HomeFeatured Mind Controlled Device Helps Stroke Patients Retrain Brain to Move Paralyzed Hands Neuroscience NewsNEUROSCIENCE NEWSMAY 27, 2017 FEATUREDNEUROLOGYNEUROSCIENCEROBOTICS9 MIN READ Summary: Researchers use BCI and exoskeleton technology to allow people with paralyzed hands following stroke to regain movement and control of their limb.
Device reads brain signals and converts them into motion.
Stroke patients who learned to use their minds to open and close a device fitted over their paralyzed hands gained some control over their hands, according to a new study from Washington University School of Medicine in St. Louis.
By mentally controlling the device with the help of a brain-computer interface, participants trained the uninjured parts of their brains to take over functions previously performed by injured areas of the brain, the researchers said.
“We have shown that a brain-computer interface using the uninjured hemisphere can achieve meaningful recovery in chronic stroke patients,” said Eric Leuthardt, MD, a professor of neurosurgery, of neuroscience, of biomedical engineering, and of mechanical engineering & applied science, and the study’s co-senior author.
The study is published May 26 in the journal Stroke.
New findings explain how the enzyme ACSS2 aids tumors in a nutrient-starved environment offering potential new treatment approaches.
All cancer tumors have one thing in common – they must feed themselves to grow and spread, a difficult feat since they are usually in a tumor microenvironment with limited nutrients and oxygen. A study at The University of Texas MD Anderson Cancer Center has revealed new details about how an enzyme called acetyl-CoA synthetase 2 (ACSS2) allows brain tumors to grow despite their harsh surroundings. The findings, published in the May 25 online issue of Molecular Cell, portends ACSS2 as a potential player in new approaches to treating this often deadly disease.
ACSS2 provides tumors a competitive edge by enhancing their ability to use a cellular salt called acetate as a carbon-based food source rather than the more desirable glucose which is often in short supply in cancer cells. This lifeline allows cancer cells at the core of the tumor to survive and even grow as it battles with nutrient deficiency.
Current therapies and the body’s own immune system are not efficient at stopping this vital nutrient pathway in cancer cells, and little is known about how these life-giving proteins are transported from cytosol, a liquid cell component, into the nucleus via a process called nuclear translocation. The ability to halt nuclear translocation of ACSS2 would cut off the cancer cell’s self-maintaining ability at its most basic level. The study, led by Zhimin Lu, Ph.D., professor of Neuro-Oncology, provided new information about nuclear translocation and how ACSS2 may offer a new approach for therapy.
“Overcoming metabolic stress is a critical step in solid tumor growth. Acetyl coenzyme A (CoA) generated via glucose and acetate uptake is a key carbon source for important cellular processes such as histone acetylation and gene expression,” said Lu. “However, how acetyl CoA is produced under nutritional stress is unclear. Our study explains the underlying mechanics of how this occurs, with ACSS2 as a novel and important method for gene expression under these circumstances.”
A Loyola University Chicago study has found that abnormal proteins found in Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease all share a similar ability to cause damage when they invade brain cells.
The finding potentially could explain the mechanism by which Alzheimer’s, Parkinson’s, Huntington’s, and other neurodegenerative diseases spread within the brain and disrupt normal brain functions.
The finding also suggests that an effective treatment for one neurodegenerative disease might work for other neurodegenerative diseases as well.
The study by senior author Edward Campbell, PhD, first author William Flavin, PhD, and colleagues is published in the journal Acta Neuropathologica.
“A possible therapy would involve boosting a brain cell’s ability to degrade a clump of proteins and damaged vesicles,” Campbell said. “If we could do this in one disease, it’s a good bet the therapy would be effective in the other two diseases.”
Neurodegenerative diseases are caused by the death of neurons and other cells in the brain, with different diseases affecting different regions of the brain. Alzheimer’s destroys memory, while Parkinson’s and Huntington’s affect movement. All three diseases are progressive, debilitating and incurable.
Previous research has suggested that in all three diseases, proteins that are folded abnormally form clumps inside brain cells. These clumps spread from cell to cell, eventually leading to cell deaths. Different proteins are implicated in each disease: tau in Alzheimer’s, alpha-synuclein in Parkinson’s and huntingtin in Huntington’s disease.
Bandi borsa di studio Nanotecnologia per il rilascio controllato di molecole bio-attive “POR FSER 2007/2013” – obiettivo Operativo 2 – Capofila Farmaceutici DAMOR SRL
Si allegano i bandi per le borse di studio "Nanotecnologia per il rilascio controllato di molecole bio-attive “POR FSER 2007/2013” – obiettivo Operativo 2 – Capofila Farmaceutici DAMOR SRL".