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Christina Coughlan on Muck Rack

Christina Coughlan

As seen in: Color Research & Application, MDPI, BioRxiv, Cell Reports Medicine, Texas Medical Center

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Christina Coughlan’s Journalist Portfolio

Leach Wallace Associates Inc. : Review of Corporate Mission

Leach Wallace Associates Inc. : Review of Corporate Mission

As a consulting engineering company operating in Eldrige, Maryland, USA, Leach Wallace Associates, Inc is rec…

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Articles

Blood measure of neuronal death is exponentially higher with age, especially in females, and halted in Alzheimer’s disease by GM-CSF treatment

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By Stefan Sillau, Christina Coughlan, Kavita V. Nair, Paula Araya, Matthew Galbraith, Alanna Ritchie, Athena Wang, Brianne M. Bettcher, Joaquin M. Espinosa, Heidi J. Chial, Timothy Boyd, Huntington Potter, Mahiuddin Ahmed, Mihret T. Elos, Neill Epperson
| Cell Reports Medicine Verified
Keywords aging neurodegeneration Alzheimer’s granulocyte-macrophage colony-stimulating factor colony-stimulating factor 2 ubiquitin C-terminal hydrolase-L1 neurofilament light glial fibrillary acidic protein senolysis neuroprotection Introduction Increasing age is the greatest risk factor for “natural” age-associated cognitive decline (AACD) and, especially in females, for developing Alzheimer’s disease (AD), but the mechanisms underlying these connections are unknown.1,2,3,4,5,6,7,8,9,10...
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"Zoster-Associated Prothrombotic Plasma Exosomes and Increased Stroke R" by Andrew N Bubak, Christina Coughlan et al.

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By Andrew Bubak, Christina Coughlan, Janelle Posey, Anthony J. Saviola
| Texas Medical Center
Abstract Herpes zoster (HZ; shingles) caused by varicella zoster virus reactivation increases stroke risk for up to 1 year after HZ. The underlying mechanisms are unclear, however, the development of stroke distant from the site of zoster (eg, thoracic, lumbar, sacral) that can occur months after resolution of rash points to a long-lasting, virus-induced soluble factor (or factors) that can trigger thrombosis and/or vasculitis.
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Possible regulation of the immune modulator tetraspanin CD81 by alpha-synuclein in melanoma

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By Christina Coughlan, Michael Graner, Stephan Witt, Nirjhar M. Aloy
| BioRxiv
Abstract Herein we probed the mechanism by which α-syn/SNCA promotes the pathogenesis of melanoma. We found that SK-MEL-28 SNCA-KO melanoma clones have very low levels of tetraspanin CD81, which is a cell-surface protein that promotes invasion, migration, immune suppression.
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