The appointment of neurointensivists is financially beneficial to the employer.

Background: Although the impact of a neurointensivist (NI) on patient outcomes has been examined in the past, the financial impact has not been estimated before.

Methods: We extracted the financial data from the Neuro-Intensive Care Unit (NICU) at Henry Ford Hospital during two 3-year periods, one before and one after the appointment of a NI. Net revenue (NR), total direct expenses (TDE), and contribution margin (CM) were compared between these two periods both for Henry Ford Hospital and the Henry Ford Medical Group.

Bone marrow stromal cells increase oligodendrogenesis after stroke.

Oligodendrocytes are sensitive to ischemic damage. The Sonic hedgehog (Shh) pathway is critical in oligodendrogenesis; Gli1 is the principal effector of Shh signaling. We investigated oligodendrogenesis and Shh/Gli1 pathway activation after bone marrow stromal cell (BMSC) treatment of stroke in rats.

Bone marrow stromal cell therapy reduces proNGF and p75 expression in mice with experimental autoimmune encephalomyelitis.

Demyelination is prominent in experimental autoimmune encephalomyelitis (EAE). The receptor p75 and its high affinity ligand proNGF are required for oligodendrocyte death after injury. We hypothesize that bone marrow stromal cells (BMSCs) provide therapeutic benefit in EAE mice by reducing proNGF/p75 expression.

Measuring adherence and persistence to disease-modifying agents among patients with relapsing remitting multiple sclerosis.

Objectives: To measure disease-modifying agent adherence and persistence among patients with multiple sclerosis (MS).

Design: Retrospective cohort study.

Setting: Multispecialty, salaried group practice in southeast Michigan, between June 1, 2004, and June 30, 2006.

Niaspan treatment improves neurological functional recovery in experimental autoimmune encephalomyelitis mice.

We investigated the treatment of experimental autoimmune encephalomyelitis (EAE) in mice with Niaspan, an agent used to elevate high-density lipoprotein (HDL). EAE mice were treated with Niaspan starting on the immunization or clinical onset day. Neurological functional recovery was significantly increased in the Niaspan treated mice (100 mg/kgbw) compared to the controls.

Bone marrow stromal cells protect oligodendrocytes from oxygen-glucose deprivation injury.

Oligodendrocyte (OLG) damage leads to demyelination, which is frequently observed in ischemic cerebrovascular diseases. In this study, we investigated the effect of bone marrow stromal cells (BMSCs) on OLGs subjected to oxygen-glucose deprivation (OGD). N20.

Evaluation of corticospinal axon loss by fluorescent dye tracing in mice with experimental autoimmune encephalomyelitis.

In both multiple sclerosis (MS) patients and experimental autoimmune encephalomyelitis (EAE) animals, axon loss has been demonstrated to correlate with neurological disability. However, it is difficult to accurately determine the location and severity of axonal damage since the lesion in MS or EAE is disseminated and is frequently in a relapsing-remitting mode. The corticospinal system is the only direct pathway from the motorsensory cortex to the spinal cord, and the major neural pathway for control of voluntary movement.

Bone marrow stromal cells reduce axonal loss in experimental autoimmune encephalomyelitis mice.

We investigated the ability of human bone marrow stromal cell (hBMSC) treatment to reduce axonal loss in experimental autoimmune encephalomyelitis (EAE) mice. EAE was induced in SJL/J mice by injection with proteolipid protein (PLP). Mice were injected intravenously with hBMSCs or PBS on the day of clinical onset, and neurological function was measured daily (score 0-5) until 45 weeks after onset.

Human bone marrow stromal cell treatment improves neurological functional recovery in EAE mice.

We investigated the treatment of remitting-relapsing experimental autoimmune encephalomyelitis (EAE) in mice with human bone marrow stromal cells (hBMSCs). hBMSCs were injected intravenously into EAE mice upon onset of paresis. Neurological functional tests were scored daily by grading clinical signs (score 0-5).

Erythropoietin treatment improves neurological functional recovery in EAE mice.

Erythropoietin (EPO), originally recognized for its central role in erythropoiesis, has been shown to improve neurological outcome after stroke. Here, we investigated the treatment of experimental autoimmune encephalomyelitis (EAE) in mice with EPO. Mice were treated with recombinant human EPO (rhEPO) upon onset of paresis.