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The therapy stops autoimmune responses that are already activated and prevents the activation of new autoimmune cells

In the trial, the MS patients' own specially processed white blood cells were used to stealthily deliver billions of myelin antigens into their bodies so their immune systems would recognize them as harmless and develop tolerance to them

Current therapies for MS suppress the entire immune system, making patients more susceptible to everyday infections and higher rates of cancer

the study did show patients who received the highest dose of white blood cells had the greatest reduction in myelin reactivity

While the trial's nine patients

were too few to statistically determine the treatment

primary aim of the study was to demonstrate the treatment's safety and tolerability

the intravenous injection of up to 3 billion white blood cells with myelin antigens caused no adverse affects in MS patients

it did not reactivate the patients' disease and did not affect their healthy immunity to real pathogens

researchers tested patients' immunity to tetanus because all had received tetanus shots in their lifetime

One month after the treatment, their immune responses to tetanus remained strong, showing the treatment's immune effect was specific only to myelin

human safety study sets the stage for a phase 2 trial to see if the new treatment can prevent the progression of MS in humans

the trial, which has already been approved in Switzerland

patients' white blood cells were filtered out, specially processed and coupled with myelin antigens by a complex GMP manufacturing process

In the phase 2 trial we want to treat patients as early as possible in the disease before they have paralysis due to myelin damage

Then billions of these dead cells secretly carrying the myelin antigens were injected intravenously into the patients

The cells entered the spleen, which filters the blood and helps the body dispose of aging and dying blood cells

During this process, the immune cells start to recognize myelin as a harmless and immune tolerance quickly develops

This therapy,

may be useful for treating not only MS but also a host of other autoimmune and allergic diseases simply by switching the antigens attached to the cells

recently published research in mice in which he used nanoparticles—rather than a patient's white blood cells—to deliver the myelin antigen

Using a patient's white blood cells is a costly and labor-intensive procedure

study showed the nanoparticles, which are potentially cheaper and more accessible to a general population, could be as effective as the white blood cells as delivery vehicles

target a particular type of brain inflammation

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.

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

given to a mouse genetically engineered to develop Alzheimer's, it prevents the development of the full-blown disease

identifies the optimal therapeutic time window for administering the drug, which is taken orally and easily crosses the blood-brain barrier.

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

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

When too many of the cytokines are produced, the synapses of the brain begin to misfire

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

drug protected against the damage associated with learning and memory impairment

before Alzheimer's memory changes are at a late stage may be a promising future approach to therapy

In M.S., overproduction of the proinflammatory cytokines damage the central nervous system and the brain

proteins directly or indirectly destroy the insulation or coverings of the nerve cells that transmit signals down the spinal cord

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.

After a traumatic brain injury, the glia cells in the brain become hyperactive and release a continuous cascade of proinflammatory cytokines

As a result of this hyperactivity, researchers believe the brain is more susceptible to serious damage following a second neurological injury.

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

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

Stroke also causes inflammation in the brain that may also be linked to long-term complications including epilepsy and cognitive deficits

ppress the immune system

the compounds boost a population of progenitor cells that can in turn repair MS-damaged nerve fibers

cautioned that benztropine is a drug with dose-related adverse side effects, and has yet to be proven effective at a safe dose in human MS patients

the newly identified compounds, a Parkinson's disease drug called benztropine, was highly effective in treating a standard model of MS in mice, both alone and in combination with existing MS therapies

MS currently affects more than half a million people in North America and Europe, and more than two million worldwide

precise triggers are unknown, but certain infections and a lack of vitamin D are thought to be risk factors

In MS, immune cells known as T cells infiltrate the upper spinal cord and brain

causing inflammation and ultimately the loss of an insulating coating called myelin on some nerve fibers

As nerve fibers lose this myelin coating, they lose their ability to transmit signals efficiently, and in time may begin to degenerate

resulting symptoms, which commonly occur in a stop-start, "relapsing-remitting" pattern, may include limb weakness, numbness and tingling, fatigue, vision problems, slurred speech, memory difficulties and depression, among other problems

Current therapies

aim to suppress the immune attack that de-myelinates nerve fibers. But they are only partially effective and are apt to have significant adverse side effects

the new study

aimed at restoring a population of progenitor cells called oligodendrocytes

These cells normally keep the myelin sheaths of nerve fibers in good repair and in principle could fix these coatings after MS damages them

oligodendrocyte numbers decline sharply in MS, due to a still-mysterious problem with the stem-like precursor cells that produce them

team screened a library of about 100,000 diverse compounds for any that could potently induce OPCs to mature or "differentiate."

Several compounds scored well

benztropine, had been well characterized and indeed was already FDA-approved for treating Parkinson's disease

tests, benztropine showed a powerful ability to prevent autoimmune disease and also was effective in treating it after symptoms had arisen

virtually eliminating the disease's ability to relapse

benztropine on its own worked about as well as existing treatments, it also showed a remarkable ability to complement these existing treatments

two first-line immune-suppressant therapies, interferon-beta and fingolimod

Adding even a suboptimal level of benztropine

allowed

to cut the dose of fingolimod by 90%

the same disease-modifying effect as a normal dose

that dose-lowering could translate into a big reduction in

potentially serious side effects

researchers confirmed that benztropine works against disease in this mouse model by boosting the population of mature oligodendrocytes

in turn restore the myelin sheaths of damaged nerves

even as the immune attack continues

benztropine-treated mice showed no change in the usual signs of inflammation, yet their myelin was mostly intact, suggesting that it was probably being repaired as rapidly as it was being destroyed

Benztropine is known to have multiple specific effects on brain cells, including the blocking of activity at acetylcholine and histamine receptors and a boosting of activity at dopamine receptors

hope to learn more about how

its molecular structure might be optimized for this purpose