Thursday, July 31, 2008

Cell changes may help Lou Gehrig's research

Cell changes may help Lou Gehrig's research


Story Published: Jul 31, 2008 at 11:22 AM PDT

By Associated Press WASHINGTON (AP) - Using a new technique to reprogram cells, scientists are growing neurons from people with Lou Gehrig's disease, a possible first step in understanding how the deadly illness develops.Technically known as amyotrophic lateral sclerosis, the disease damages the nerve cells in the brain and spinal cord, eventually leading to death. The ALS Association estimates that as many as 30,000 Americans may have the disease at any given time."What we now have in the culture dish is cells that have the same genetic makeup as the ALS patient and they are the same cells that are affected by the disease," said Dr. Chris Henderson, co-director of the Center for Motor Neuron Biology and Disease at Columbia University.That means that, for the first time, scientists hope to be able to observe the development of the disease in the cells and, from that, possibly begin studies of treatments."There is no way we could go to an ALS patient and take these cells," Henderson pointed out.Instead, they used skin cells from two patients, aged 82 and 89, and were able to reprogram the cells into a type of adult stem cell, and from that into nerve cells, the researchers report in Friday's edition of the journal Science.Co-author Dr. Kevin Eggan of the Harvard Stem Cell Institute said what they hope to do next is study the cells in the lab and compare them with cells of someone who doesn't have that disease.ALS is a slowly developing disease and the test cells have not yet begun to show illness, they noted. But in similar studies in mouse cells the cultured neurons did develop the disease.Dr. Lucie Bruijn, science director and vice president of the ALS Association, called the work a first step."This is the beginning," she said in a telephone interview. "It's a most important approach.""Now we have to figure out whether these motor neurons are able to mature," she added. "For these to be useful for drug development we need mature motor neurons."The researchers worked with a form of ALS that is caused by a defect in a single gene, a rare form of the disease.But Henderson said that they even though the vast majority of cases are caused by different triggers, they hope to learn about the mechanism of the disease, how it develops after being triggered."Up until now, it's been impossible to get access to the neurons affected by ALS and, although everyone was excited by the potential of the new technology, it was uncertain that we would be able to obtain them from patients' skin cells," Henderson said. "Our paper now shows that we can generate hundreds of millions of motor neurons that are genetically identical to a patient's own neurons. This will be an immense help as we try to uncover the mechanisms behind this disease and screen for drugs that can prolong life."The research was supported by the Harvard Stem Cell Institute, Project ALS, the SMA Foundation, MDA Wings Over Wall Street, the Spina and Bowen families, the New York Stem Cell Foundation, the National Science Foundation and the John D. and Catherine T. McArthur Foundation

Wednesday, July 30, 2008

World Stem Cell Summit

There is a World Stem Cell Summit held in Madison by the Waisman Center on September 22 -24. There are several therapies under discussion for human trial in early 2009.
Here is a link to the program:

Thursday, July 24, 2008

these are some of the answers people gave to the question: What is your biggest ALS fear?


  1. Total paralysis, I'm scared of it
  2. losing the ability to walk.
  3. I'm with Sheila on this one. Total paralysis. I nearly drowned when I was a kid, and I've had a fear of being helpless ever since. I've become claustrophobic because of this. The idea of being trapped in my body, not even able to move my head, scares the crap out of me. I believe this will drive me insane.
  4. my mother having to watch me die.
  5. No cure.
  6. I can't spend time fearing what is ahead for me...I'll go nuts. I only focus on today and what I can still do. Everyday I pray for 3 things...strength, courage, and inner peace.
  7. I fear being alive when the body bag is zipped!
  8. A long drawn-out diminishing until I actually die. I have a slow form of MND - that is great in the earlier stages as I have longer to enjoy doing the things I can still do but that benefit is amply balanced by the fact that the later stages when total paralysis kicks in will last much longer too. I have no fear of death itself but I certainly fear the stage before when I am unable to do anything except just be there.

Wednesday, July 23, 2008

Jul 22 What is your biggest ALS fear?

Jul 22
What is your biggest ALS fear?
Created by TipaCow on

my answer:
it is not DYING that scares-i'm okay w/ that. it's GETTING dead that keeps me awake at night....

Monday, July 21, 2008

World’s First Genome-Wide Spinal Cord Atlas Unveiled

July 21, 2008
World’s First Genome-Wide Spinal Cord Atlas Unveiled

Co-Funded by The ALS Association
The ALS Association has joined a funding consortium of non-profit and private organizations to fund the Allen Spinal Cord Atlas, which was unveiled as the world’s first genome-wide map of the mouse spinal cord, key to the study of amyotrophic lateral sclerosis and other diseases, disorders and traumatic injuries of the spinal cord.
Created by the Seattle, Wash.-based Allen Institute for Brain Science, the atlas enables researchers to access the free online data to advance their research surrounding these conditions.
“The atlas enables scientists to determine the location of genes and their expression patterns at the cellular level in the spinal cord,” said Lucie Bruijn, Ph.D., science director and vice president of The Association. “This will provide an important reference when trying to understand gene changes and how these are linked to disease in mouse models of ALS.”
From Lou Gehrig’s Disease (ALS) to Spinal Muscular Atrophy, spinal cord related diseases and disorders affect people of all ages. As many as 30,000 Americans, including military veterans, suffer from ALS at any given time; and multiple sclerosis affects 2.5 million people worldwide, to name a few. Nearly one-quarter of a million Americans—including several thousand troops who have served in Iraq—have suffered or suffer from a spinal cord injury.
The Institute’s unique funding model, designed to transform public, private and foundation funds into breakthrough scientific discoveries, supported the Spinal Cord Atlas’ dedicated consortium of public and private entities—including The Association, PVA Research Foundation, Wyeth Research, PEMCO Insurance, National Multiple Sclerosis Society, International Spinal Research Trust and philanthropist and Institute founder Paul G. Allen, as well as numerous anonymous donors.
“We were so thrilled to work with such a diverse array of funders with a shared goal of supporting this important project—which the Institute would never have completed without their support,” said Elaine Jones, chief operating officer at the Allen Institute. “The Allen Spinal Cord Atlas serves as a successful example of how major scientific projects can be funded, and we are eternally grateful to our partners.”
The atlas will be completed in a 12-month time frame. While inaugural data—approximately 2,000 genes—from the Allen Spinal Cord Atlas is now available (, the Institute will continue to follow its founding mission and upload additional information until the projected completion by the end of 2008. It is estimated that hundreds of users from universities, research institutes, pharmaceutical companies and government organizations will use the atlas.
When completed, the Allen Spinal Cord Atlas will detail approximately 20,000 genes including data from youth and adult developmental stages. It will also feature data across the full length of the spinal cord as well as anatomical reference sections.
The ALS Association is the only not-for-profit voluntary health organization dedicated solely to the fight against ALS through research, patient care, advocacy and public education. The mission of The Association is to lead the fight to cure and treat ALS through global, cutting-edge research, and to empower people with Lou Gehrig’s Disease and their families to live fuller lives by providing them with compassionate care and support.

Thursday, July 17, 2008

If everyone cared and nobody cried
If everyone loved and nobody lied
If everyone shared and swallowed their pride
Then we'd see the day when nobody died

When nobody died....We'd see the day,
we'd see the day
When nobody died
We'd see the day, we'd see the day
When nobody died
We'd see the day when nobody died

Wednesday, July 16, 2008

it's at the 9-12 month mark when will know if it works

Dear all,

You are receiving this message because you or your PALS are participating in or have participated in or requested information about the online worldwide ALS lithium study. We wanted to let you know that the preliminary three month study report is now available for download. Please go to and download the report from the latest "updates" link at the bottom of the page. Please note that this is a preliminary report which has not yet been edited or approved by PatientsLikeMe.We will continue to collected data through the 6 month point after which we will write up a final report. All data collection and analysis after that point will be done by PatientsLikeMe.Our basic results so far are, in summary:At the three month point:

Lithium does not affect ALS progression rates, at least for most PALS

Taking riluzole with lithium does not make a difference

Reaching a blood level of 0.4 does not make a difference

The ALSFRS-R score when lithium was started doesn't make a difference

Lithium may relieve cramps and fascics and spasticity for some at low doses (0.2 mmol/l blood concentration)Although not in the 3 month report, it seems that PALS who are taking an Omega 3 supplement are progressing a bit more slowly. There was also an interesting research report that came out yesterday that calcium supplements may be helpful (Medications and laboratory parameters as prognostic factors in amyotrophic lateral sclerosis. Qureshi M, Shui A, Dibernardo AB, Brown Jr RH, Schoenfeld DA, Cudkowicz ME.) The research abstract didn't give the dosage, but a quick search of PLM indicated that many PALS on calcium are taking ~1200 mg/day.

Thank you so, so much to everyone who has provided data for the lithium trial. So far our research results have been disappointing, but it is so much better to get results quickly so that we can move onto the next thing rather than to have to wait 2 to 3 years for the traditional research machinery to do its work. You have shown what a dedicated groups of PALS and CALS can do!Best wishes to everyone -- I'll be in touch,Karen

Hope is the Thing with Feathers
Posted: 15 Jul 2008 03:21 PM CDT
“Hope” is the thing with feathers
That perches in the soul
And sings the tune without the words
And never stops at all,
And sweetest in the gale is heard;
And sore must be the storm
That could abash the little bird
That kept so many warm.
I’ve heard it in the chillest land
And on the strangest sea,
Yet never, in extremity,
It asked a crumb of me.
By: Emily Dickinson
- Emily Dickinson

Monday, July 14, 2008

Life is not about waiting for the storm to clear, it's about learning to dance in the rain

Saturday, July 12, 2008

a great friend sent this to me

makes sense.....

I can see clearly now, the rain is gone,
I can see all obstacles in my way
Gone are the dark clouds that had me blind
It's gonna be a bright (bright), bright (bright)Sun-Shiny day. (I FUCKING HOPE SO!!)

Johnny Nash ~ I Can See Clearly Now

Friday, July 11, 2008

good news

Michigan stem cell research proposal advances
Associated Press WriterTue Jul 8, 4:06 AM ET
Supporters of a ballot measure that would loosen Michigan's restrictions on embryonic stem cell research took a big step toward placing it on the November ballot.
The Stem Cell Research Ballot Question Committee said Monday it turned in more than 570,000 voter signatures backing the measure. More than 380,000 of them must be ruled valid for the proposal to reach voters.
Backers say embryonic stem cell research holds the potential to help treat or cure diseases such as Alzheimer's, Parkinson's, cancer, sickle cell anemia and diabetes.
The politically diverse group that helped launch the campaign Monday included former Republican U.S. Rep. Joe Schwarz and former Democratic gubernatorial hopeful Larry Owen.
"It is research that we know has a high chance of curing many diseases and saving many lives," said Owen, the campaign chairman.
Opponents raise ethical concerns because the research involves the use and destruction of human embryos. The Michigan Catholic Conference and Right to Life of Michigan oppose the proposal and an opposition group called Michigan Citizens Against Unrestricted Science and Experimentation is forming.
"The proposal is deliberately deceptive," group spokesman David Doyle said. "It's the confusing legalese that is the problem."
Ballot proposal supporters countered that their opponents are the ones misrepresenting the issues. Supporters are trying to make the ballot because their efforts to change state law have failed in the Legislature.
Some embryonic stem cell research is allowed in Michigan. But the state's laws related to the research are among the nation's most restrictive, allowing only the use of stem cell lines from California, Illinois or other states with less restrictive laws. Those lines sometimes are patented by other researchers.
Ballot proposal supporters say changing Michigan's law would help broaden the type of available stem cell lines, opening up new avenues for potential cures and eventually drawing more research money to the state.
The proposal would change Michigan law to allow research on donated embryos created during fertility treatments that otherwise would be discarded. It's now a state felony to use new embryonic stem cells for research.
Supporters of the proposal to amend the constitution say it protects and strengthens Michigan's ban on human cloning. The proposal says nothing in it "shall alter Michigan's current prohibition on human cloning."
Opponents say the proposal does not explicitly put a ban on human cloning in the state constitution, so cloning could be allowed if state law is ever changed to permit it.
Stem cells are rare cells in tissues that give rise to most other cells. While many scientists say embryonic stem cell research holds the most medical versatility and potential, critics are upset that stem cells are harvested from adults or umbilical cords.
On the Net:
Stem Cell Research Ballot Question Committee:
Michigan Citizens Against Unrestricted Science and Experimentation:

Thursday, July 10, 2008

A POEM: — anon·y·mous·ly SENT TO ME

Three Little Letters
In Honor of Robert J Cram

A life altering change at a blink of an eye,
a debilitating disease can leave you wondering “Why”?

Weakness and Strength is the bodies constant fight,
no cure to the illness leaves a future un-bright.

Speaking with no words is a challenge to conquest,
faith and patience is what does it best.

Courage and Hope is your medication for pain,
time is the enemy with nothing to gain.

Day to day struggles makes it difficult to see,
that God has a plan and knows what’s best for me.

Education and awareness is priority no less,
with hopes to finding a cure and strike out ALS.

-Ashley Meadows
June 2008

Wednesday, July 9, 2008

Turning an adversity into opportunity is possible

ALS Association Wins Fight for Power Wheelchairs

ALS Association Wins Fight for Power Wheelchairs
Dear Drew,
Thanks to the outreach of ALS advocates in key states across the country, the U.S. Senate this afternoon passed legislation (HR 6331) that would exclude power wheelchairs from Medicare's new competitive bidding program. The bill, which passed by a 69-30 vote, also would delay implementation of the program for 18 months. This is a tremendous victory for people with ALS and their families and helps to ensure PALS will continue to have access to needed power wheelchairs!
For nearly two years, The ALS Association has worked with Congress to exclude high-end power chairs from the new program for fear that it would limit the types of chairs available to PALS, reduce services and force PALS to obtain chairs from suppliers who do not know the unique medical needs of people with ALS.
The Association held a breakout session on competitive bidding during our Advocacy Conference in May and worked closely with PALS and Chapters to educate Congress on the unique needs of people with ALS, making it clear that one-size-fits-all policies like competitive bidding are not appropriate when it comes to this disease. In fact, the participation of PALS at a press conference on competitive bidding last year helped to highlight the concerns of the ALS community and clearly demonstrated that the chairs needed by PALS are much different than those used by most Medicare beneficiaries.
With today's vote, we are one step closer to ensuring that competitive bidding will not limit the ability of PALS to access to the power chairs they need when they need them.
The House of Representatives already has passed HR 6331 with broad support so the bill now heads to the President for his signature. The President has signaled that he may veto the bill due to concerns about other unrelated provisions. However, both the Senate and House passed the bill with enough support to override a veto and enact HR 6331 into law.
We would like to thank all of the PALS, families and Chapters who have helped to reach out to Congress in support of this issue over the past two years. Your outreach has continued to make a difference!
If you have any questions about today's vote or would like additional information, please contact the Advocacy Department at or 1-877-444-ALSA.
Thank you!

Tuesday, July 8, 2008

Stem cells 'halt nerve disease'

Stem cells 'halt nerve disease'

The injection contained immature foetal glial cells
An injection of stem cells has been used to cure mice with a normally fatal nervous system condition.
The therapy which helped repair faulty nerve wiring raises hopes of treatments for children with rare and deadly nervous leukodystrophy disorders.
A UK expert said human treatments were still some way off - but potentially the technique could be used to treat conditions such as multiple sclerosis.
The US study features in the journal Cell: Stem Cell.
It's extremely exciting to think about not only treating but actually curing a disease, particularly an awful disease that affects children Professor Steven GoldmanUniversity of Rochester Medical Center
The scientists from the University of Rochester Medical Center believe it may be the first time that this type of "shiverer" mouse has been cured.
Its genetic makeup means that its nerve cells do not have enough myelin, a fatty coating which acts like the sheath on an electrical wire.
Without it, nerve signals do not travel properly from cell to cell, causing the trademark shaking and wobbling symptoms, and normally death within four months.
There are dozens of rare human disorders which involve genetic myelin-related faults in the nervous system, most of which are fatal in childhood or young adulthood.
One of the most well-known of these affected Lorenzo Odone, who died last week after decades battling adrenoleukodystrophy.
Surviving minority
The US team did not use "true" stem cells, which have the ability to turn into any cell in the body, but precursor stem cells, which can become one of a limited number of cell types.
The "glial cells" used here can become among other things, oligdendrocytes, the cells which produce the myelin sheath.
The cells were injected in different places in the central nervous system in a bid to see if this could make any difference to the overall symptoms.
For most, it made none, with three-quarters of the 26 mice injected dying around the same time as mice who had received no treatment.
However, for six mice, the difference was stark - in just two months, the cells had spread around, multiplying, and covering nerve cells in the brain and spinal cord, and producing myelin to coat them.
Two of the mice lived longer than usual, but the other four were still alive a year later, free from virtually all symptoms.
'Awful disease'
Professor Steven Goldman, who led the study, said: "We kept expecting them to die, but not only did they not die, they improved day by day.
"It's extremely exciting to think about not only treating but actually curing a disease, particularly an awful disease that affects children.
Professor David Attwell, from University College London, said the study represented an "important proof of principle" that transplantation of these "precursor" cells could help restore myelin not only within people with leukodystrophies, but in theory within those affected by other conditions involving loss of myelin, such as multiple sclerosis, cerebral palsy and spinal cord injury.
However, he said: "The work is still a long way from being applied in humans, and the paper raises several issues which could affect the chances of that happening.
"Only a small fraction of the mice were cured, and it is unclear why."
He said that other potential hurdles were whether within humans, defective myelin-producing cells would be as readily replaced by the new transplanted in versions, and whether, as in the mice, the immune system would have to be suppressed prior to treatment.
6 Mark this post as helpful

Saturday, July 5, 2008

ALS toxic assault

ALS toxic assault
Date: 07/04/2008
Align Center
Leaky blood vessels that lose their ability to protect the spinal cord from toxins may play a role in the development of amyotrophic lateral sclerosis, better known as ALS or Lou Gehrig's disease, according to research published in the April issue of Nature Neuroscience.
The results mark the first time that scientists have witnessed molecular changes occurring long before key nerve cells start dying. The unexpected finding opens up a new front in studies of ALS, a disease in which motor neurons in the spinal cord die off for unknown reasons, resulting in dramatically weakened muscles. Patients lose their strength, their ability to move or swallow, and eventually lose their ability even to breathe. Most patients live only a few years after diagnosis.
"We believe these changes contribute to or possibly initiate the onset of ALS," said lead author Berislav Zlokovic, M.D., Ph.D., of the University of Rochester Medical Center. "It's clear that these changes occur before the loss of neurons, and it's well known that the types of changes we are seeing certainly injure or kill these types of cells, which are extremely sensitive to their biochemical environment."
The results, discovered by studying mutant mice that have an inherited form of the disease, were made by a collaboration of neuroscientists from the University of Rochester Medical Center working together with a team of ALS experts from the University of California at San Diego. Zlokovic, a pioneer in learning how the body's vascular system plays a role in neurodegenerative diseases like Alzheimer's disease and ALS, led the team, and the first author is post-doctoral researcher Zhihui Zhong, Ph.D.
While it's unlikely the new findings will help ALS patients immediately, the results open up a new and unexpected way to think about the disease. Zlokovic's team is currently testing in the laboratory a compound that may help seal up leaky vessels and protect the neurons targeted by ALS.
The team studied mice with a mutation in a gene for superoxide dismutase 1 (SOD-1), which in healthy people and mice plays an important role keeping cells safe from damaging molecules known as free radicals. Scientists estimate that SOD-1 mutations play a role in a small number of cases of ALS overall in people, about one-quarter of the 10 percent or so of cases that are inherited. But those cases provide a unique window to study the disease's initial steps.
In the Nature Neuroscience paper, the group from Rochester's Center for Neurodegenerative and Vascular Brain Disorders and UCSD showed that a breakdown in the natural barrier between the blood and the spinal cord breaks down early on in mice destined to get ALS, long before nerve cells appear sick or die.
In this work, the team showed that the barrier between the blood and the spinal cord weakens in all three types of genetically based ALS cases that involve SOD-1 mutations, allowing toxic substances to flood into the spinal cord and directly affect neurons.
That barrier is crucial for the health of our central nervous system, which is treated like the inner sanctum of the body. Like a high-performance race car that demands a choice fuel, our neurons work well only if the chemical environment in the brain and spinal cord is precisely maintained within a strict, narrow set of conditions.
To maintain that select environment, the body has strict barriers or gateways for substances entering or exiting the central nervous system. Blood vessels run through our brain and spinal cord and supply oxygen and other nutrients, and the lining of those blood vessels constitutes a biochemical barrier to protect the central nervous system from toxins, inflammatory cells, red blood cells, blood products, and a variety of other potential toxic insults.
The barrier between the blood and the spinal cord isn't some stand-alone structure that keeps all substances away from the spinal cord. Rather, the word "barrier" describes an elaborate molecular lattice that lines the insides of the blood vessels that weave throughout the spinal cord. The lattice controls which molecules can cross from the blood to the neurons in the spinal cord, and which cannot. It's a bit like netting with very small openings that line the inside of blood vessels.
Oxygen and many nutrients get the OK to pass through the barrier in measured amounts. And the barrier readily accepts waste products from the spinal cord, transporting them away from the central nervous system and eventually out of the body. But the "netting" should be taut and should bar substances in the blood that have no business being near neurons.
The team found that a SOD-1 mutation disrupted key building blocks in the barrier. Essentially, the mutations loosened the lattice, creating bigger holes in the barrier that allowed molecular interlopers to pass from the blood to the spinal cord.
Mice with the mutation had lower levels of three types of "tight junction proteins" that are key components of the barrier: ZO-1, occludin and claudin-5. In mice just two months old, the numbers of those important tight junction proteins in the linings of blood vessels were reduced by about half, by 40 to 60 percent, allowing the lattice to loosen abnormally.
The weakened barrier brought about several problems. Neurons were exposed directly to biochemical byproducts of haemoglobin, which forms reactive oxygen molecules that injure neurons. Where the barrier had weakened, tiny hemorrhages dotted the spinal column. The smallest blood vessels crucial to nerve health shrunk: Mice with the mutation had total capillary length in the spinal cord 10 to 15 percent less than healthy mice, and their blood flow in the spinal cord was reduced by 30 to 45 percent.
Scientists must investigate whether the same processes happen in forms of ALS that are not inherited. Zlokovic notes that from what is known so far, the disease progresses exactly in inherited forms and forms that are not inherited.
"The vascular system is crucial to health - it's how oxygen and other nutrients are delivered to cells, and how toxins are removed," said Zlokovic, who is professor of Neurosurgery and Neurology and director of the Center for Neurodegenerative and Vascular Brain Disorders. "Any damage to the vascular system is a serious threat to the organism. It's clear now that the vascular system is certainly involved in the development of ALS."
Zlokovic first began doing research on the disease in 2004, when a former classmate from medical school who had been diagnosed with ALS and was looking for new treatments contacted him. By the time his friend died two years later, Zlokovic was well underway in studies investigating the possible role of the vascular system.
During the last 15 years, Zlokovic has pioneered the view that the vascular system plays a central role in many neurodegenerative diseases. He has found that a breakdown in the barriers between the blood and the central nervous system may be at the root of diseases like Alzheimer's. In January, Zlokovic reviewed the evidence for involvement of the barrier in diseases like Alzheimer's, ALS, and multiple sclerosis in a 24-page review in Neuron.

Thursday, July 3, 2008

A SONG.....

It used to seem to me
That my life ran on too fast
And I had to take it slowly
Just to make the good parts last

But when youre born to run
Its so hard to just slow down
So dont be surprised to see me
Back in that bright part of town

Ill be back in the high life again
All the doors I closed one time will open up again
Ill be back in the high life again

All the eyes that watched me once will smile and take me in

appropriate for my challenge

There are really only two ways to approach life - as victim or as gallant fighter - and you must decide if you want to act or react, deal your own cards or play with a stacked deck. And if you don't decide which way to play with life, it always plays with you.--Merle Shain

Wednesday, July 2, 2008

If you're never scared or embarrassed or hurt, it means you never take any chances.--Julia Soul

If you're never scared or embarrassed or hurt, it means you never take any chances.--Julia Soul

Tuesday, July 1, 2008

Devices known as brain-machine interfaces could someday be used routinely to help paralyzed patients and amputees control prosthetic limbs with just t

Devices known as brain-machine interfaces could someday be used routinely to help paralyzed patients and amputees control prosthetic limbs with just their thoughts.

--Now, University of Florida researchers have taken the concept a step further, devising a way for computerized devices not only to translate brain signals into movement but also to evolve with the brain as it learns.
Instead of simply interpreting brain signals and routing them to a robotic hand or leg, this type of brain-machine interface would adapt to a person's behavior over time and use the knowledge to help complete a task more efficiently, sort of like an assistant, say UF College of Medicine and College of Engineering researchers who developed a model system and tested it in rats.
Until now, brain-machine interfaces have been designed as one-way conversations between the brain and a computer, with the brain doing all the talking and the computer following commands. The system UF engineers created actually allows the computer to have a say in that conversation, too, according to findings published this month online in the Institute of Electrical and Electronics Engineers journal IEEE Transactions on Biomedical Engineering.
"In the grand scheme of brain-machine interfaces, this is a complete paradigm change," said Justin C. Sanchez, Ph.D., a UF assistant professor of pediatric neurology and the study's lead author. "This idea opens up all kinds of possibilities for how we interact with devices. It's not just about giving instructions but about those devices assisting us in a common goal. You know the goal, the computer knows the goal and you work together to solve the task."
Scientists at UF and other institutions have been studying and refining brain-machine interfaces for years, developing and testing numerous variations of the technology with the goal of creating implantable, computer-chip-sized devices capable of controlling limbs or treating diseases.
The devices are programmed with complex algorithms that interpret thoughts. But the algorithms, or code, used in current brain-machine interfaces don't adapt to change, Sanchez said.
"The status quo of brain-machine interfaces that are out there have static and fixed decoding algorithms, which assume a person thinks one way for all time," he said. "We learn throughout our lives and come into different scenarios, so you need to develop a paradigm that allows interaction and growth."
To create this type of brain-machine interface, Sanchez and his colleagues developed a system based on setting goals and giving rewards.
Fitted with tiny electrodes in their brains to capture signals for the computer to unravel, three rats were taught to move a robotic arm toward a target with just their thoughts. Each time they succeeded, the rats were rewarded with a drop of water.
The computer's goal, on the other hand, was to earn as many points as possible, Sanchez said. The closer a rat moved the arm to the target, the more points the computer received, giving it incentive to determine which brain signals lead to the most rewards, making the process more efficient for the rat. The researchers conducted several tests with the rats, requiring them to hit targets that were farther and farther away. Despite this increasing difficulty, the rats completed the tasks more efficiently over time and did so at a significantly higher rate than if they had just aimed correctly by chance, Sanchez said.
"We think this dialogue with a goal is how we can make these systems evolve over time," Sanchez said. "We want these devices to grow with the user. (Also) we want users to be able to experience new scenarios and be able to control the device."
Dawn Taylor, Ph.D., an assistant professor of biomedical engineering at Case Western Reserve University, said the results of the study add a new dimension to brain-machine interface research. That UF researchers were able to train rats to use the robotic arm and then obtain significant results from animals lacking the mental prowess of primates or humans is also impressive, she said.
"It's a clear demonstration of a methodology that will work in situations when other implementations would fall apart," Taylor said.
Source : University of Florida