Posts tagged enzymes
Articles and news from the latest research reports.
Missing Enzyme Linked to Drug Addiction
A missing brain enzyme increases concentrations of a protein related to pain-killer addiction, according to an animal study. The results were presented at The Endocrine Society’s 95th Annual Meeting in San Francisco.
Opioids are pain-killing drugs, derived from the opium plant, which block signals of pain between nerves in the body. They are manufactured in prescription medications like morphine and codeine, and also are found in some illegal drugs, like heroin. Both legal and illegal opioids can be highly addictive.
In addition to the synthetic opioids, natural opioids are produced by the body. Most people have heard of the so-called feel-good endorphins, which are opioid-like proteins produced by various organs in the body in response to certain activities, like exercise.
Drug addiction occurs, in part, because opioid-containing drugs alter the brain’s biochemical balance of naturally produced opioids. Nationwide, drug abuse of opioid-containing prescription drugs is skyrocketing, and researchers are trying to identify the risk factors that differentiate people who get addicted from those who do not.
In this particular animal model, researchers eliminated an enzyme called prohormone convertase 2, or PC2, which normally converts pre-hormonal substances into active hormones in certain parts of the brain. Previous research by this team demonstrated that PC2 levels increase after long-term morphine treatment, according to study lead author Theodore C. Friedman, MD, PhD, chairman of the internal medicine department at Charles R. Drew University of Medicine and Science in Los Angeles.
“This raises the possibility that PC2-derived peptides may be involved in some of the addiction parameters related to morphine,” Friedman said.
For this study, Friedman and his co-researchers analyzed the effects of morphine on the brain after knocking out the PC2 enzyme in mice. Morphine normally binds to a protein on cells known as the mu opioid receptor, or MOR. They found that MOR concentrations were higher in mice lacking PC2, compared to other mice.
To analyze the effects of PC2 elimination, the researchers examined MOR levels in specific parts of the brain that are related to pain relief, as well as to behaviors associated with reward and addiction. They measured these levels using a scientific test called immunohistochemistry, which uses specific antibodies to identify the cells in which proteins are expressed.
“In this study, we found that PC2 knockout mice have higher levels of MOR in brain regions related to drug addiction,” Friedman said. “We conclude that PC2 regulates endogenous opioids involved in the addiction response and in its absence, up-regulation of MOR expression occurs in key brain areas related to drug addiction.”
(Source: newswise.com)
OHSU researchers discover how enzyme may prevent nervous system repair in multiple sclerosis
Discovery could be ‘life-changer’ for millions with MS, stroke and other conditions that cause brain damage
Researchers at Oregon Health & Science University have discovered that blocking a certain enzyme in the brain can help repair the brain damage associated with multiple sclerosis and a range of other neurological disorders.
The discovery could have major implications for multiple sclerosis, complications from premature birth and other disorders and diseases caused by demyelination – a process where the insulation-like sheath surrounding nerve cells in the brain becomes damaged or destroyed. Demyelination disrupts the ability of nerve cells to communicate with each other, and produces a range of motor, sensory and cognitive problems in MS and other disorders.
The study was published this week in the online edition of the Annals of Neurology. The study was conducted by a team of researchers led by Larry Sherman, Ph.D., who is a professor of cell and development biology at OHSU and a senior scientist in the Division of Neuroscience at the Oregon National Primate Research Center.
"What this means is that we have identified a whole new target for drugs that might promote repair of the damaged brain in any disorder in which demyelination occurs," Sherman said. "Any kind of therapy that can promote remyelination could be an absolute life-changer for the millions of people suffering from MS and other related disorders."
Possible new approach to fighting chronic inflammatory diseases
30 July 2012
Researchers from The University of Queensland’s Institute for Molecular Bioscience have discovered a potential new approach to treating chronic inflammatory diseases such as arthritis.
Professor David Fairlie and his colleagues have developed an experimental treatment that has proven effective at reducing symptoms and stopping the progression of the disease in models of arthritis.
“Human enzymes called proteases stimulate the secretion of immune cells that, when the correct amount is released, play important roles in digestion, fighting infections and healing wounds,” Professor Fairlie said.
“But in chronic inflammatory diseases such as arthritis, these enzymes continuously stimulate the release of immune cells, which cause inflammation when present at high levels. This leads to ongoing tissue damage.”
Professor Fairlie and his team have developed experimental compounds that block this stimulation and successfully reduce chronic inflammatory arthritis in experimental models.
If the treatment could be transferred to humans, it has the potential to reduce both the health and economic impacts of chronic inflammatory diseases.
Almost four million Australians suffer from chronic joint pain and disability caused by various forms of arthritis, including osteoarthritis, rheumatoid arthritis and gout.
Related healthcare and loss of employment cost Australia over $20 billion per year, an amount that is expected to increase dramatically as our population ages.
These promising new findings are published in the current hard-copy edition of The Federation of American Societies For Experimental Biology Journal, the world’s most cited scientific journal in biology.
Journal subscribers can access the paper at this address: http://bit.ly/Pg8lgk
Source: The University of Queensland