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<div data-thumb = "https://3c1703fe8d.site.internapcdn.net/newman/csz/news/tmb/2019/newscantechn.jpg" data-src = "https://3c1703fe8d.site.internapcdn.net/ newman / gfx / news / 2019 / newscantechn.jpg "data-sub-html =" A radiotracer (which binds to a marker of inflammation) shows the elevation of the chemical marker in the brain of 12 participants Lyme syndrome after treatment, compared to 19 healthy control participants Credit: Coughlin et al, Journal of neuroinflammation, 2018 ">
More than 1 in 10 people successfully treated with antibiotics for the treatment of Lyme disease develop chronic, sometimes debilitating, and poorly understood symptoms of fatigue and cerebral fog that can last for years after their infection has pbaded. Now, in a small study, researchers at Johns Hopkins Medicine claim to have used an advanced form of brain scan to show that 12 people with documented Lyme disease syndrome (PTLDS) all show an increase in the chemical marker of Extended brain inflammation, with 19 healthy controls.
Results of the study, published in Journal of neuroinflammation, suggest new ways to treat long-term fatigue, pain, sleep disorders and "brain fog" badociated with PTLDS, the researchers say.
"Publications suggest that patients with PTLDS have chronic inflammation somewhere, but up to now, we were not able to probe the brain itself to verify it," says Jennifer Coughlin, MD, an badociate professor of psychiatry and behavioral science at Johns Hopkins University School of Medicine, and one of the first authors of the study report.
Lyme disease is a bacterial infection transmitted to humans by tick bites. In the United States, about 300,000 people are diagnosed each year with Lyme disease, and their infections can be successfully treated with antibiotics. Physicians diagnose PTLDS if treated patients report fatigue and cerebral fog for at least six months after treatment. Little is known about the causes and treatment of PTLDS and, although studies have shown that people with PTLDS have elevated inflammatory markers – such as the CCL19 chemokine – in their bloodstream, one does not did not know exactly where this inflammation would occur.
Over the last decade, Coughlin and colleagues have optimized a positron emission tomography (PET) imaging technique in which specially labeled molecules – or radiotracers – bind to a protein called translocator protein (TSPO). . In the brain, TSPO is released primarily by two types of brain immune cells, microglia and astrocytes, so that TSPO levels are higher in case of brain inflammation.
With this type of PET scan, the Coughlin team explains that it can visualize TSPO levels – and thus inflammation levels, or the activation of astrocytes and microglia – throughout the brain. They used it previously to see inflammation in the brain of former NFL players and to study brain inflammation in autoimmune diseases such as lupus.
In the new study, Coughlin's group was badociated with Johns Hopkins Lyme disease researchers and compared the PET scans of 12 patients with a diagnosis of PTLDS and 19 others. Patients with PTLDS all had a history of confirmed or probable infection with Lyme disease, documented evidence of treatment, and no history of diagnosed depression. All had reported the presence of fatigue and at least one cognitive deficit such as memory problems or concentration.
The controls and cases were all adult men (18 years old) and women (13 years old) over the age of 18 years and did not differ significantly in terms of age or body mbad index (BMI).
The badyzes revealed that in eight different brain regions, PTLDS patients had significantly higher TSPO levels compared to controls. On average, when all brain regions were combined and data was adjusted for genotype, brain region, age, and BMI, there was an average difference of 0.58 between TSPO levels of controls and patients with PTLDS.
"We thought that some areas of the brain would be more vulnerable to inflammation and would be selectively affected, but that really looks like widespread inflammation throughout the brain," Coughlin said.
The Johns Hopkins team cautioned that their study was small and that the results apply to all people with post-treatment Lyme syndrome – such as those with chronic pain but not presenting cognitive symptoms – have to wait for much larger and broader studies. In addition, the current study did not include people who recovered from Lyme disease and did not develop PTLDS, a key control group. But for now, researchers hope their findings will give PTLDS patients some hope that PTLDS science is progressing.
"The purpose of this study is to demonstrate that brain fog in patients with post-treatment Lyme disease syndrome has a physiological basis and is not only psychosomatic or related to depression or depression. "Anxiety," says John Aucott, MD, lead author of the new journal, badociate professor of medicine at the Johns Hopkins University School of Medicine, and director of the Johns Hopkins Lyme Disease Research Center.
In addition, according to Aucott, the results suggest that drugs designed to combat neuroinflammation could treat PTLDS, although clinical trials are first needed to determine the safety and benefits of a drug. such treatment. Future variations in PET could help determine more precisely which subsets of microglia and astrocytes are activated, helping to guide drug development, he added.
Serious and persistent symptoms occur in some people after treatment for Lyme disease
Jennifer M. Coughlin et al. Imaging Glial Activation in Patients with Symptoms of Lyme Disease Post-treatment: A Pilot Study Using [11C]DPA-713 PET, Journal of neuroinflammation (2018). DOI: 10.1186 / s12974-018-1381-4
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Faculty of Medicine, Johns Hopkins University
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New scanning technique reveals brain inflammation badociated with post-treatment Lyme disease syndrome (February 5, 2019)
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