Syndicate content

Archive - Apr 13, 2017

Comprehensive Neuropsychological Study of Living Ex-Pro Hockey Players Shows No Significant Brain Impairment, But High Levels of Emotional, Behavioral, & Cognitive Challenges; Scott Thornton Participates, Worried About His Memory

Researchers at Baycrest Health Sciences' Rotman Research Institute in Toronto, Canada, have reported the most comprehensive neuropsychological study of retired professional ice hockey players to date. They found that the alumni involved in the study, most of whom played in the Nzational Hockey League (NHL), were free from significant brain impairment on objective testing. Yet the players reported a high level of emotional, behavioral and cognitive challenges on questionnaires rating subjective complaints. “The study was published in the the Journal of Neurology, Neurosurgery, and Psychiatry. The open-access article is titled “Cognitive and Psychosocial Function in Retired Professional Hockey Players.” The ongoing study, which began in 2010, is led by Dr. Brian Levine, neuropsychologist and senior scientist at the Rotman Research Institute and Professor of Psychology and Medicine (Neurology) at the University of Toronto, Both institutions are in Toronrto, Canada. The study focuses on retired professional ice hockey players' cognitive and behavioral functioning in relation to their age, concussion history, and genetic risk. "There has been a lot of attention on repeated concussions and neurodegenerative disease, particularly in post-mortem samples of ex-athletes," says Dr. Levine. "There is a need for more comprehensive assessment of mental and behavioral changes during life. This longitudinal study will allow us to track changes over time to better understand aging and brain health in retired professional athletes." Thirty-three retired professional athletes were tested along with eighteen age-matched healthy males recruited from the community as a comparison group with no history of professional contact sports.

Exosomes Delivered by Nasal Spray Can Limit Brain Damage Caused by Seizure Disorder; Inflammation Relieved Is Similar to That Seen in Alzheimer’s, Parkinson’s, Multiple Sclerosis, & Traumatic Injury, Author States

Tiny sub-cellular vesicles (exosomes) isolated from adult mesenchymal stem cells (MSCs) and administered intranasally can limit the damage to the brain of animal models caused by a seizure disorder called status epilepticus, according to research published online on April 10, 2017 in PNAS. The open-access article is titled “Intranasal MSC-Derived A1-Exosomes Ease Inflammation, and Prevent Abnormal Neurogenesis and Memory Dysfunction After Status Epilepticus.” Status epilepticus is the formal name for a single seizure lasting longer than 30 minutes or a series of seizures in which the person does not regain consciousness in between them. If it is not quickly stopped, even one episode can cause brain damage, loss of cognitive function, and memory loss. “Saving the brain from injury and disease is certainly one of the holy grails of medicine,” said Darwin J. Prockop, M.D., Ph.D., the Stearman Chair in Genomic Medicine, Professor at the Texas A&M College of Medicine, and co-senior author of the article. “Our paper suggests one way that this might be done, and not by a procedure that requires brain surgery or even injection into a vein: All that would be required is a nasal spray that a patient might receive in a doctor’s office.” The material in the nasal spray is anti-inflammatory exosomes, which Dr. Prockop and his team isolated from cultures of mesenchymal stem cells, a type of adult stem cell. Ashok K. Shetty, Ph.D., a Professor in the Department of Molecular and Cellular Medicine at the Texas A&M College of Medicine, Associate Director of the Institute for Regenerative Medicine, research career scientist at the Olin E. Teague Veterans Medical Center, and co-senior author of the paper, and his team tested the efficiency of these exosomes in a status epilepticus model with damage from a period of acute seizures.

CRISPR Gene-Editing Alternative Corrects Duchenne Muscular Dystrophy Mutations in Human Cells in Vitro & in Mice in Lab

Using the new gene-editing enzyme CRISPR-Cpf1, researchers at the University of Texas (UT) Southwestern Medical Center have successfully corrected Duchenne muscular dystrophy in human cells in vitro and mice in the lab. The UT Southwestern group had previously used CRISPR-Cas9, the original gene-editing system, to correct the Duchenne defect in a mouse model of the disease and in human cells. In the current work, they used a new variation of the gene-editing system to repair the defect in both a mouse model and in human cells. “We took patient-derived cells that had the most common mutation responsible for Duchenne muscular dystrophy and we corrected them in vitro to restore production of the missing dystrophin protein in the cells. This work provides us with a promising new tool in the CRISPR toolbox,” said author Dr. Eric Olson (phpto), Chairman of Molecular Biology, Co-Director of the UT Southwestern Wellstone Muscular Dystrophy Cooperative Research Center, and Director of the Hamon Center for Regenerative Science and Medicine, all at UT Southwestern. The research appeared in the April 12, 2017 issue of Science Advances. The article is titled “CRISPR-Cpf1 Correction of Muscular Dystrophy Mutations in Human Cardiomyocytes and Mice.” CRISPR-Cpf1 differs from CRISPR-Cas9 in a number of key ways. Cpf1 is much smaller than the Cas9 enzyme, which makes it easier to package inside a virus and therefore easier to deliver to muscle cells. Also, Cpf1 recognizes a different sequence of DNA than Cas9 does, which provides greater flexibility in terms of use. “There will be some genes that may be difficult to edit with Cas9, but may be easier to modify with Cpf1, or vice versa.