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Immunology

Immunology, Neuroscience, Research, Stanford News

Blocking a receptor on brain’s immune cells counters Alzheimer’s in mice

Blocking a receptor on brain’s immune cells counters Alzheimer’s in mice

brain in motionAttention, nerve cells: It’s not all about you.

As a new study in the Journal of Clinical Investigation led by Stanford neuroscientist Kati Andreasson, MD, shows, blocking the action of a single molecule situated on the surfaces of entirely different brain cells reversed memory loss and a bunch of other Alzheimer’s-like features in experimental mice.

The very term “neuroscience” strongly suggests that nerve cells, a.k.a. neurons, are the Big Enchilada in brain research – and, let’s face it, you wouldn’t want to leave home without them. But they’re far from the entire picture. In fact, neurons account for a mere 10 percent of all the cells in the brain. It may be that the mass die-off of nerve cells in the brains of people with Alzheimer’s disease may largely occur because, during the course of aging, another set of key players ensconced in that mysterious organ inside our skull and  known collectively as microglia begin to fall down on the job.

In  a release I wrote to explain the study’s findings in lay terms, I described microglia as the brain’s very own, dedicated immune cells:

A microglial cell serves as a front-line sentry, monitoring its surroundings for suspicious activities and materials by probing its local environment. If it spots trouble, it releases substances that recruit other microglia to the scene … Microglia are tough cops, protecting the brain against invading bacteria and viruses by gobbling them up. They are adept at calming things down, too, clamping down on inflammation if it gets out of hand. They also work as garbage collectors, chewing up dead cells and molecular debris strewn among living cells – including clusters of a protein called A-beta, notorious for aggregating into gummy deposits called Alzheimer’s plaques, the disease’s hallmark anatomical feature. … A-beta, produced throughout the body, is as natural as it is ubiquitous. But when it clumps into soluble clusters consisting of a few molecules, it’s highly toxic to nerve cells. These clusters are believed to play a substantial role in causing Alzheimer’s.

“The microglia are supposed to be, from the get-go, constantly clearing A-beta, as well as keeping a lid on inflammation,” Andreasson told me. If their job performance heads downhill – as seems to occur during the aging process – things get out of control. A-beta builds up in the brain, inducing toxic inflammation.

But by blocking the activity of a single molecule – a receptor protein on microglial cells’ surfaces  – Andreasson’s team got those microglia back on the job. They resumed chewing up A-beta, quashing runaway neuro-inflammation, squirting out neuron-nurturing chemicals. Bottom line: the Alzheimer’s-prone experimental animals’ IQs (as measured by mousey memory tests) rose dramatically.

Aspirin and similar drugs also tend to shut down the activity of this microglial receptor, which may or may not explain why their use seems to stave off the onset of Alzheimer’s in people who start using them regularly (typically for unrelated reasons) before this memory-stealing syndrome’s symptoms show up. But aspirin et al. do lots of other things, too – some good, some bad. The new findings suggest a compound carefully tailored to block this receptor and do nothing else might be a weapon in the anti-Alzheimer’s arsenal.

Previously: Another big step toward building a better aspirin tablet, Untangling the inflammation/Alzheimer’s connection and Study could lead to new class of stroke drugs
Photo by Henry Markham

Clinical Trials, Immunology, Research, Transplants

Transplant without lifelong drugs gives patient another chance

Transplant without lifelong drugs gives patient another chance

"DCIM100GOPRO"Imagine learning you have an illness. It’s the same illness that killed your mother. You watched her fade, the last years of her life dreadful to watch, unimaginably tough to endure. The same fate awaits you. Until… it doesn’t. Now there’s a therapy that just might save you.

That’s the story of San Francisco Bay Area resident Cynthia Alcaraz-Jew, featured in the fall issue of Stanford Medicine Magazine. Now in her late 40s, Alcaraz-Jew, like her mother, suffers from a rare genetic condition called Alport Syndrome. The ailment leads to kidney, ear and eye problems.

Alcaraz-Jew didn’t immediately luck out. Her kidneys failed first and her younger brother, Xavier, a perfect immunologic match, offered to donate his kidney. Great news, of course, but a transplant usually means years of immunosuppressive drugs, which leave bones brittle and can lead to infections, heart disease, or even, ironically kidney failure.

Thanks to her perfectly matched kidney, Alcaraz-Jew was able to enroll in a trial led by Stanford immunologist Samuel Strober, MD, that aims to wean transplant patients off immunosuppressive drugs. From the article:

Of the 24 kidney transplant patients with perfectly matched donors who enrolled in the trial beginning in 2000, 16, including Alcaraz-Jew, are living drug free, and three others are working to get off the medications, Strober says. The team is planning to publish a paper summarizing the research results in the near future.

And the photo? That’s Alcaraz-Jew and her husband swimming with whale sharks in Mexico earlier this year.

Previously: Stanford Medicine magazine traverses the immune system, Kidney-transplant recipients party without drugs — immune-suppressing anti-rejection drugs, that is, Might kidney-transplant recipients be able to toss their pills?  and Marked improvement in transplant success on the way, says Stanford immunologist
Photo courtesy of Cynthia Alcaraz-Jew

Chronic Disease, Imaging, Immunology, Neuroscience, Research, Stanford News

Patients' reaction to ME/CFS coverage in Stanford Medicine magazine

Patients' reaction to ME/CFS coverage in Stanford Medicine magazine

me-cfs-brain-zeineh

In the last few weeks, Stanford published two articles on chronic fatigue syndrome, a.k.a. myalgic encephalomyelitis, and the outpouring of positive feedback from ME/CFS patients has been tremendous. In my long-form Stanford Medicine story and video, I describe a young woman’s seven-year battle with the disease and the groundbreaking research being done by her physician, José Montoya, MD, and immunologist Mark Davis, PhD, to identify the biomarkers and root causes of ME/CFS. My colleague Bruce Goldman followed up with an elegantly written article describing the distinct differences between the brains of ME/CFS patients with those of healthy people, in a newly released study from this same research team.

While our primary job as medical science writers is to explain new research accurately, it’s a bonus to know that we captured the patient experience in a compassionate way, and that we have in some way eased their suffering with hope.

Here is a sampling of a few of these letters from around the world:

From British Columbia, Canada:
Thank you for an article that is very well done. I will be printing it for my MD and forwarding it to family and a few close friends because it captures this devastating illness so well. I will keep a copy for myself to remind me (on those dark days) that Dr. Montoya is in my corner.

From Sweden:
I would like to thank you for your very informative and interesting article! This kind of information of what research is going on at Stanford, etc., is very important for us patients with ME all over the world! There is a lot of disinformation coming out about this disease and I therefore very much appreciate your article and especially Dr. Montoya’s passionate engagement with this disease.

From Cali, Colombia:
Here in Cali, Colombia, the city of birth of Dr. Montoya, I feel very happy reading your excellent article, and learning the marvelous and difficult investigation performed by these brilliant scientists. I was moved to tears. Thank you.

From the San Francisco Bay Area:
I want to thank you very much for the powerful piece you wrote about ME/CFS. You tell the story in a very engaging way, which is so compelling. It’s not the usual doom/gloom/dark room story which my daughter and I have encountered frequently in what people write about ME/CFS. Family and friends with whom I have shared the article are appreciative of your writing so descriptively and articulately about all aspects of ME/CFS: the science, the inequity of research funding, the personal experience of a patient, the work of Drs. Montoya/Mark Davis/Holden Maecker.

From India:
Today I have gone through your article about Erin’s story. How she recovered from CFS had given me a ray of hope as I am also suffering from such an ailment for the last 6-8 years.

From Atlanta, Georgia:
I just read your beautifully written article on Immune System Disruption. First soccer caught my eye, then “swimming in the primordial soup of creative disruption” locked me in. I read every word … and I am going to spend the rest of the night in Atlanta copying [my internal medicine doctor] on the article.

From Australia:
Just wanted to thank you for your excellent article. It could really make a difference in raising awareness and I appreciate the quality of your writing. I have suffered from CFS/ME for many years in Australia and find the research project and your understanding very encouraging.

From the blogosphere:
I just wanted to thank you for taking the time to write such an in-depth, accurate article on our oft-ignored illness. Dr. Montoya is a hero within the ME/CFS community, but I didn’t know about the others at Stanford also working on ME/CFS — that gives me some hope for a better future! I plan to share your article on my ME/CFS blog and in several Facebook groups for ME/CFS that I belong to.

Previously: Some headway on chronic fatigue syndrome: Brain abnormalities pinpointedUnbroken: A chronic-fatigue patient’s long road to recovery, Deciphering the puzzle of chronic-fatigue syndrome and Stanford Medicine magazine traverses the immune system
Image, showing white matter differences between a ME/CFS patient sample an a healthy control, by Michael Zeineh/Stanford

Biomed Bites, Immunology, Infectious Disease, Research, Stanford News

Figuring out a parasite's secrets – insights from studying Toxoplasma gondii

Figuring out a parasite's secrets - insights from studying Toxoplasma gondii

Welcome to Biomed Bites, a weekly feature that highlights some of Stanford’s most innovative research and introduces Scope readers to innovators in a variety of disciplines. 

You’ve probably heard that pregnant women shouldn’t get near the litter box. The reason is that many kitties carry a parasite called Toxoplasma gondii, which is transmitted through their feces. The parasite infects about 2 billion people worldwide, according to Stanford microbiologist John Boothroyd, PhD.

Boothroyd, who also serves as the associate vice provost for graduate education, directs a lab that has uncovered some of the basic biology of this single-celled protozoan parasite. Here’s Boothroyd in the video above:

Most of the time, this causes no significant disease, very few symptoms and probably something that most of these people will never know they were infected with. Occasionally, however, this parasite can cause devastating disease. It can affect the brain of the unborn child, it can cause severe neurological problems, it can even kill the developing fetus.

Toxoplasmosis, or infection with the parasite, can also cause serious complications in immunocompromised individuals. Boothroyd said he was drawn to the study of the T. gondii because it is clinically significant — he has the opportunity to help millions of people: “I wanted something where I felt the work we were doing was worth the many, many hours that I and the people I worked with put in to the daily effort.” T. gondii is also related to the Plasmodium parasites that cause malaria and some of the work from Boothroyd’s lab has been translated into insights into malaria.

Boothroyd’s team also identified the T. gondii protein that triggers the immune response in humans. With that knowledge, the investigators were able to insert the gene coding for that protein into yeast, letting the yeast produce the protein, “instead of having to grow the parasite in literally hundreds of thousands of mice a year and then killing those mice to get the parasite,” Boothroyd said. He went on to explain:

The situation in which Toxoplasma presents the most significant problem for the doctor and for the patient is in the pregnant woman. The challenge becomes first, is she infected, and if so, has the parasite crossed the placenta and reached the fetus. And third, what is the consequence of the infection in the fetus? All three of those we have addressed through our work.

Although much about the parasitic diseases remains unknown, Boothroyd is glad he picked T. gondii to focus on: “I think we’ve been able to do some real good with this work.”

Learn more about Stanford Medicine’s Biomedical Innovation Initiative and about other faculty leaders who are driving biomedical innovation here.

Previously: Stanford microbiologist’s secret sauce for disease detection, Cat guts, car crashes and warp-speed Toxoplasma infections and Patrick House discusses Toxoplasma gondii, parasitic mind control and zombies

Global Health, Immunology, Pregnancy, Public Health, Stanford News, Technology

Stanford-developed smart phone blood-testing device wins international award

Stanford-developed smart phone blood-testing device wins international award

When I worked as an epidemiologist, one of my jobs was with a program that prevented perinatal hepatitis B infections. That’s when a woman with a chronic hepatitis B infection passes it on to her baby. Babies are more likely than almost any other group to develop chronic infections that can cause them years of health problems and will most likely cut their lives short.

In the U.S., most states have comprehensive testing programs to detect pregnant women with infections and strict protocols that require delivery hospitals to treat babies born to them with vaccination and antibodies to prevent infection with the virus. But a program like this requires a huge administrative and laboratory investment – and in many poverty-stricken parts of the world, this simply isn’t possible. In fact, in California, the vast majority of cases identified by the prenatal testing program are women who were born outside the United States, including many from Asia.

So when I heard the recent news that a team of four Stanford graduate students had won the Nokia Sensing XCHALLENGE, an international competition to for diagnostic devices, for a mobile test that could detect hepatitis B infections, I was pretty impressed and curious about how it could be implemented in those places. The competition is run by XPrize, the same group that has run several competitions for space exploration, and others for super-fuel efficient vehicles and ocean clean-up efforts.

The mobile version of the winning test was one of five awarded top prizes among 90 entrants. It was developed by engineering PhD candidates Daniel Bechstein, Jung-Rok Lee, Joohong Choi and Adi W. Gani, building on work previously done by Stanford professor of materials science and engineering Shan Wang, PhD, and Stanford immunologist  Paul Utz, MD. The device works because magnetic nanoparticles are grafted onto two biological markers: the hepatitis B virus and the antibody that our bodies make in response to the virus. Current tests for hepatitis B requires a full laboratory facility. A Stanford press release describes the device:

The students used a diagnostic strip that takes a finger prick of blood. The patient’s blood flows into a tiny chamber where it mixes with magnetic nanoparticles to form magnetically tagged biomarkers.

The test strip is inserted into a small magnetic detector… The smartphone is plugged into the detector, and its microprocessor helps to perform the test. It takes only a few minutes.

If the test finds the hepatitis B antigen in the blood, the patient is infected and needs treatment. For a newborn with an infected mother, the child needs both vaccination and antibody therapy.

Continue Reading »

Genetics, History, Immunology, Research, Science, Stanford News

Knight in lab: In days of yore, postdoc armed with quaint research tools found immunology's Holy Grail

Knight in lab: In days of yore, postdoc armed with quaint research tools found immunology's Holy Grail

charging knightA human has only about 25,000 genes. So, it’s tough to imagine just how our immune systems can manage to recognize potentially billions of differently shaped microbial or tumor-cell body parts. But that’s precisely what our immune systems have to do, and with exquisite precision, in order to stomp invading pathogens and wanna-be cancer cells and leave the rest of our bodies the heck alone.

How do they do it?

Stanford immunologist Mark Davis, PhD, tore the cover off of immunology in the early 1980s by solving that riddle. As I wrote in  “The Swashbuckler,” an article in the latest issue of Stanford Medicine, T cells are one of two closely related, closely coordinated workhorse-warrior cell types that deserve much of the credit for the vertebrate immune system’s knack of carefully picking bad guys of various stripes out of the lineup and attacking them:

[Q]uite similar in many respects, B cells and T cells are more like fraternal than identical twins. B cells are specialized to find strange cells and strange substances circulating in the blood and lymph. T cells are geared toward inspecting our own cells for signs of harboring a virus or becoming cancerous. So it’s not surprising that the two cell types differ fundamentally in the ways they recognize their respective targets. B cells’ antibodies recognize the three-dimensional surfaces of molecules. T cells recognize one-dimensional sequences of protein snippets, called peptides, on cell surfaces. All proteins in use in a cell eventually get broken down into peptides, which are transported to the cell surface and displayed in molecular jewel cases that evolution has optimized for efficient inspection by patrolling T cells. Somehow, our inventory of B cells generates antibodies capable of recognizing and binding to a seemingly infinite number of differently shaped biological objects. Likewise, our bodies’ T-cell populations can recognize and respond to a vast range of different peptide sequences.

In the late 1970s, scientists (including then-graduate student Davis, who is now director of Stanford’s Institute for Immunity, Transplantation and Infection) unraveled the genetic quirks behind B cells’ ability to recognize a mind-blowingly diverse  set of different pathogens’ and tumor-cells’ characteristic molecular shapes. As a follow-on, Davis and a handful of colleagues – working with what would today be considered the most primitive of molecular-biology tools – isolated the gene underlying the T-cell receptor: an idiosyncratic and very important surface protein that is overwhelmingly responsible for T cells’ recognition of myriad pathogen- and cancer-cell-specific peptide sequences. And they figured out how it works.

The result? (Again from my article:)

With the T-cell receptor gene in hand, scientists can now routinely sort, scrutinize, categorize and utilize T cells to learn about the immune system and work toward improving human health. Without it, they’d be in the position of a person trying to recognize words by the shapes of their constituent letters instead of by phonetics.

Previously: Stanford Medicine magazine traverses the immune systemBest thing since sliced bread? A (potential) new diagnostic for celiac disease, Deja vu: Adults’ immune systems “remember” microscopic monsters they’ve never seen before, Immunology escapes from the mousetrap, Immunology meets infotech and Mice to men: Immunological research vaults into the 21st century
Photo by davidmclaughlin

Aging, Chronic Disease, Clinical Trials, Immunology, Research, Stanford News

Is osteoarthritis an inflammatory disorder? New thinking gets clinical test

Is osteoarthritis an inflammatory disorder? New thinking gets clinical test

SM arthritis imageOsteoarthritis sort of comes with the territory of aging. If you live long enough, you’ll probably get it.

For those fortunate enough not to have a working acquaintance with the disease, I describe its onset in a just-published Stanford Medicine article, “When Bones Collide”:

You start to feel some combination of pain, stiffness and tenderness in a thumb, a knee, a hip, a toe or perhaps your back or neck. It takes root, settles in and, probably, gets worse. And once you’ve got it, it never goes away. Eventually, it can get tough to twist off a bottle cap or to get around, depending on the joint or joints affected.

All too many of us, of course, are perfectly familiar with the symptoms of osteoarthritis. An estimated 27 million people in the United States have been diagnosed with it. By 2030, due mainly to the aging of the population, the number will be more like 50 million. Anything so common is all too easy to look at as inevitable: basically, the result of the same kind of wear and tear on your joints that causes the treads on a commuter car’s set of tires to disappear eventually.

But Stanford rheumatologists Bill Robinson, MD, PhD, and Mark Genovese, MD, think that just may not be the way it works. Almost four years ago I wrote about Robinson’s discovery that osteoarthritis is propelled by a sequence of inflammatory events similar to ones associated with Alzheimer’s disease, cardiovascular disease, and type-2 diabetes. That discovery and a steady stream of follow-up work in his lab have spawned a clinical trial, now underway and led by Genovese, to see if a regimen of anti-inflammatory medicines that’s been shown to roll back osteoarthritis’s progression in mice can do the same thing in people.

That’s the kind of progress most of us could live without.

Previously: New thinking about osteoarthritis, older people’s nemesis and Inflammation, not just wear and tear, spawn arthritis
Illustration by Jeffrey Decoster

Autoimmune Disease, Behavioral Science, Immunology, Pediatrics, Research

What happens when the immune system attacks the brain? Stanford doctors investigate

What happens when the immune system attacks the brain? Stanford doctors investigate

SM PANS image - smallerThe first time he flew into a psychotic rage, Paul Michael Nelson was only 7 years old. He stabbed at a door in his family’s home with a knife, tore at blankets with his teeth, spoke in gibberish. His very worried parents, Paul and Mary Nelson, rushed him to their local emergency room, where the medical staff thought that perhaps the little boy had simply had a bad temper tantrum.

But his rages got worse. Over the weeks and months that followed the first March 2009 emergency room visit, as Paul Michael cycled in and out of psychiatric hospitals, his parents and doctors struggled to understand what was wrong. Finally, they came to a surprising conclusion: Paul Michael had an autoimmune disease. His immune system appeared to be attacking his brain.

As strange as the case seems, the Nelsons are far from alone. As I describe in a recent story for Stanford Medicine magazine, Paul Michael was the first of more than 70 children who have been evaluated at a new clinic at Lucile Packard Children’s Hospital Stanford for pediatric acute-onset neuropsychiatric syndrome, a disease (or, more likely, a group of diseases) that doctors are still working to define. The suddenness and severity of the syndrome are frightening. Healthy children abruptly begin to show psychiatric symptoms that can include severe obsessive-compulsive behavior; anorexia; intense separation anxiety at the thought of being away from a parent; deterioration in their school work, and many other problems. From my story:

“In some ways, it’s like having your kid suddenly become an Alzheimer’s patient, or like having your child revert back to being a toddler,” says Jennifer Frankovich, MD, clinical assistant professor of pediatric rheumatology at the School of Medicine and one of the clinic’s founders.

“We can’t say how many kids with psychiatric symptoms have an underlying immune or inflammatory component to their disorder, but given the burgeoning research indicating that inflammation drives mood disorders and other psychiatric problems, it’s likely to be a large subset of children and even adults diagnosed with psychiatric illnesses,” says Kiki Chang, MD, professor of psychiatry and behavioral sciences.

To shed light on the disease, Frankovich and Chang are working with scientists from around the world on defining the parameters of the illness and launching urgently-needed research. In a special issue of the Journal of Child and Adolescent Psychopharmacology that published online this month, the researchers lay out several aspects of the problem. The Stanford experts are co-authors of a scientific article describing how doctors should evaluate children with the disease, known by its acronym, PANS. Other researchers have written about disordered eating in PANS and given a detailed description of the disease phenotype.

Recognition and treatment of the disease are still an uphill battle, but the growth of research efforts is a hopeful step. As Frankovich says at the conclusion of the Stanford Medicine story, “We cannot give up on this. There are so many of these cases out there.”

Previously: Stanford Medicine magazine traverses the immune system and My descent into madness – a conversation with author Susannah Cahalan
Illustration by Jeffrey Decoster

Imaging, Immunology, Infectious Disease, Neuroscience, Research, Stanford News

Some headway on chronic fatigue syndrome: Brain abnormalities pinpointed

Some headway on chronic fatigue syndrome: Brain abnormalities pinpointed

patchbrainHow can you treat a disease when you don’t know what causes it? Such a mystery disease is chronic fatigue syndrome, which not so long ago was written off by many physicians as a psychiatric phenomenon because they just couldn’t figure out what else might be behind it. No one was even able to identify an anatomical or physiological “signature” of the disorder that could distinguish it from any number of medical lookalikes.

“If you don’t understand the disease, you’re throwing darts blindfolded,” Stanford neuroradiologist Mike Zeineh, MD, PhD, told me about a week ago. Zeineh is working to rip that blindfold from CFS researchers’ eyes.

From a release I wrote about some breaking CFS research by Zeineh and his colleagues:

CFS affects between 1 million and 4 million individuals in the United States and millions more worldwide. Coming up with a more precise number of cases is tough because it’s difficult to actually diagnose the disease. While all CFS patients share a common symptom — crushing, unremitting fatigue that persists for six months or longer — the additional symptoms can vary from one patient to the next, and they often overlap with those of other conditions.

A study just published in Radiology may help to resolve those ambiguities. Comparing brain images of 15 CFS patients with those from 14 age- and sex-matched healthy volunteers with no history of fatigue or other conditions causing similar symptoms, Zeineh and his colleagues found distinct differences between the brains of patients with CFS and those of healthy people.

The 15 patients were chosen from a group of 200 people with CFS whom Stanford infectious-disease expert Jose Montoya, MD, has been following for several years in an effort to identify the syndrome’s underlying mechanisms and speed the search for treatments. (Montoya is a co-author of the new study.)

In particular, the CFS patients’ brains had less overall white matter (cable-like brain infrastructure devoted to carrying signals rather than processing information), aberrant structure in a portion of a white-matter tract called the right arcuate fasciculus, and thickened gray matter (that’s the data-crunching apparatus of the brain) in the two places where the right arcuate fasciculus originates and terminates.

Exactly what all this means is not clear yet, but it’s unlikely to be spurious. Montoya is excited about the discovery. “In addition to potentially providing the CFS-specific diagnostic biomarker we’ve been desperately seeking for decades, these findings hold the promise of identifying the area or areas of the brain where the disease has hijacked the central nervous system,” he told me.

No, not a cure yet. But a well-aimed ray of light that can guide long-befuddled CFS dart-throwers in their quest to score a bullseye.

Previously: Unbroken: A chronic-fatigue patient’s long road to recovery, Deciphering the puzzle of chronic-fatigue syndrome and Unraveling the mystery of chronic-fatigue syndrome
Photo by Kai Schreiber

Autoimmune Disease, Chronic Disease, Immunology, Stanford News, Videos

Unbroken: A chronic fatigue syndrome patient’s long road to recovery

Unbroken: A chronic fatigue syndrome patient’s long road to recovery

“Fatigue is what we experience, but it is what a match is to an atomic bomb,” said Laura Hillenbrand, the author of Unbroken, about how it feels to live with chronic fatigue syndrome.

I recently finished a Stanford Medicine story and video (above) about another CFS patient, “Erin,” who asked that her real name not be used. After an acute illness in rural Mexico, Erin went from being an elite soccer player to one of the 17 million people worldwide who suffer from the condition.

Most people who acquire hit-and-run infections go back to their normal lives after a few days. But these patients don’t. They become virtual shut-ins, prisoners of a never-ending cycle of flu-like symptoms, many of them bedridden for years. CFS, also called myalgic encephalomyelitis or ME/CFS, has no known cause or cure, frustrating both patients and physicians.

What makes Erin’s CFS story somewhat rare is its happy ending. With the help of Stanford infectious disease expert José Montoya, MD, and cardiac electrophysiologist Karen Friday, MD, Erin is back to working fulltime and playing soccer.

“Dr. Montoya and doctors like him are heroes for taking up an unpopular disease and patients that most doctors shun,” said Lori Chapo-Kroger, a registered nurse and CEO of the patient charity, PANDORA Org. “He combines his medical expertise and a creative approach with a truly caring heart for suffering patients.”

Dr. Montoya is also collaborating with immunologist Mark Davis, PhD, on the Stanford Initiative on Infection-Associated Chronic Diseases, a research project using cutting-edge technologies to identify the biomarkers and root causes of ME/CFS. Working at the Human Immune Monitoring Center, team members are searching 600 blood samples for infectious microbes, inflammation-related molecules and genetic flaws. In addition, they’re conducting brain scans and physical exams to look for physical abnormalities among these patients.

Early results are promising — the team has discovered a number of measurable biological markers that indicate that ME/CFS patients may be suffering from out-of-control inflammation.

The team’s goal: To find out what is wrong with the immune systems of patients with infection-triggered diseases such ME/CFS and Lyme disease, then figure out how to help them get better.

Previously: Deciphering the puzzle of chronic fatigue syndrome

The HIMC is partially funded by Spectrum, Stanford’s NIH Clinical and Translational Science Award.

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