I bet this didn't make our non-existent stroke leaders ears perk up and get to writing an RFP to researchers to test this out in humans. Of course not, SOMEONE ELSE WILL TO SOLVE THE PROBLEM. Our fucking failures of stroke associations don't even have two functioning neurons to know that they are totally fucking useless to survivors.
http://neurosciencenews.com/stroke-p7c3-neurons-6194/
Summary: A
compound called P7C3 provides both protection for neurons following a
stroke and improves physical and cognitive outcomes, a new study
reports.
Source: University of Iowa Health Care.
P7C3 compound protects mature and newborn neurons in rats, and also improves physical and cognitive outcomes, following stroke.
Researchers
from the University of Iowa Carver College of Medicine and the
University of Miami Miller School of Medicine have shown that a
neuroprotective compound tested in rats provides two-pronged protection
for brain cells during stroke and improves physical and cognitive
outcomes in the treated animals.
Every year, nearly 800,000
Americans have a stroke and almost 130,000 die. Survivors often are left
with long-term physical and cognitive disability that significantly
alters their lives.
When a stroke interrupts the brain’s blood
supply, mature brain cells (neurons) die. In addition, reestablishing
blood flow, known as reperfusion, also leads to processes that cause
cell death. A part of the brain’s natural response to stroke injury is
to increase production of new brain cells in two specific regions (the
subgranular zone of the hippocampal dentate gyrus and the subventricular
zone of the lateral ventricles), which normally make a smaller number
of new brain cells every day. Unfortunately, the vast majority of these
newborn cells die within one to two weeks, limiting the benefit of this
potential repair process. Minimizing the loss of brain cells is a
primary goal for new stroke therapies.
“If we could prevent the
mature brain cells from dying that would be beneficial,” says Andrew
Pieper, MD, PhD, professor of psychiatry in the UI Carver College of
Medicine and co-senior study author. “But if we could also support or
enhance this surge in neurogenesis (birth of new neurons), we might be
able to further foster recovery, especially in terms of cognitive
function, which is critically dependent on the hippocampus.”
Using
rats, Pieper and his colleagues Zachary B. Loris and W. Dalton
Dietrich, PhD, tested the effects of a compound called P7C3-A20 on these
two aspects of neuroprotection following ischemic stroke. Blood flow to
the rats’ brains was interrupted for 90 minutes and then the blockage
was cleared allowing reperfusion. One group of rats was given the
P7C3-A20 compound twice daily for seven days following the stroke.
P7C3-A20 has previously been shown to prevent brain cell death in other
animal models of neurologic injury, including Parkinson’s disease,
amyotrophic lateral sclerosis, stress-associated depression, and
traumatic brain injury.
In terms of the brain itself, the P7C3-A20
compound reduced loss of brain tissue (atrophy) and increased survival
of newborn neurons six weeks after stroke. In addition to the improved
survival of both mature and newborn neurons, rats that received the
P7C3-A20 compound for seven days after stroke also had better physical
and cognitive outcomes than untreated rats. Treated rats had improved
balance and coordination one week after stroke, and improved learning
and memory one month after stroke. The findings were published recently
in the journal Experimental Neurology.
“There is no previous
demonstration of a pharmacologic agent that both protects mature neurons
from dying and also boosts the net magnitude of neurogenesis,” Pieper
says. “Our compound is beneficial in this animal model of stroke, and
we’re hopeful that it might eventually benefit patients.”
“Currently
there are limited treatments for acute stroke that make a real
difference in patient’s lives. There is an urgent need to identify,
test, and translate new therapies to the clinic,” adds Dietrich,
co-senior study author and Scientific Director of The Miami Project to
Cure Paralysis, professor of neurological surgery, neurology, biomedical
engineering and cell biology at the University of Miami where the
studies were conducted. “The ability to both protect and repair the
injured nervous system has major implications on how we think about
improving outcomes in millions of people each year with acute
neurological injuries.”
The neuronal protection provided by the
P7C3-A20 compound was also associated with a boost in the levels of a
substance called nicotinamide adenine dinucleotide (NAD) in the rats’
brains. NAD is emerging as an important player in neuronal health and
survival. Levels of this substance are depleted during stroke, and it
has been proposed that increasing NAD levels may be a therapeutic target
for treating stroke. In this study, P7C3-A20 treatment restored NAD to
normal levels in the rats’ cortex after a stroke.
Importantly, the
study examined the effects of P7C3-A20 on cognitive and physical
outcomes well beyond the time of the initial stroke. The sustained
physical and cognitive improvement seen in the rats up to one month
after the stroke suggests that the P7C3-A20 compound provides a
long-term benefit.
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