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Kahlilia C Morris-Blanco

Researcher at University of Wisconsin-Madison

Publications -  15
Citations -  334

Kahlilia C Morris-Blanco is an academic researcher from University of Wisconsin-Madison. The author has contributed to research in topics: Medicine & Neuroprotection. The author has an hindex of 5, co-authored 9 publications receiving 179 citations. Previous affiliations of Kahlilia C Morris-Blanco include United States Department of Veterans Affairs.

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Impact of microRNAs on ischemic stroke: From pre- to post-disease.

TL;DR: This review lists miRNAs that have been reported to regulate various stroke risk factors and pre-disease mechanisms, including hypertension, atherosclerosis, and diabetes, followed by an in-depth analysis of mi RNAs in ischemic stroke pathogenesis, such as excitotoxicity, oxidative stress, inflammation, apoptosis, angiogenesis and neurogenesis.
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The microRNA miR-7a-5p ameliorates ischemic brain damage by repressing α-synuclein

TL;DR: It is found that treating rodents with an oligonucleotide mimicking the microRNA miR-7 either before or within 30 min (but not 2 hours) after focal cerebral ischemia reduced the amount of brain damage and improved motor recovery and quality of life after a stroke.
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Epigenetic mechanisms of neurodegenerative diseases and acute brain injury

TL;DR: This review aims to highlight ways in which epigenetics applies to several commonly researched neurodegenerative diseases and forms of acute brain injury as well as shed light on the benefits of epigenetics-based treatments.
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Induction of DNA Hydroxymethylation Protects the Brain After Stroke

TL;DR: TET3 activation by ascorbate provided robust protection against ischemic injury in young and aged mice of both sexes and improved motor function recovery in both male and female mice, indicating the potential of TET3 and 5hmC as novel stroke therapeutic targets.
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Inhibition of the Epigenetic Regulator REST Ameliorates Ischemic Brain Injury

TL;DR: It is demonstrated that direct inhibition of the epigenetic remodeler REST prevents secondary brain damage in the cortex and improves functional outcome potentially via de-repression of plasticity-related genes after stroke.