So get your researcher involved, So much to remember at the hospital for my next stroke since I'm sure my doctors won't have knowledge of these off-label drugs.
But I can hope that
Dr. Algorithm is on duty.
http://www.eurekalert.org/pub_releases/2012-07/nu-ndc072312.php
1-size-fits-all drug targets harmful brain inflammation in many diseases
CHICAGO --- A new class of drug developed at Northwestern University
Feinberg School of Medicine shows early promise of being a
one-size-fits-all therapy for Alzheimer's disease, Parkinson's disease,
multiple sclerosis and traumatic brain injury by reducing inflammation
in the brain.
Northwestern has recently been issued patents to cover this new drug
class and has licensed the commercial development to a biotech company
that has recently completed the first human Phase 1 clinical trial for
the drug.
The drugs in this class target a particular type of brain
inflammation, which is a common denominator in these neurological
diseases and in traumatic brain injury and stroke. This brain
inflammation, also called neuroinflammation, is increasingly believed to
play a major role in the progressive damage characteristic of these
chronic diseases and brain injuries.
By addressing brain inflammation, the new class of drugs --
represented by MW151 and MW189 -- offers an entirely different
therapeutic approach to Alzheimer's than current ones being tested to
prevent the development of beta amyloid plaques in the brain. The
plaques are an indicator of the disease but not a proven cause.
A new preclinical study published today in the
Journal of Neuroscience,
reports that when one of the new Northwestern drugs is given to a mouse
genetically engineered to develop Alzheimer's, it prevents the
development of the full-blown disease. The study, from Northwestern's
Feinberg School and the University of Kentucky, identifies the optimal
therapeutic time window for administering the drug, which is taken
orally and easily crosses the blood-brain barrier.
"This could become part of a collection of drugs you could use to
prevent the development of Alzheimer's," said D. Martin Watterson, a
professor of molecular pharmacology and biological chemistry at the
Feinberg School, whose lab developed the drug. He is a coauthor of the
study.
In previous animal studies,
the same drug reduced the neurological
damage caused by closed-head traumatic brain injury and inhibited the
development of a multiple sclerosis-like disease. In these diseases as
well as in Alzheimer's, the studies show the therapy time window is
critical.
MW151 and MW189 work by preventing the damaging overproduction of
brain proteins called proinflammatory cytokines.
Scientists now believe
overproduction of these proteins contributes to the development of many
degenerative neurological diseases as well as to the neurological damage
caused by traumatic brain injury and stroke.
When too many of the cytokines are produced, the synapses of the
brain begin to misfire. Eventually the entire organization of the brain
falls into disarray, like a computer failing. The neurons lose their
connections with each other and can eventually die. The resulting damage
in the cortex and hippocampus can compromise memory and
decision-making.
"In Alzheimer's disease, many people now view the progression from
mild cognitive impairment to full-blown Alzheimer's as an indication of
malfunctioning synapses, the pathways that allow neurons to talk to each
other," said Watterson, the John G. Searle Professor of Molecular
Biology and Biochemistry. "And high levels of proinflammatory cytokines
can contribute to synaptic malfunction."
Because this harmful inflammatory mechanism also appears to be a
major player in other neurodegenerative disorders in addition to
Alzheimer's, the class of drugs represented by MW151 might hold bright
potential as co-therapies for Parkinson's disease, frontotemporal
dementia, amyotrophic lateral sclerosis, M.S. and the longer term
complications of brain injury, Watterson said.
"We need more studies of therapeutic time windows in models of these
other diseases so we can better plan future clinical trials," Watterson
noted.
In the new study by Northwestern's Watterson and Linda Van Eldik,
director of the University of Kentucky Sanders-Brown Center on Aging, a
mouse model of Alzheimer's received MW151 three times a week starting at
six months of age, right at the time the proinflammatory cytokines
began to rise. This would be the comparable stage when a human patient
would begin to experience mild cognitive impairment.
When the mice brains were later evaluated at 11 months (at a time
when disease pathology is usually present), cytokine levels in the mice
receiving the drug were restored to normal levels and their synapses
were functioning normally. The inflammatory cytokine levels of the mice
not receiving the drug, however, were still at abnormally high levels,
and the mice had misfiring synapses.
"The drug protected against the damage associated with learning and
memory impairment," Van Eldik noted. "Giving this drug before
Alzheimer's memory changes are at a late stage may be a promising future
approach to therapy."
DRUG INHIBITS MULTIPLE SCLEROSIS DEVELOPMENT
In M.S., overproduction of the proinflammatory cytokines damage
the central nervous system and the brain. The proteins directly or
indirectly destroy the insulation or coverings of the nerve cells that
transmit signals down the spinal cord. When the insulation is stripped,
messages aren't properly conducted down the spinal cord.
When mice that were induced to develop an M.S.-like disease received MW151 orally, they did not develop disease as severe.
"We inhibited the development of the disease," said William Karpus,
the Marie A. Fleming Research Professor of Pathology at the Feinberg
School. "Now we need to learn if the drug can prevent relapses of M.S."
That study is ongoing in mice and the results will determine whether a
patient trial will be planned.
The only current oral drug treatment for M.S. acts at the level of
the lymph nodes, Karpus said. Because the brain is the site of the
inflammation and damage, a drug that works in the brain is an ideal
therapy.
DRUG PROTECTS BRAIN AFTER TRAUMATIC BRAIN INJURY
After a traumatic brain injury, the glia cells in the brain
become hyperactive and release a continuous cascade of proinflammatory
cytokines that -- in the long term -- can result in cognitive impairment
and epilepsy. As a result of this hyperactivity, researchers believe
the brain is more susceptible to serious damage following a second
neurological injury.
In a study with mice, Mark Wainright, M.D., professor of pediatric
neurology at Northwestern's Feinberg School and a physician at the Ann
& Robert H. Lurie Children's Hospital of Chicago, showed that when
MW151 is given during an early therapeutic window three to six hours
after the injury, it blocks glial activation and prevents the flood of
proinflammatory cytokines after a traumatic brain injury.
"If you took a drug like this early on after traumatic brain injury
or a even a stroke, you could possibly prevent the long-term
complications of that injury including the risk of seizures, cognitive
impairment and, perhaps, mental health issues," Wainwright said.
Stroke also causes inflammation in the brain that may also be linked
to long-term complications including epilepsy and cognitive deficits.
As in traumatic brain injury, this inflammatory response is part of the
recovery mechanisms used by the brain, so the use of brief and focused
treatments like MW151 could prevent the harmful effects of inflammation
while allowing the protective effects to occur unimpeded.
In another study, Wainwright showed MW151, when given after a
traumatic brain injury, prevented the increased risk of epileptic
seizures.
