Posts tagged science
Articles and news from the latest research reports.
Visualising plastic changes to the brain
Painless therapy
Transcranial magnetic stimulation (TMS) is a painless, non-invasive stimulation method, where an electromagnetic coil held above the head is used to generate a strong magnetic field. This method is deployed to activate or inhibit specific brain regions. Even though the number of its medical applications is constantly on the increase, TMS’ precise neuronal mechanisms of action are not, as yet, very well understood. That is because imaging used for humans, such as fMRI (functional magnetic resonance imaging), do not possess the temporal resolution necessary for recording neural activities in milliseconds. More rapid measurement methods, such as EEG or MEG, on the other hand, are affected by the induced magnetic field, with the results that strong interferences are generated that cover important information regarding immediate TMS-based changes to brain activities.
Observing effect on neurons in real time
High-res images of TMS effects have now for the first time been successfully generated by RUB researchers in animal testing. The work group headed by PD Dr Dirk Jancke, Institut für Neuroinformatik, utilises voltage-sensitive dyes which, anchored in cell membranes, send out fluorescent light signals once neurons get activated or inhibited. By using light, the researchers avoided the problem of measurement of artefacts occurring due to magnetic fields. “We can now demonstrate in real time how one single TMS pulse suppresses brain activity across a considerable region, most likely through mass activation of inhibiting brain cells,” says Dr Jancke. With higher TMS frequencies, each additional TMS pulse generates an incremental increase in brain activity. “This results in a higher cortical activation state, which opens up a time window for plastic changes,” explains Dr Vladislav Kozyrev, the first author of the study.
Chances for patients
The increased neuronal excitability may be utilised to effect specific reorganisation of cell connections by means of targeted learning processes. For example, through visual training after TMS, the ability to identify image contours improves; moreover, a combination of these methods enhances contrast perception in patients with amblyopia - a disorder of sight acquired during child development. For many neurological diseases of the brain, such as epilepsy, depression and stroke, specific models have been developed. “Deployed in animal testing, our technology has delivered high spatiotemporal resolution imaging data of cortical activity changes,” says Dirk Jancke. “We are hoping that these data will enable us to optimise TMS parameters and learning processes in a targeted manner, which are going to be used in future to adapt this technology for medical treatment of humans.”
Stanford scientists reveal complexity in the brain’s wiring diagram
When Joanna Mattis started her doctoral project she expected to map how two regions of the brain connect. Instead, she got a surprise. It turns out the wiring diagram shifts depending on how you flip the switch.
"There’s a lot of excitement about being able to make a map of the brain with the idea that if we could figure out how it is all connected we could understand how it works," Mattis said. "It turns out it’s so much more dynamic than that."
Mattis is a co-first author on a paper describing the work published August 27 in the Journal of Neuroscience. Julia Brill, then a postdoctoral scholar, was the other co-first author.
Mattis had been a graduate student in the lab of Karl Deisseroth, professor of bioengineering and of psychiatry and behavioral sciences, where she helped work on a new technique called optogenetics. That technique allows neuroscientists to selectively turn parts of the brain on and off to see what happens. She wanted to use optogenetics to understand the wiring of a part of the brain involved in spatial memory – it’s what makes a mental map of your surroundings as you explore a new city, for example.
Scientists already knew that when an animal explores habitats, two parts of the brain are involved in the initial exploring phase and then in solidifying a map of the environment – the hippocampus and the septum.
When an animal is exploring an environment, the neurons in the hippocampus fire slow signals to the septum, essentially telling the septum that it’s busy acquiring information. Once the animal is done exploring, those same cells fire off intense signals letting the septum know that it’s now locking that information into memory. The scientists call this phase consolidation. The septum uses that information to then turn around and regulate other signals going into the hippocampus.
"I wanted to study the hippocampus because on the one hand so much was already known – there was already this baseline of knowledge to work off of. But then the question of how the hippocampus and septum communicate hadn’t been accessible before optogenetics," Mattis said.
Neurons in the hippocampus were known to fire in a rhythmic pattern, which is a particular expertise of John Huguenard, a professor of neurology. Mattis obtained an interdisciplinary fellowship through Stanford Bio-X, which allowed her to combine the Deisseroth lab’s expertise in optogenetics with the rhythmic brain network expertise of Julia Brill from the Huguenard lab.
Mattis and Brill used optogenetics to prompt neurons of the hippocampus to mimic either the slow firing characteristic of information acquisition or the rapid firing characteristic of consolidation. When they mimicked the slow firing they saw a quick reaction by cells in the septum. When they mimicked the fast consolidation firing, they saw a much slower response by completely different cells in the septum.
Same set of wires – different outcome. That’s like turning on different lights depending on how hard you flip the switch. “This illustrates how complex the brain is,” Mattis said.
Most scientific papers answer a question: What does this protein do? How does this part of the brain work? By contrast, this paper raised a whole new set of questions, Mattis said. They more or less understand the faster reaction, but what is causing the slower reaction? How widespread is this phenomenon in the brain?
"The other big picture thing that we opened up but didn’t answer is: How can you then tie this back to the circuit overall and learning memory?" Mattis said. "Those would be exciting things to follow up on for future projects."
Yoga Relieves Multiple Sclerosis Symptoms
Paula Meltzer was only 38 when out of nowhere everything she looked at was blurry. For the single mother, who had a lucrative career as a gemologist and spent hours examining valuable pieces of jewelry, it seemed as if – in a split second – her life changed.
At first doctors thought Meltzer had a brain tumor. What they determined after further tests, however, was that she had multiple sclerosis, an autoimmune disease that affects the brain and central nervous system and was causing optic neuritis, an inflammation of the optic nerve that can cause a partial or complete loss of vision.
“I was living independently, doing my job, taking care of my child – and then I had to look to my parents to take care of me,” Meltzer said.
Almost two decades later, Meltzer, out of a wheelchair and walking without a cane, was one of 14 women with moderate disability due to MS who participated in a pilot trial conducted by the Rutgers School of Health Related Professions. A specially-designed yoga program for these MS patients not only improved their physical and mental well-being but also enhanced their overall quality of life.
“I felt like I became steadier and stronger in my core,” Meltzer said. Prior to yoga, she described herself as a “wall walker,” someone who felt safer holding onto the wall in order to get around. “To be able to stand on one leg and feel balanced is amazing.”
Susan Gould Fogerite, director of research for the Institute for Complementary and Alternative Medicine in the School of Health Related Professions, said that although there is widespread evidence that yoga is being used as a form of exercise by those with MS, much of the feedback has been anecdotal and there isn’t much empirical data regarding its safety and efficacy.
This is why she and her colleagues, Evan Cohen and David Kietrys, physical therapists and associate professors in the School of Health Related Professions at Stratford, decided to undertake the small pilot study, believing that a specialized yoga program for MS patients – which incorporates mind, body and spirit – would be beneficial to everyday living.
What they discovered at the end of the eight-week trial was that those who participated were better able to walk for short distances and longer periods of time, had better balance while reaching backwards, fine motor coordination, and were better able to go from sitting to standing. Their quality of life also improved in perceived mental health, concentration, bladder control, walking, and vision, with a decrease in pain and fatigue.
“Yoga is not just exercise, it is a whole system of living,” said Fogerite, an associate professor, who, along with Kietrys, will present the results on September 26 at the Symposium on Yoga Research at the Kripalu Institute in Massachusetts. “The panel of experts who advised us on the trial wanted to make sure that we provided a fully integrated program that included philosophy, breathing practices, postures, relaxation and meditation.”
The yoga pilot trial was held at Still Point Yoga Center in Laurel Springs, a southern New Jersey town close to Philadelphia. Of the 72 individuals who were interested in participating, only 16 were eligible based on medical and other criteria and availability. Of those, 15 were enrolled and 14 completed the program after one person had to withdraw because of an unrelated health problem.
Meltzer and the other women who participated in the trial ranged in age from 34 to 64. Some had been diagnosed with MS within the last two years while others had been living with the illness for up to 26 years. For 90 minutes, twice a week for two months, they practiced techniques and exercises that would improve their posture, help to increase stamina, and teach them how to relax and focus.
“This study, I hope, is one of many that will give us the clinical information we need,” said Fogerite. “Yoga is not currently being widely prescribed for people with MS, although it might turn out to be a very helpful treatment.”
The yoga practices were done by the women in the study sitting, standing, or lying on yoga mats, and using metal folding chairs situated close to the wall to provide them with more support.
“What was so nice about this experience was that although everyone was at a different level of the disease, we felt like we were all together, so I think the camaraderie helped,” said Meltzer. “And it wasn’t just about gaining more mobility and balance in our legs but our arms and necks felt stronger as well.”
Fogerite said a larger randomized controlled trial would be needed to determine whether yoga could be used as a prescribed treatment for individuals with moderate disability due to MS. More than 2.3 million people – two to three times more women than men – throughout the world are diagnosed with this disease which can cause poor coordination, loss of balance, slurred speech, tremors, numbness, extreme fatigue and problems with memory and concentration.
“When I was first diagnosed I no longer felt safe in my own body,” Meltzer said. “I didn’t trust my body at all. What the program did was really bring that trust back.”
(Source: news.rutgers.edu)
Can Sleep Loss Affect Your Brain Size?
Sleep difficulties may be linked to faster rates of decline in brain volume, according to a study published in the September 3, 2014, online issue of Neurology®, the medical journal of the American Academy of Neurology.
Sleep has been proposed to be “the brain’s housekeeper”, serving to repair and restore the brain.
The study included 147 adults 20 and 84 years old. Researchers examined the link between sleep difficulties, such as having trouble falling asleep or staying asleep at night, and brain volume.
All participants underwent two MRI brain scans, an average of 3.5 years apart, before completing a questionnaire about their sleep habits.
A total of 35 percent of the participants met the criteria for poor sleep quality, scoring an average of 8.5 out of 21 points on the sleep assessment. The assessment looked at how long people slept, how long it took them to fall asleep at night, use of sleeping medications, and other factors.
The study found that sleep difficulties were linked with a more rapid decline in brain volume over the course of the study in widespread brain regions, including within frontal, temporal and parietal areas.
The results were more pronounced in people over 60 years old.
“It is not yet known whether poor sleep quality is a cause or consequence of changes in brain structure,” said study author Claire E. Sexton, DPhil, with the University of Oxford in the United Kingdom. “There are effective treatments for sleep problems, so future research needs to test whether improving people’s quality of sleep could slow the rate of brain volume loss. If that is the case, improving people’s sleep habits could be an important way to improve brain health.”
Nature or nurture? It’s all about the message
Were Albert Einstein and Leonardo da Vinci born brilliant or did they acquire their intelligence through effort?
No one knows for sure, but telling people the latter – that hard work trumps genes – causes instant changes in the brain and may make them more willing to strive for success, indicates a new study from Michigan State University.
The findings suggest the human brain is more receptive to the message that intelligence comes from the environment, regardless of whether it’s true. And this simple message, said lead investigator Hans Schroder, may ultimately prompt us to work harder.
“Giving people messages that encourage learning and motivation may promote more efficient performance,” said Schroder, a doctoral student in clinical psychology whose work is funded by the National Science Foundation. “In contrast, telling people that intelligence is genetically fixed may inadvertently hamper learning.”
In past research by Stanford University psychologist Carol Dweck, elementary students performing a task were either praised for their intelligence (“You’re so smart!”) or for their effort (“You worked really hard!”) after correct responses. As the task became harder, children in the first group performed worse after their mistakes compared to the group that had heard effort was important.
The MSU study, which appears online in the journal Biological Psychology, offers what could be the first physiological evidence to support those findings, in the form of a positive brain response. “These subtle messages seem to have a big impact, and now we can see they have an immediate impact on how the brain handles information about performance,” Schroder said.
For the study, two groups of participants read different articles. One article reported that intelligence is largely genetic, while the other said the brilliance of da Vinci and Einstein was “probably due to a challenging environment. Their genius had little to do with genetic structure.”
Participants were instructed to remember the main points of the article and completed a simple computer task while their brain activity was recorded. The findings, in a nutshell:
- The group that read intelligence was primarily genetic paid more attention to their responses, as if they were more concerned with their performance. This extra attention, however, did not relate to performance on trials after errors, suggesting a disconnect between brain and behavior.
- In contrast, those who had read that intelligence was due to a challenging environment showed a more efficient brain response after they made a mistake, possibly because they believed they could do better on the next trial. The more attention these participants paid to mistakes, the faster their responses were on the next trial.
The study does not weigh in on the age-old “nature vs. nurture” debate, Schroder noted. Rather, it investigates the messages about the nature of abilities people are exposed to on a regular basis, from a teacher comforting a student (“It’s OK, not everyone can be a math person.”) to the sports announcer commenting on a player’s skill (“Wow, what a natural!”). These messages are thought to contribute to the attitudes or “mindsets” people hold about their intelligence and abilities.
The research started as part of Schroder’s honors thesis as an undergraduate at MSU working in the Clinical Psychophysiology Lab directed by Jason Moser, MSU assistant professor. Moser co-authored the study along with Tim Moran, an MSU graduate student in cognitive psychology, and Brent Donnellan, a former MSU professor who now works at Texas A&M University.
As an undergraduate and graduate student, Schroder has already co-written nine papers that have appeared in academic journals, including five as lead author. His work is supported by a three-year grant from the NSF’s Graduate Research Fellowship Program.
Longitudinal study explores white matter damage, cognition after traumatic axonal injury
Traumatic Axonal Injury is a form of traumatic brain injury that can have detrimental effects on the integrity of the brain’s white matter and lead to cognitive impairments. A new study from the Center for BrainHealth at The University of Texas at Dallas investigated white matter damage in the acute and chronic stages of a traumatic axonal injury in an effort to better understand what long-term damage may result.
The study, published online July 21 in the Journal of Neurotrauma, looked at 13 patients ages 16 to 60 with mild to severe brain injuries from the intensive care unit at a Level I trauma center. This group was matched to a cohort of 10 healthy individuals resembling the age, gender, and ethnicity of the patients. White matter integrity was measured using diffusion tensor imaging (DTI) in the acute stage of injury, at day one, and again at the chronic stage, seven months post-injury. In addition, neuropsychological assessments measured cognitive performance including processing speed, attention, learning and memory at both stages after injury.
“We intended to determine whether DTI could not only identify early compromise to white matter, but also demonstrate an association with functional and neuropsychological outcomes months post-injury,” said Carlos Marquez de la Plata, Ph.D., Assistant Director of Rehabilitation Research at Pate Rehabilitation in Dallas, Texas.
The study’s findings suggest DTI may be used to detect meaningful changes in white matter as early as one day after a traumatic brain injury. White matter integrity measured at the chronic stage was also found to significantly correlate with cognitive processing speed.
“On the first day after the injury, we found white matter integrity was compromised due to swelling in the brain,“ said the study’s lead author Alison Perez. “As the swelling subsided over time and the brain began to repair itself, we found that many of the damaged neurons that were unable to repair themselves began to die off, which appears to slow the speed of cognitive processing.”
Interestingly, the degree of white matter compromise detected early after injury was associated with markers of injury severity such as the number of days in the intensive care unit and hospital, but not to outcomes months later.
At seven months post-injury, many of the patients’ cognitive performance improved including processing speed, divided attention, and short and long-term memory. In addition, patients with better white matter integrity at the chronic stage had the fastest processing speed.
By studying the long-term effects of a traumatic axonal injury at both the acute and chronic stages, researchers hope to assist in the advancement of future assessment and treatment options after a traumatic brain injury.
Researchers unlock new mechanism in pain management
It’s in the brain where we perceive the unpleasant sensations of pain, and researchers have long been examining how calcium channels in the brain and peripheral nervous system contribute to the development of chronic pain conditions.
Neuroscientist Gerald Zamponi, PhD, and his team at the University of Calgary’s Hotchkiss Brain Institute have discovered a new mechanism that can reverse chronic pain. Using an animal model, their research has found that pain signals in nerve cells can be shut off by interfering with the communication of a specific enzyme with calcium channels, a group of important proteins that control nerve impulses.
Their Canadian Institutes of Health Research-funded study was published in the September issue of Neuron — one of the most influential journals in the field of neuroscience.
Zamponi is now applying his research and partnering with the Centre for Drug Research and Development (CDRD) in Vancouver to develop a drug that could one day improve the lives of those with inflammatory pain such as arthritis, irritable bowel disease or neuropathic pain. Their approach may be able to reduce the pain associated with these conditions.
Opening the door to new treatments
“Chronic pain can be a debilitating condition that affects many people and is often poorly controlled by currently available treatments. Therefore, new treatment avenues are needed. Our discovery opens the door towards new treatments, and based on the data that we have so far, it is a viable strategy,” says Zamponi, the lead author of the study and senior associate dean of research at the Cumming School of Medicine.
With CDRD, Zamponi and his team are screening more than 100,000 molecules in hopes of finding one that would stop the enzyme from communicating with the calcium channel. If they can isolate the right molecule, they can potentially turn it into a drug. So far, they have already found two viable molecules that have been validated by his group as painkillers in animals.
Promising innovation from basic research
Commercialization of the project Zamponi and his team are working on is one of six funded through the competition of the Alberta/Pfizer Translational Research Fund Opportunity. “AIHS is delighted that the strong partnership created with Pfizer, Western Economic Diversification, and Alberta Innovation and Advanced Education is helping to develop promising innovations from basic research into technologies, drugs, and tools to improve health,” says Dr. Cy Frank, president and CEO of Alberta Innovates – Health Solutions.
The Alberta/Pfizer Translational Research Fund Opportunity is a partnership between Pfizer Canada Inc., Alberta Innovates – Health Solutions, Alberta’s Ministry of Innovation and Advanced Education, and Western Economic Diversification Canada. This partnership will provide opportunities to focus on the development and commercialization of innovations in health. More than $3.25 million has been committed to identify and support promising health-care innovations with market potential.
(Image caption: A thalamocortical, or TC neuron labeled with fluorescent dye, as used in Dr. Augustinaite’s study. The image shows a voltage recording device, at bottom left, entering the yellow cell body, and a stimulation device, at top, reaching the dendrites. Color in this image shows the depth in the slice.)
The brain is a complicated network of small units called neurons, all working to carry information from the outside world, create an internal model, and generate a response. Neurons sense a signal through branching dendrites, carry this signal to the cell body, and send it onwards through a long axon to signal the next neuron. However, neurons can function in many different ways; some of which researchers are still exploring. Some signals that the dendrites receive do not continue to the next neuron; instead they seem to change the way that the neuron handles the subsequent signals. This could help neurons function as part of a large network, but researchers still have many questions. Dr. Sigita Augustinaite, a researcher in the Optical Neuroimaging Unit at the Okinawa Institute of Science and Technology Graduate University, suggested one mechanism explaining how neurons help the network function. Her findings, part of collaboration between the University of Oslo and OIST, were published August 13, 2014 as the cover article in The Journal of Neuroscience.
Dr. Augustinaite studies the visual pathway, where signals from the retina are sent to the visual cortex, where the brain interprets signals from the eye. Between the eye and the visual cortex, the signals must pass through the visual thalamus, that is, through thalamocortical, or TC neurons. These neurons can switch between a “sleeping” state and a “waking” state depending on input they receive from neurons and other brain areas. When an animal is awake, TC neurons transmit the incoming retinal signals on to the cortex, but when the animal is asleep, the neurons block retinal signals.
The visual cortex also sends a massive input back to TC neurons to control retinal signals traveling through the thalamus. But Dr. Augustinaite says that the suggested mechanisms of this control bring more questions than answers. To understand more, she conducted experiments in acute brain slices, small pieces of brain tissue where neurons stay alive and maintain their physiological properties. She added glutamate to dendrites far from the cell body to emulate a feedback signal from the visual cortex. Then she measured the neuron’s response, shown as a voltage difference between inside and outside of the membrane.
Dr. Augustinaite found that stimulating the neurons in this way depolarizes their membranes, creating something called NMDA spike/plateau potentials. If strong enough, depolarization can cause a neuron to fire an action potential, which travels through the axon to activate other neurons. Action potentials look like a sharp, one-millisecond increase in membrane voltage, and they transmit signals from retina to cortex. But if NMDA spike/plateaus induces action potentials, signals from the cortex and signals from the retina would be indistinguishable. With her experiments, Dr. Augustinaite showed that the NMDA spike/plateau potentials in TC neurons do not trigger action potentials. Instead, they lift the voltage of the membrane, changing the neuron’s properties for few hundred milliseconds, creating conditions for reliable signal transmission from retina to cortex.
“The research gives, for the first time, a clear view on what dendritic potentials are good for,” explained Prof. Bernd Kuhn, who leads the lab where Dr. Augustinaite works. “It points directly to the mechanism,” he concluded. Showing how dendritic plateaus function is just one important step toward understanding how neurons function as a network. “This mechanism could also be used in many other neuronal circuits, where one input regulates how another input moves through the network,” Dr. Augustinaite said. “This mechanism is an exciting logical element in the neuronal network, but just the start of putting the puzzle together.”
Seizures and sudden death: When SUMO ‘wrestles’ potassium channels
A gene crucial for brain and heart development may also be associated with sudden unexplained death in epilepsy (SUDEP), the most common cause of early mortality in epilepsy patients.
Scientists at The University of Texas MD Anderson Cancer Center have created a new animal model for SUDEP and have shown that mice who have a partial deficiency of the gene SENP2 (Sentrin/SUMO-specific protease 2) are more likely to develop spontaneous seizures and sudden death. The finding occurred when observing mice originally bred for studying a link between SENP2 deficiency and cancer.
"SENP2 is highly present in the hippocampus, a critical brain region for seizure genesis," said Edward Yeh, M.D., chair of cardiology at MD Anderson. "Understanding the genetic basis for SUDEP is crucial given that the rate of sudden death in epilepsy patients is 20-fold that of the general population, with SUDEP the most common epilepsy-related cause of death."
Yeh’s findings were published in this month’s issue of Neuron.
Although it’s not yet known what causes SUDEP in humans, inactivation of potassium channels genes have been linked to SUDEP in animal models. Potassium channels are found in most cell types and control a large variety of cell functions.
"These animal models demonstrated an important connection between the brain and heart. However, it remains unclear whether seizure and sudden death are two separate manifestations of potassium channel deficiency in the brain and the heart, or whether seizures predispose the heart to lethal cardiac arrhythmia," said Yeh.
The study revealed that when SENP2 was deficient in the brain, seizures activated a part of the nervous system responsible for regulating the heart’s electrical system. This resulted in a phenomenon known as atrioventricular conduction block, which effectively slowed down and then stopped the heart.
Yeh’s team observed that the SENP2-deficient mice appeared normal at birth, but by 6 to 8 weeks, experienced convulsive seizures, and then sudden death. He believes the reason may lie with protein modifiers called SUMO. SENP2 deficiency results in a process known as hyper-SUMOylation, which dramatically impacts potassium channels in the brain.
"One of the channels, Kv7, is significantly diminished or ‘closed’ due to the lack of SENP2," said Yeh. "In mice this led to seizures and cardiac arrest."
In humans, the good news is that an FDA-approved drug, retigabine works by “opening” the Kv7 channel. The therapy was developed for treating partial-onset seizures. The findings in Yeh’s new mouse model clearly demonstrate a previously unknown cause of SUDEP, which may open up new opportunities for study and treatment in the future.
(Source: eurekalert.org)
Why HIV patients develop dementia
Immune cells in the brain under suspicion
“HIV-associated neurocognitive disorders” (HAND) include disorders of the cognitive functions, motor capacities as well as behavioural changes. How exactly HAND occur has not, as yet, been fully understood. “Scientists assume that HIV is harmful to cells directly and that it also triggers indirect mechanisms that lead to nerve cell damage,” explains Dr Simon Faissner (RUB clinic for neurology, St. Josef-Hospital). The researchers strongly suspect that, once activated in the brain and the spinal cord, immune cells keep up a chronic inflammation level which then results in the destruction of nerve cells. An immune activation in peripheral tissue as well as therapeutic consequences may likewise contribute to nerve cell damage in the brain.
First steps of HIV infection are sufficient
The HI virus overcomes the blood-brain barrier hitchhiking on infected immune cells, the monocytes and probably the T cells. The researchers from Bochum tested the hypothesis that HIV-infected monocytes activate specific immune cells in the brain, the so-called microglial cells. These cells, in turn, respond by releasing harmful substances, such as reactive oxygen metabolites and inflammatory signalling molecules, i.e. cytokines. To test this hypothesis, the researchers developed a cell culture system in which they initially examined the effect of HIV-infected monocytes on microglial cells. The researchers simulated the individual steps of HIV infection and measured the concentration of the cytokines released at each stage. Thus, they were able to demonstrate that releasing the viral RNA in the monocytes was a sufficient trigger for maximal microglial activation. Subsequent infection phases – reverse transcription into DNA and the resulting formation of HIV proteins – did not augment activation any further.
Released substances result in neuronal cell death
In the second step, they analysed nerve cells from rat brains to determine if the substances released by the microglial cells could lead to cell death. Compared with the control group, the amount of cell death was indeed twice as high. Studies of liquor cerebrospinalis received from HIV-infected patients have shown a positive correlation with marker of neuronal degeneration in patients who did not as yet present any neurocognitive disorders.
Detailed understanding necessary for therapeutic strategies
“Thanks to our research, we have gained a better understanding of the mechanisms of HIV-associated neurodegeneration,” concludes Prof Dr Andrew Chan. “These results are likely to contribute to HAND biomarkers becoming established. In the long term, these data may be used to develop therapeutic strategies aiming at retarding HAND progression in HIV-infected patients.” Starting points may include activation of microglial cells – a method that is applied in other autoimmune diseases of the central nervous system, for example in multiple sclerosis.
Start-up through FoRUM funds
The research, which was initiated following a collaboration between clinics for neurology and dermatology, St. Josef Hospital, as well as the Department for Molecular and Medical Virology, has been made possible through start-up funding provided by the Faculty of Medicine at Ruhr-Universität (FoRUM). The collaboration has evolved into an international consortium of clinics and basic research organisations in Bochum, Langen, Strasbourg and Mailand. One objective of the follow-up study, for which an application for EU funds is pending, is going to be an in-depth analysis of inflammatory processes in the central nervous system. The researchers will attempt to inhibit inflammatory processes with different drugs. They are, moreover, planning to study direct cell-cell interaction by means of state-of-the-art microscopy, in collaboration with the University of Strasbourg.
(Image credit: Mehau Kulyk/Science Photo Library)