Abstract P811: Oral Curcumin Treatment Facilitates Recovery of Function in a Rhesus Monkey Model of Cortical Injury

 Fascinating, but I'm sure this is not enough for your doctor to be able to extrapolate from Rhesus monkeys to humans. Don't do this on your own. Notice they only did male monkeys.

Abstract P811: Oral Curcumin Treatment Facilitates Recovery of Function in a Rhesus Monkey Model of Cortical Injury

 

Monica A Pessina

,

Bethany G Bowley

,

Maria Medalla

,

Douglas L Rosene

,

Tara L Moore

Originally published11 Mar 2021https://doi.org/10.1161/str.52.suppl_1.P811Stroke. 2021;52:AP811

Abstract

Curcumin is a primary component of the spice turmeric, and is a potent anti-inflammatory and anti-oxidant compound. In rodent models of brain damage from stroke or trauma, curcumin acts primarily on microglia and astrocytes to inhibit pro-inflammatory signaling pathways and to reduce inflammation and levels of reactive oxygen species (ROS). Further, rats with cortical injury treated with curcumin have smaller lesions and fewer neurological impairments than those treated with vehicle. However, it is not clear whether curcumin exerts the same biological effect in primate brains as in rodent brains, and the effects of curcumin have not yet been extensively tested in monkey models of brain injury. Data from our laboratory has demonstrated that curcumin enhances spatial working memory and motor function in normal aging rhesus monkeys given daily doses of dietary curcumin over two years. The question remains as to whether chronic dietary curcumin can enhance neuroprotection and dampen or ameliorate functional motor deficits after cortical injury. Thus, we administered curcumin to adult, male rhesus monkeys daily for two weeks prior to(So you will need pre-knowledge of when your stroke is going to occur.) and 12 weeks following induced cortical injury to the hand-representation of primary motor cortex (M1). Monkeys given daily treatment with oral doses of curcumin, but not those given vehicle, demonstrated significantly enhanced recovery of function in terms of time to retrieve a food reward on our hand dexterity task (HDT). In addition, treated monkeys returned to pre-injury finger-thumb grasp patterns on the HDT, while monkeys that received vehicle developed a compensatory whole hand grasp pattern and never returned to pre-injury grasp. These findings provide evidence that the anti-inflammatory compound, curcumin, is an effective treatment for facilitating recovery of function following cortical injury. Studies investigating the effect of curcumin on the microglia and astrocytes in the brains from these monkeys will provide evidence of the role of curcumin in reducing inflammation and ROS following injury.

This happens in our mind when we take a gamble

So would damage in this area explain who is willing to take the challenges/risks necessary to recover better?
http://www.futurity.org/risk-decisions-1213152-2/
Scientists have located a region of the brain that kicks into gear when we make decisions that we’re not completely sure about.
The discovery could lead to treatments for psychological and psychiatric disorders that involve misjudging risk, such as problem gambling and anxiety disorders.
“We know from human imaging studies that certain parts of the brain are more or less active in risk-seeking people, but the neural circuits involved are largely unknown,” says Ilya Monosov, assistant professor of neuroscience at Washington University in St. Louis. “We found a population of value-coding neurons that are specifically suppressed when animals make a risky choice.”
Value-coding neurons are cells whose activity reflects the value of a stimulus—in this study, the more juice that was offered to a monkey, the bigger the neurons’ response. However, shortly before the subject made a risky choice, these neurons became suppressed.

A single brain connection predicts risky gambling

The researchers also found a separate group of neurons that signal information about uncertainty after the choice but before the risky outcome. Their findings appear in the Journal of Neuroscience.

“It makes sense that choosing an uncertain option is an important part of learning.”

As they go about their everyday lives, people often must choose between a safe option and a better, but riskier, option. Do you stay in a secure job or quit to start your own business? Do you keep $2 in your pocket or use the money to buy a lottery ticket?
When the system of evaluating risk goes awry, it can have a severe impact on people’s lives. Maladaptive risky behaviors are a feature of compulsive gambling, bipolar disorder, and attention deficit hyperactivity disorder. People with anxiety, on the other hand, err too far on the side of caution.
To study the neuronal circuits of risk-taking, researchers gave rhesus monkeys—whose brains are structured very similarly to humans—a choice between a small amount of juice or a 50-50 chance of receiving either double that amount of juice or nothing at all. Over time, the amount of juice received under either condition would be the same, but one option was safe and the other risky.

Living on the edge

It turns out rhesus monkeys like to live on the edge. The monkeys chose the risky option more often than the safe option. Moreover, a group of value-coding neurons in a part of the brain called the ventral pallidum were selectively suppressed when monkeys chose a risky option over a safe one.
The ventral pallidum plays an important role in controlling levels of dopamine—a molecule that transmits signals between neurons and makes us feel good.
“The ventral pallidum inhibits dopamine neurons, and suppression of this area during risky behavior may increase dopamine release,” says Monosov, who is also an adjunct professor of biomedical engineering.
The results of the study may fit with observations showing an increase in risky behavior among people who take drugs that increase dopamine—such as methamphetamine users and Parkinson’s disease patients treated with L-dopa.

Can brain scans predict risky sex and drinking?

The study also found neurons in a nearby brain area called the medial basal forebrain became most active after the monkeys made a risky choice but before they learned the outcome of their choice—juice or no juice. That part of the brain provides inputs to a wide network of cortical brain regions involved in learning and memory.
“It makes sense that choosing an uncertain option is an important part of learning,” Monosov says. “When people are uncertain, they are driven to resolve the uncertainty. They approach the uncertain option, explore it, and learn from the outcome of their actions.” Modulating the medial basal forebrain by uncertainty could promote or influence learning. However, this remains to be tested.
Monosov is now studying whether temporarily turning off the ventral pallidum and the medial basal forebrain with targeted drug treatments affect the monkeys’ risk preferences and the strategies they use to learn.
“There are no anatomically targeted treatments for psychiatric disorders associated with misjudging risk, such as pathological gambling and anxiety,” Monosov says “Now that we know where uncertainty is processed in the brain, we can start looking for ways to modulate it.”
The Edward Mallinckrodt Jr. Foundation and the Brain and Behavior Research Foundation funded the work.
Source: Washington University in St. Louis

Original Study DOI: 10.1523/JNEUROSCI.1123-16.2016

Inosine Treatment Helps Recovery of Motor Functions after Brain Injury

Well shit, has nothing been done since this came out in April 2011? Every single stroke leader since then who has done nothing should be fired, including boards of directors and hospital staff.
More proof we have fucking failures of stroke associations. No followup on anything possibly useful.

Molecular Therapy for Improved Post-Stroke Motor Recovery April 2011 

The latest here:

Inosine Treatment Helps Recovery of Motor Functions after Brain Injury

Brain tissue can die as the result of stroke, traumatic brain injury, or neurodegenerative disease. When the affected area includes the motor cortex, impairment of the fine motor control of the hand can result. In a new study published in Restorative Neurology and Neuroscience, researchers found that inosine, a naturally occurring purine nucleoside that is released by cells in response to metabolic stress, can help to restore motor control after brain injury.
Based on evidence from rodent studies, researchers used eight rhesus monkeys ranging in age from 5 to 10 years (approximately equivalent to humans from 15 to 30 years of age). All received medical examinations and motor skills were tested, including video recording of fine motor functions used to retrieve small food rewards. All monkeys were given initial MRI scans to ensure there were no hidden brain abnormalities.
Brain injuries were created in the area controlling each monkey’s favored hand. Four monkeys received inosine treatment, while four received a placebo. Research staff were not informed regarding which monkeys were included in the treatment vs placebo groups. Recovery of motor function was then measured for a period of 14 weeks after surgery.
While both the treated and placebo groups recovered significant function, three out of four of the treated monkeys were able to return to their pre-operative grasping methods. The placebo group developed a compensatory grasping method for retrieving food rewards unlike the original thumb-and-finger method.
“In the clinical context, the enhanced recovery of grasp pattern suggests that inosine facilitates greater recovery from this type of cortical injury and motor impairment,” explained lead investigator Tara L. Moore, PhD, of the Department of Anatomy & Neurobiology and the Department of Neurology, Boston University School of Medicine, Boston, MA, USA. “To our knowledge, this is the first study to demonstrate the positive effects of inosine for promoting recovery of function following cortical injury in a non-human primate.”
Inosine has also been administered in human clinical trials for multiple sclerosis and Parkinson’s disease and has been proven to be safe in doses up 3000 mg/day. Athletes have used inosine as a nutritional supplement for decades, and inosine supplements are widely available commercially. “Given the effectiveness of inosine in promoting cortical plasticity, axonal sprouting, and dendritic branching, the present evidence of efficacy after cortical injury in a non-human primate, combined with a long history of safe use, indicates a need for clinical trials with inosine after cortical injury and spinal cord injury,” noted Dr. Moore.
The study points to neural plasticity, whereby the brain essentially “re-wires” connections between neurons to reestablish control pathways, as a therapeutic target for the recovery of fine motor control and grasping ability. Further study of cortical tissue from these monkeys is currently being completed and may provide further insights into the mechanisms underlying recovery.
http://www.iospress.nl/ios_news/inosine-treatment-helps-recovery-of-motor-functions-after-brain-injury/

• Full bibliographic information“Inosine Enhances Recovery of Grasp Following Cortical Injury to the Primary Motor Cortex of the Rhesus Monkey,” by Tara L. Moore, Monica A. Pessina, Seth P. Finklestein, Ronald J. Killiany, Bethany Bowley, Larry Benowitz, and Douglas L. Rosene. Published online in advance of Restorative Neurology and Neuroscience, Volume 34, Issue 5, (September 2016). DOI 10.3233/RNN-160661, published by IOS Press.