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Clinical Trial-Ready Patient Cohorts for Multiple System Atrophy: Coupling Biospecimen and iPSC Banking to Longitudinal Deep-Phenotyping.
Cerebellum
February 2024
Department of Neurology, Building for Transformative Medicine Room 10016L, Brigham and Women's Hospital and Harvard Medical School, 60 Fenwood Road, Boston, 02115, USA.
Article Synopsis
- Multiple System Atrophy (MSA) is a deadly neurodegenerative disease linked to protein aggregation and shares similarities with Parkinson's disease; its complexity and fast progression make drug development challenging.
- Researchers have created a cohort of 69 carefully assessed MSA patients and are recruiting them into a unique clinical trial setup that tracks individual patient progress over time.
- The study includes extensive patient phenotyping, collection of biospecimens, and development of induced pluripotent stem cell (iPSC) models to enhance understanding of MSA and improve chances of successful therapies through personalized medicine.
Classification of pseudocalcium visual responses from mouse retinal ganglion cells.
Vis Neurosci
November 2021
Department of Molecular and Cellular Mechanisms of Neurodegeneration, Paul Flechsig Institute for Brain Research, University of Leipzig, Leipzig, Germany.
Recently, a detailed catalog of 32 retinal ganglion cell (RGC) visual response patterns in mouse has emerged. However, the 10,000 samples required for this catalog-based on fluorescent signals from a calcium indicator dye-are much harder to acquire from the extracellular spike train recordings underlying our bionic vision research. Therefore, we sought to convert spike trains into pseudocalcium signals so that our data could be directly matched to the 32 predefined, calcium signal-based groups.
View Article and Find Full Text PDFCerebral Microbleeds, Cerebral Amyloid Angiopathy, and Their Relationships to Quantitative Markers of Neurodegeneration.
Neurology
April 2022
From the Departments of Neurology (C.B., K.K., M.L., A.J.S.-A., D.Z., A.M., A.F.T., M.S.V.E., D.R., J.G.) and Pathology and Cell Biology (X.E.F., S.P.L., J.P.V., A.F.T.), Columbia University Irving Medical Center, New York, NY; Department of Neurology (C.B.), UCLA Medical Center, Los Angeles, CA; Memory Aging and Cognition Center (S.H., C.C.), National University Health System, Singapore; Department of Pharmacology (S.H., C.C.), Yong Loo Lin School of Medicine, National University of Singapore; Saw Swee Hock School of Public Health (S.H.), National University of Singapore and National University Health System, Singapore; College of Medicine (G.P.-S.), SUNY Upstate Medical University, Syracuse, NY; Singapore Eye Research Institute (C.-Y.C.), Singapore National Eye Centre; Ophthalmology and Visual Sciences Academic Clinical Program (C.-Y.C.), Duke-NUS Medical School, National University of Singapore; Istanbul University Cerrahpasa School of Medicine (B.A.), Turkey; Department of Neurology and Evelyn F. McKnight Brain Institute (V.J.D.B., T.R., R.L.S.), Miller School of Medicine, University of Miami Miller School of Medicine, FL; National Institutes of Health (C.W.), Bethesda, MD; Department of Pathology (E.C.), Icahn School of Medicine at Mount Sinai, New York, NY; and Department of Epidemiology (M.S.V.E.), Mailman School of Public Health, Columbia University, New York, NY.
Background And Objectives: Age-related cognitive impairment is driven by the complex interplay of neurovascular and neurodegenerative disease. There is a strong relationship between cerebral microbleeds (CMBs), cerebral amyloid angiopathy (CAA), and the cognitive decline observed in conditions such as Alzheimer disease. However, in the early, preclinical phase of cognitive impairment, the extent to which CMBs and underlying CAA affect volumetric changes in the brain related to neurodegenerative disease remains unclear.
View Article and Find Full Text PDFNeuroradiological findings expand the phenotype of OPA1-related mitochondrial dysfunction.
J Neurol Sci
February 2015
INSERM, U-1051, Institut des Neurosciences, Montpellier, France; CHU Montpellier, Centre of Reference for Genetic Sensory Diseases, Montpellier, France.
Objective: OPA1 mutations are responsible for more than half of autosomal dominant optic atrophy (ADOA), a blinding disease affecting the retinal ganglion neurons. In most patients the clinical presentation is restricted to the optic nerve degeneration, albeit in 20% of them, additional neuro-sensorial symptoms might be associated to the loss of vision, as frequently encountered in mitochondrial diseases. This study describes clinical and neuroradiological features of OPA1 patients.
View Article and Find Full Text PDFNeurodegeneration behind bars: from molecules to jurisprudence.
Front Psychiatry
September 2014
Evidence Based Health Care, University of Oxford, Oxford , UK.
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