A5036724567- Multiple Sclerosis Research Studies
- Long-Term Effects of COVID-19
- Mitochondrial Function and Pathology
- Ubiquitin and proteasome pathways
- Autophagy in Disease and Therapy
- Peripheral Neuropathies and Disorders
- COVID-19 and Mental Health
- Autoimmune Neurological Disorders and Treatments
- Infectious Encephalopathies and Encephalitis
- Fibromyalgia and Chronic Fatigue Syndrome Research
- Cytokine Signaling Pathways and Interactions
- SARS-CoV-2 and COVID-19 Research
- Systemic Lupus Erythematosus Research
- COVID-19 Clinical Research Studies
- Intracerebral and Subarachnoid Hemorrhage Research
- Intracranial Aneurysms: Treatment and Complications
- Anesthesia and Pain Management
- Genetic Neurodegenerative Diseases
- Stroke Rehabilitation and Recovery
- Pathogenesis and Treatment of Hiccups
- Herpesvirus Infections and Treatments
- History of Medicine Studies
- Parkinson's Disease Mechanisms and Treatments
- Protein Degradation and Inhibitors
- Spine and Intervertebral Disc Pathology
Johns Hopkins University
2023-2025
Johns Hopkins Medicine
2023-2025
Cedars-Sinai Medical Center
2024
University of California, Los Angeles
2024
University of Calgary
2018-2023
University of Alberta
2023
Women and Children’s Health Research Institute
2023
Centre for Mental Health
2023
Deleted Institution
2023
Montreal Neurological Institute and Hospital
2013-2022
Parkin Enhanced? Inactivation of parkin, an E3 ubiquitin ligase, is responsible for a familial form Parkinson's disease and may be involved in sporadic forms as well. Trempe et al. (p. 1451 , published online 9 May) present the crystal structure full-length parkin autoinhibited configuration. Guided by structure, mutations were designed that activated both vitro cells. Because neuroprotective, provides framework enhancing function therapeutic strategy disease.
A 28-year-old Black woman presented with both typical and atypical features of multiple sclerosis in the setting multimorbidity including psychiatric history, complicating diagnosis treatment. This case illustrates importance differential longitudinal follow-up before committing to disease-modifying therapy. Individualized treatment decision-making is highlighted.
We used a robotic exoskeleton to quantify specific patterns of abnormal upper limb motor behaviour in people who have had transient ischemic attack (TIA). A cohort with TIA was recruited within two weeks symptom onset. All individuals completed robotic-based assessment 8 behavioural tasks related and proprioceptive function, as well cognitive function. Robotic task performance compared large controls without neurological impairments corrected for the influence age. Impairment defined below...
Mutations in Parkin and PINK1 cause early-onset familial Parkinson's disease. is a RING-In-Between-RING E3 ligase that transfers ubiquitin from an E2 enzyme to substrate two steps: (i) thioester intermediate formation on (ii) acyl transfer lysine. The process triggered by PINK1, which phosphorylates damaged mitochondria, turn recruits activates Parkin. This leads the ubiquitination of outer mitochondrial membrane proteins clearance organelle. While targets mitochondria are known, factors...
The long-term impact of COVID-19 among those with mild infections is not well characterized. Among 81 adults who completed online assessments at 3- and 12-months following infection, quality life scores did significantly improve over time. 62 subjects also telephone interviews, respiratory symptoms or exercise limitation were reported by 42% a median follow-up 387 days (IQR 251-402 days). Those persistent scored lower on the EQ-5D visual analog score compared to without. Persistent...
Various neurologic manifestations have been reported in patients with COVID-19, mostly retrospective studies of admitted to hospital, but there are few data on mild COVID-19. We examined the frequency and persistence neurologic/neuropsychiatric symptoms COVID-19 a 1-year prospective cohort study, as well assessment use health care services patient-reported outcomes.Participants Alberta HOPE trial (hydroxychloroquine v. placebo for 5 d), managed outpatients, were prospectively assessed 3...
Herein we describe a case of relapsing anti-GAD65-associated encephalitis which was responsive to the combination thymoma resection, external beam radiotherapy, and immunomodulatory therapy. The illustrates value remaining vigilant for possibility paraneoplastic syndromes in context anti-GAD65 antibodies thymoma. It also that tumor-directed therapies may offer additional benefit beyond therapy alone.
To compare anti-GAD65-associated neurological disorders that impact cerebellar function.
Previous reports of patients with myelitis associated rheumatologic disease may have had unrecognized aquaporin-4 (AQP4)-IgG seropositive neuromyelitis optica spectrum disorder (NMOSD) or myelin oligodendrocyte glycoprotein (MOG)-IgG-associated (MOGAD). We clinicoradiologically and serologically characterized evaluated in the era availability MOG-IgG more sensitive AQP4-IgG cell-based assays.
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Accurate anti-aquaporin-4 (AQP4) and anti-myelin oligodendrocyte glycoprotein (MOG) autoantibody assays are needed to effectively diagnose neuromyelitis optica spectrum disorder MOG antibody-associated disease. A proportion of patients at our centre have been tested for anti-AQP4 anti-MOG autoantibodies locally, followed by an outsourced test as part real-world practice. Outsourced testing is costly unproven utility. We conducted a quality improvement project determine the value...
Abstract Mutations in Parkin and PINK1 cause an early-onset familial Parkinson’s disease. is a RING-In-Between-RING (RBR) E3 ligase that transfers ubiquitin from E2 enzyme to substrate two steps: 1) thioester intermediate formation on Parkin, 2) acyl transfer lysine. The process triggered by PINK1, which phosphorylates damaged mitochondria, turn recruits activates Parkin. This leads the ubiquitination of outer mitochondrial membrane proteins clearance organelle. While targets mitochondria...
Mutations in the Parkin gene are responsible for an autosomal recessive form of Parkinson's disease. The parkin protein is a RING1-In-Between-RING2 (RBR) E3 ubiquitin ligase, which functions through two-step mechanism involving parkin~ubiquitin thioester intermediate [1]. However, compared to other ligases, exhibits low basal activity and requires activation both vitro cells. As neuroprotective various models disease, understanding how it catalyses transfer will be critical. We previously...
An abstract is not available for this content so a preview has been provided. As you have access to content, full PDF via the ‘Save PDF’ action button.
April 27, 2018April 10, 2018Free AccessCommunication Priorities in Spontaneous Intracerebral Hemorrhage (CPsICH): A Survey-based Study Incorporating Patient and Physician Perspectives (P6.335)Jonathan Krett, Cally Martin, Colleen Murphy, J. Gordon Boyd, Nicole Chenier-Hogan, Phyllis Davis, Vivian Bethell, Albert JinAuthors Info & AffiliationsApril 2018 issue90 (15_supplement)https://doi.org/10.1212/WNL.90.15_supplement.P6.335 Letters to the Editor