Posts Tagged ‘neurology’

Having a parent with Alzheimer’s disease has been known to raise a person’s risk of developing the disease, but new research published in Neurology suggests that having second- and third-degree relatives who have had Alzheimer’s may also increase risk.

“Family history is an important indicator of risk for Alzheimer’s disease, but most research focuses on dementia in immediate family members, so our study sought to look at the bigger family picture,” said Lisa A. Cannon-Albright, PhD, University of Utah School of Medicine, Salt Lake City, Utah. “We found that having a broader view of family history may help better predict risk. These results potentially could lead to better diagnoses and help patients and their families in making health-related decisions.”

For the study, researchers looked at the Utah Population Database, which includes the genealogy of Utah pioneers from the 1800s and their descendants up until modern day. The database is linked to Utah death certificates, which show causes of death, and in a majority of cases, contributing causes of death.

In that database, researchers analysed data from over 270,800 people who had at least 3 generations of genealogy connected to the original Utah pioneers including genealogy data for both parents, all 4 grandparents, and at least 6 of 8 great-grandparents. Of those, 4,436 have a death certificate that indicates Alzheimer’s disease as a cause of death.

Results showed that people with 1 first-degree relative with Alzheimer’s disease (18,494 people) had a 73% increased risk of developing the disease. Of this group of people, 590 developed Alzheimer’s disease; the researchers would have expected this group to have 341 cases.

People with 2 first-degree relatives were 4 times more likely to develop the disease; those with 3 were 2.5 times more likely; and those with 4 were nearly 15 times more likely to develop Alzheimer’s disease.

Of the 21 people in the study with 4 first-degree relatives with Alzheimer’s, 6 had the disease. The researchers would have expected only 0.4 people to develop the disease.

Those with 1 first-degree relative and 1 second-degree relative had a 21 times greater risk. Examples of this would be a parent and one grandparent with the disease, or a parent and one aunt or uncle. There were 25 people in this category in the study; 4 of them had the disease when researchers would have expected 0.2 cases.

Those who had only third-degree relatives, and 3 such relatives, with Alzheimer’s disease had a 43% greater risk of developing the disease. An example of this would be two great-grandparents with the disease, along with one great uncle, but no parents or grandparents with the disease. Of the 5,320 people in this category, 148 people had the disease when researchers would have expected 103.

“More and more, people are increasingly seeking an estimate of their own genetic risk for Alzheimer’s disease,” said Dr. Cannon-Albright. “Our findings indicate the importance of clinicians taking a person’s full family history that extends beyond their immediate family members.”

She noted that among all of the study participants, 3% had a family history that doubled their risk of Alzheimer’s disease, and a little over one-half of a percent had a family history that increased their risk by ≥3 times that of a person without a family history of the disease.

Limitations of the study include that not all individuals dying from Alzheimer’s disease may have had a death certificate listing it as cause of death. Dr. Cannon-Albright said death certificates are known to underestimate the prevalence of the disease.

“There are still many unknowns about why a person develops Alzheimer’s disease,” she said. “A family history of the disease is not the only possible cause. There may be environmental causes, or both. There is still much more research needed before we can give people a more accurate prediction of their risk of the disease.”

Reference:
https://n.neurology.org/content/early/2019/03/13/WNL.0000000000007231

https://dgnews.docguide.com/having-great-grandparents-cousins-alzheimer-s-linked-higher-risk?overlay=2&nl_ref=newsletter&pk_campaign=newsletter&nl_eventid=20119

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A normal brain of a 70-year-old (left slice), compared with the brain of a 70-year-old with Alzheimer’s disease.Credit: Jessica Wilson/Science Photo Library

Neuroscientists have amassed more evidence for the hypothesis that sticky proteins that are a hallmark of neurodegenerative diseases can be transferred between people under particular conditions — and cause new damage in a recipient’s brain.

They stress that their research does not suggest that disorders such as Alzheimer’s disease are contagious, but it does raise concern that certain medical and surgical procedures pose a risk of transmitting such proteins between humans, which might lead to brain disease decades later.

“The risk may turn out to be minor — but it needs to be investigated urgently,” says John Collinge, a neurologist at University College London who led the research, which is published in Nature1 on 13 December.

The work follows up on a provocative study published by Collinge’s team in 20152. The researchers discovered extensive deposits of a protein called amyloid-beta during post-mortem studies of the brains of four people in the United Kingdom. They had been treated for short stature during childhood with growth-hormone preparations derived from the pituitary glands of thousands of donors after death.

The recipients had died in middle-age of a rare but deadly neurodegenerative condition called Creutzfeldt-Jakob disease (CJD), caused by the presence in some of the growth-hormone preparations of an infectious, misfolded protein — or prion — that causes CJD. But pathologists hadn’t expected to see the amyloid build up at such an early age. Collinge and his colleagues suggested that small amounts of amyloid-beta had also been transferred from the growth-hormone samples, and had caused, or ‘seeded’, the characteristic amyloid plaques.

Seeds of trouble
Amyloid plaques in blood vessels in the brain are a hallmark of a disease called cerebral amyloid angiopathy (CAA) and they cause local bleeding. In Alzheimer’s disease, however, amyloid plaques are usually accompanied by another protein called tau — and the researchers worry that this might also be transmitted in the same way. But this was not the case in the brains of the four affected CJD patients, which instead had the hallmarks of CAA.

The team has now more directly tested the hypothesis that these proteins could be transmitted between humans through contaminated biological preparations. Britain stopped the cadaver-derived growth hormone treatment in 1985 and replaced it with a treatment that uses synthetic growth hormone. But Collinge’s team was able to locate old batches of the growth-hormone preparation stored as powder for decades at room temperature in laboratories at Porton Down, a national public-health research complex in southern England.

When the researchers analysed the samples, their suspicions were confirmed: they found that some of the batches contained substantial levels of amyloid-beta and tau proteins.

Mouse tests
To test whether the amyloid-beta in these batches could cause the amyloid pathology, they injected samples directly into the brains of young mice genetically engineered to be susceptible to amyloid pathology. By mid-life, the mice had developed extensive amyloid plaques and CAA. Control mice that received either no treatment or treatment with synthetic growth hormone didn’t have amyloid build up.

The scientists are now checking in separate mouse experiments whether the same is true for the tau protein.

“It’s an important study, though the results are very expected,” says Mathias Jucker at the Hertie Institute for Clinical Brain Research in Tubingen, Germany. Jucker demonstrated in 2006 that amyloid-beta extracted from human brain could initiate CAA and plaques in the brains of mice3. Many other mouse studies have also since confirmed this.

Surgical implications
That the transmissibility of the amyloid-beta could be preserved after so many decades underlines the need for caution, says Jucker. The sticky amyloid clings tightly to materials used in surgical instruments, resisting standard decontamination methods4. But Jucker also notes that, because degenerative diseases take a long time to develop, the danger of any transfer may be most relevant in the case of childhood surgery where instruments have also been used on old people.

So far, epidemiologists have not been able to assess whether a history of surgery increases the risk of developing a neurodegenerative disease in later life — because medical databases tend not to include this type of data.

But epidemiologist Roy Anderson at Imperial College London says researchers are taking the possibility seriously. Major population cohort studies, such as the US Framingham Heart Study, are starting to collect information about participants’ past surgical procedures, along with other medical data.

The 2015 revelation prompted pathologists around the world to reexamine their own cases of people who had been treated with similar growth-hormone preparations — as well as people who had acquired CJD after brain surgery that had involved the use of contaminated donor brain membranes as repair patches. Many of the archived brain specimens, they discovered, were full of aberrant amyloid plaques5,6,7. One study showed that some batches of growth-hormone preparation used in France in the 1970s and 1980s were contaminated with amyloid-beta and tau — and that tau was also present in three of their 24 patients.8

Collinge says he applied unsuccessfully for a grant to develop decontamination techniques for surgical instruments after his 2015 paper came out. “We raised an important public-health question, and it is frustrating that it has not yet been addressed.” But he notes that an actual risk from neurosurgery has not yet been established.

https://www.nature.com/articles/d41586-018-07735-w?utm_source=fbk_nnc&utm_medium=social&utm_campaign=naturenews&sf204283628=1

Thank to Kebmodee for bringing this to the It’s Interesting community.

SS39069

By Alan Mozes

People with attention-deficit/hyperactivity disorder (ADHD) may be more than twice as likely to develop an early onset form of Parkinson’s, new research warns.

What’s more, among “those ADHD patients who had a record of being treated with amphetamine-like drugs — especially Ritalin [methylphenidate] — the risk dramatically increased, to between eight- to nine-fold,” said senior study author Glen Hanson.

But his team did not prove that ADHD or its medications actually caused Parkinson’s risk to rise, and one ADHD expert noted that the absolute risk of developing Parkinson’s remains very small.

For the study, researchers analyzed nearly 200,000 Utah residents. All had been born between 1950 and 1992, with Parkinson’s onset tracked up until the age of 60.

Prior to any Parkinson’s diagnosis, roughly 32,000 had been diagnosed with ADHD.

Hanson, a professor of pharmacology and toxicology at the University of Utah, said that ADHD patients were found to be “2.4 times more likely to develop Parkinson’s disease-like disorders prior to the age of 50 to 60 years,” compared with those with no history of ADHD. That finding held up even after accounting for a number of influential factors, including smoking, drug and alcohol abuse, and other psychiatric disorders.

“Although we cannot accurately say how much time elapsed between ADHD and [a] Parkinson’s-like disorder diagnosis, it was probably between 20 to 50 years,” he said.

As to what might explain the link, Hanson said that both ADHD and most forms of Parkinson’s source back to a “functional disorder of central nervous system dopamine pathways.”

In addition, Hanson said that “the drugs used to treat ADHD apparently work because of their profound effects on the activity of these dopamine pathways.” Theoretically, the treatment itself might trigger a metabolic disturbance, promoting dopamine pathway degeneration and, ultimately, Parkinson’s, he explained.

Still, Hanson pointed out that, for now, “we are not able to determine if the increased risk associated with stimulant use is due to the presence of the drug or the severity of the ADHD,” given that those treated with ADHD drugs tend to have more severe forms of the disorder.

And while demonstrating “a very strong association” between ADHD and Parkinson’s risk, the findings are preliminary, the study authors added.

Also, the absolute risk of developing Parkinson’s remained low, even in the most pessimistic scenario.

For example, the findings suggest that the risk of developing early onset Parkinson’s before the age of 50 would be eight or nine people out of every 100,000 with ADHD. This compares with one or two out of every 100,000 among those with no history of ADHD, the researchers said.

But the scientists noted that the results should raise eyebrows, because Parkinson’s primarily strikes people over the age of 60. Given the age range of those tracked so far in the study, Hanson said that his team was not yet able to ascertain Parkinson’s risk among ADHD patients after the age of 60.

Hanson also pointed out that because ADHD was only first diagnosed in the 1960s, only about 1.5 percent of the people in the study had an ADHD diagnosis, despite current estimates that peg ADHD prevalence at 10 percent. That suggests that the current findings may underestimate the scope of the problem.

“Clearly, there are some critical questions left to be answered concerning what is the full impact of this increased risk,” Hanson said.

Dr. Andrew Adesman is chief of developmental and behavioral pediatrics at Cohen Children’s Medical Center of New York with Northwell Health in New York City. He was not involved with the study and said the findings “surprised” him.

But, “we need to keep in mind that this study needs to be replicated and that the incidence of these conditions was very low, even among those with ADHD,” Adesman said. “The reality is that this would not affect 99.99 percent of individuals with ADHD.”

Meanwhile, Adesman said, “given that this study needs to be replicated, given that it is unclear whether ADHD medications further increase the risks of Parkinson’s, and given the very low risk in an absolute sense, I believe individuals with ADHD should not be hesitant to pursue or continue medical treatment for their ADHD.”

The report was published online Sept. 12 in the journal Neuropsychopharmacology.

Glen Hanson, DDS, Ph.D., vice dean and professor, pharmacology, School of Dentistry, University of Utah, Salt Lake City; Andrew Adesman, M.D., chief, developmental and behavioral pediatrics, Steven & Alexandra Cohen Children’s Medical Center of New York, Northwell Health, New York City; Sept. 12, 2018, Neuropsychopharmacology, online

https://consumer.healthday.com/cognitive-health-information-26/parkinson-s-news-526/adhd-tied-to-raised-risk-of-early-parkinson-s-737637.html

By Jim Dryden

It may be possible in the future to screen patients for Alzheimer’s disease using an eye exam.

Using technology similar to what is found in many eye doctors’ offices, researchers at Washington University School of Medicine in St. Louis have detected evidence suggesting Alzheimer’s in older patients who had no symptoms of the disease.

Their study, involving 30 patients, is published Aug. 23 in the journal JAMA Ophthalmology.

“This technique has great potential to become a screening tool that helps decide who should undergo more expensive and invasive testing for Alzheimer’s disease prior to the appearance of clinical symptoms,” said the study’s first author, Bliss E. O’Bryhim, MD, PhD, a resident physician in the Department of Ophthalmology & Visual Sciences. “Our hope is to use this technique to understand who is accumulating abnormal proteins in the brain that may lead them to develop Alzheimer’s.”

Significant brain damage from Alzheimer’s disease can occur years before any symptoms such as memory loss and cognitive decline appear. Scientists estimate that Alzheimer’s-related plaques can build up in the brain two decades before the onset of symptoms, so researchers have been looking for ways to detect the disease sooner.

Physicians now use PET scans and lumbar punctures to help diagnose Alzheimer’s, but they are expensive and invasive.

In previous studies, researchers examining the eyes of people who had died from Alzheimer’s have reported that the eyes of such patients showed signs of thinning in the center of the retina and degradation of the optic nerve.

In the new study, the researchers used a noninvasive technique — called optical coherence tomography angiography — to examine the retinas in eyes of 30 study participants with an average age in the mid 70s, none of whom exhibited clinical symptoms of Alzheimer’s.

Those participants were patients in The Memory and Aging Project at Washington University’s Knight Alzheimer’s Disease Research Center. About half of those in the study had elevated levels of the Alzheimer’s proteins amyloid or tau as revealed by PET scans or cerebrospinal fluid, suggesting that although they didn’t have symptoms, they likely would develop Alzheimer’s. In the other subjects, PET scans and cerebrospinal fluid analyses were normal.

“In the patients with elevated levels of amyloid or tau, we detected significant thinning in the center of the retina,” said co-principal investigator Rajendra S. Apte, MD, PhD, the Paul A. Cibis Distinguished Professor of Ophthalmology and Visual Sciences. “All of us have a small area devoid of blood vessels in the center of our retinas that is responsible for our most precise vision. We found that this zone lacking blood vessels was significantly enlarged in people with preclinical Alzheimer’s disease.”

The eye test used in the study shines light into the eye, allowing a doctor to measure retinal thickness, as well as the thickness of fibers in the optic nerve. A form of that test often is available in ophthalmologist’s offices.

For this study, however, the researchers added a new component to the more common test: angiography, which allows doctors to distinguish red blood cells from other tissue in the retina.

“The angiography component allows us to look at blood-flow patterns,” said the other co-principal investigator, Gregory P. Van Stavern, MD, a professor of ophthalmology and visual sciences. “In the patients whose PET scans and cerebrospinal fluid showed preclinical Alzheimer’s, the area at the center of the retina without blood vessels was significantly larger, suggesting less blood flow.”

Added Apte: “The retina and central nervous system are so interconnected that changes in the brain could be reflected in cells in the retina.”

Of the patients studied, 17 had abnormal PET scans and/or lumbar punctures, and all of them also had retinal thinning and significant areas without blood vessels in the centers of their retinas. The retinas appeared normal in the patients whose PET scans and lumbar punctures were within the typical range.

More studies in patients are needed to replicate the findings, Van Stavern said, but he noted that if changes detected with this eye test can be used as markers for Alzheimer’s risk, it may be possible one day to screen people as young as their 40s or 50s to see whether they are at risk for the disease.

“We know the pathology of Alzheimer’s disease starts to develop years before symptoms appear, but if we could use this eye test to notice when the pathology is beginning, it may be possible one day to start treatments sooner to delay further damage,” he said.

O’Bryhim BE, Apte RS, Kung N, Coble D, Van Stavern GP. Optical coherence tomography angiography findings in pre-clinical Alzheimer’s disease. JAMA Ophthalmology, Aug. 23, 2018.

https://source.wustl.edu/2018/08/alzheimers-one-day-may-be-predicted-during-eye-exam/


Migraines are not typical headaches; they are extremely painful events and are often accompanied by nausea, blurred vision, or ultrasensitivity to smells, light, or sounds. These episodes can be debilitating and highly disruptive to day-to-day life. More women than men tend to experience them, and researchers ask why.

Ny Maria Cohut

Scientists at the Universitas Miguel Hernández in Elche, Spain, believe that the answer as to why migraines are more common among women may lie with the activity of sex hormones.

“We can observe significant differences in our experimental migraine model between males and females and are trying to understand the molecular correlates responsible for these differences,” says Prof. Antonio Ferrer-Montiel.

The trigeminovascular system is made up of neurons that are found in a cranial nerve known as the trigeminovascular nerve. Researchers have suggested that this system is involved in migraine mechanisms.

In the new study, Prof. Ferrer-Montiel and his team argue that the activity of sex-specific hormones interact with the trigeminal system in a way that renders its nerve cells more sensitive to migraine triggers.

These findings now appear in the journal Frontiers in Molecular Biosciences, as part of a special issue focusing on the importance of targeting proteins in cell membranes as an effective therapeutic approach in medicine.

In the future, Prof. Ferrer-Montiel and colleagues hope that their findings may lead to a better, more personalized approach to migraine management.

The researchers conducted a review of existing studies about sex hormones, what drives migraine sensitivity, and how nerves react to migraine triggers. In doing so, they were looking to understand how specific sex hormones might facilitate the development of migraines.

Soon enough, they found that certain sex hormones — such as testosterone — actually appear to play a protective role. However, other hormones — such as prolactin — seem to intensify the severity of migraines, according to the scientists.

Yhese hormones, the authors say, either boost cells’ sensitivity to migraine triggers or desensitize them, by interacting with the cells’ ion channels. These are a type of membrane protein that allow ions (charged particles) to pass through and influence the cells’ sensitivity to various stimuli.

Through their research, Prof. Ferrer-Montiel and team identified the hormone estrogen as a key player in the development of migraines.

At first, the team saw that estrogen was tied to higher migraine prevalence in women experiencing menstruation. Moreover, they also found that certain types of migraine were linked to changes in hormone levels around menstruation.

Specifically, Prof. Ferrer-Montiel and colleagues noticed that changes in estrogen levels means that trigeminal nerve cells may become more sensitive to external stimuli, which can lead to a migraine episode.

At the same time, the researchers warn that nobody should jump to any conclusions based on the evidence gathered so far. This study, they say, is preliminary, and much more research is needed to determine the exact roles that hormones play in the development and prevention of migraine.

Also, the new study has focused on findings from research conducted in vitro, or on animal models, so Prof. Ferrer-Montiel and colleagues advise that in the future, it will be important to conduct longitudinal studies with human participants.

If their findings are confirmed and consolidated, the scientists believe they could lead to improved strategies for the management of migraines.

“If successful, we will contribute to better personalized medicine for migraine therapy,” concludes Prof. Ferrer-Montiel.

https://www.medicalnewstoday.com/articles/322767.php


Researchers believe that large cells called nucleus gigantocellularis neurons, pictured here, modulate blood flow by releasing nitric oxide.

There is no shortage of wonders that our central nervous system produces—from thought and language to movement to the five senses. All of those dazzling traits, however, depend on an underappreciated deep brain mechanism that Donald Pfaff, head of the Laboratory of Neurobiology and Behavior at The Rockefeller University, calls generalized arousal, or GA for short. GA is what wakes us up in the morning and keeps us aware and in touch with ourselves and our environment throughout our conscious hours.

“It’s so fundamental that we don’t pay attention to it,” says Pfaff, “and yet it’s so important that we should.”

Pfaff and his team of researchers certainly do. Now, in a series of experiments involving a particular type of brain cell, they have advanced our understanding of the roots of consciousness. Their work may potentially prove relevant in the study of some psychiatric diseases.

The big cells in the black box

The findings, published this month in Proceedings of the National Academy of Sciences, shed light on an area of the brainstem that is so little understood the first author of the paper, Inna Tabansky, a research associate in Pfaff’s lab, calls it “the black box.” That term is certainly simpler than its actual name—the nucleus gigantocellularis (NGC), which is part of a structure called the medullary reticular formation.

In her work, using mice, Tabansky focused on a subtype of extremely large neurons in the NGC with links to virtually the entire nervous system, including the thalamus, where neurons can activate the entire cerebral cortex. “If you just look at the morphology of NGC neurons, you know they’re important,” Pfaff says. “It’s just a question of what they’re important for. I think they’re essential for the initiation of any behavior.”

To discover what role the NGC neurons might play in GA, Tabansky and her colleagues, including Joel Stern, a visiting professor in the Pfaff lab, began by identifying the genes that these neurons express. They used a technique known as “retro-TRAP,” developed in the lab of Rockefeller scientist Jeffrey Friedman.

To Tabansky’s surprise, the NGC neurons were found to express the gene for an enzyme, endothelial nitric oxide synthase (eNOS), which produces nitric oxide, which in turn relaxes blood vessels, increasing the flow of oxygenated blood to tissue. (No other neurons in the brain are known to produce eNOS.) They also discovered that the eNOS-expressing NGC neurons are located close to blood vessels.

In Pfaff’s view, the neurons are so critical for the normal functions of the central nervous system that they have evolved the ability to control their own blood supply directly. ‘“We’re pretty sure that if these neurons need more oxygen and glucose, they will release nitric oxide into these nearby blood vessels in order to get it,” he says.

The circumstances that would prompt such a response were the subject of further experiments. The scientists found evidence that changes in the environment, such as the introduction of novel scents, activated eNOS in the NGC neurons and produced increased amounts of nitric oxide in mice.

“There is some low level of production when the animal is in a familiar setting,” says Tabansky, “which is what you expect as they maintain arousal. But it is vastly increased when the animal is adapting to a new environment.” This activation of the NGC neurons supports the case for their central role in arousal, Tabansky says.

From cells to psychiatry

Going forward, Tabansky says she’s interested in exploring if their findings might help fill a gap in the understanding of certain disorders, such as bipolar disorder, suicidality, and ADHD. Some genetic research has implicated a role for the neurons she studied in these diseases, but the mechanism behind this link is not known.

“By showing that this gene and its associated pathways have a particular role, at least in the rodent brain, that relates to a fundamental function of the nervous system, is a hint about how this gene can cause psychiatric disease,” she says. “It’s very preliminary, and there is a lot more work to be done, but it potentially opens a new way to study how this gene can alter an individual’s psychology.”

https://www.rockefeller.edu/news/23275-giant-neurons-in-the-brain-may-play-similarly-giant-role-in-awareness-and-cognition/


The Dr. Peter Stys lab within the Hotchkiss Brain Institute at the Cumming School of Medicine, University of Calgary, is equipped with highly specialized microscopes used for researching multiple sclerosis, Alzheimer’s and other neurodegenerative disease. In this customized lab, the researchers can’t wear white lab coats, they have to wear dark clothing. Photons could reflect off light clothing and interfere with the experiments. From left: Megan Morgan, research assistant, and Craig Brideau, engineering scientist. Photo by Pauline Zulueta, Cumming School of Medicine

By Kelly Johnston, Cumming School of Medicine

Ridiculous. That’s how Andrew Caprariello says his colleagues described his theory about multiple sclerosis (MS) back when he was doing his PhD in Ohio.

Caprariello’s passion to explore controversial new theories about MS propelled him to seek out a postdoctoral fellowship with a like-minded thinker, whom he found in University of Calgary’s Dr. Peter Stys, a member of the Hotchkiss Brain Institute at the Cumming School of Medicine (CSM).

The collaboration paid off. Caprariello, Stys and their colleagues have scientific proof published in the Proceedings of the National Academy of Sciences (PNAS) that their somewhat radical theory has merit. “I’ve always wondered ‘what if’ MS starts in the brain and the immune attacks are a consequence of the brain damage,” says Caprariello, PhD, and lead author on the study.

Currently, MS is considered to be a progressive autoimmune disease. Brain inflammation happens when the body’s immune system attacks a protective material around nerve fibers in the brain called myelin. Conventional thinking is that rogue immune cells initially enter the brain and cause myelin damage that starts MS.

“In the field, the controversy about what starts MS has been brewing for more than a decade. In medical school, I was taught years ago that the immune attack initiates the disease. End of story,” says Stys, a neurologist and professor in the Department of Clinical Neurosciences at the CSM. “However, our findings show there may be something happening deeper and earlier that damages the myelin and then later triggers the immune attacks.”

To test the theory, the research team designed a mouse model of MS that begins with a mild myelin injury. In this way, researchers could mirror what they believe to be the earliest stages of the disease.

“Our experiments show, at least in this animal model, that a subtle early biochemical injury to myelin secondarily triggers an immune response that leads to additional damage due to inflammation. It looks very much like an MS plaque on MRI and tissue examination,” says Stys. “This does not prove that human MS advances in the same way, but provides compelling evidence that MS could also begin this way.”

With that result, the researchers started to investigate treatments to stop the degeneration of the myelin to see if that could reduce, or stop, the secondary autoimmune response.

“We collaborated with researchers at the University of Toronto and found that by targeting a treatment that would protect the myelin to stop the deterioration, the immune attack stopped and the inflammation in the brain never occurred,” says Stys. “This research opens a whole new line of thinking about this disease. Most of the science and treatment for MS has been targeted at the immune system, and while anti-inflammatory medications can be very effective, they have very limited benefit in the later progressive stages of the disease when most disability happens.”

It can be very hard to find funding to investigate an unconventional theory. The research team was funded by the Brain and Mental Health Strategic Research Fund, established by the Office of the Vice-President (Research) at UCalgary to support innovative, interdisciplinary studies within the Brain and Mental Health research strategy.

“We chose high-risk, novel projects for these funds to support discoveries by teams who did not have the chance to work together through conventional funding sources,” said Ed McCauley, PhD, vice-president (research). “The MS study shows the potential of brain and mental health scholars to expand capacity by tapping into new approaches for conducting research. Their work also exemplifies the type of interdisciplinary research that is propelling the University of Calgary as an international leader in brain and mental health research.”

http://www.ucalgary.ca/utoday/issue/2018-05-04/ucalgary-scientists-discover-new-way-battle-multiple-sclerosis