Tag Archives: brain

Diabetics die 3 times more of Covid-19

From the outset of the pandemic, data coming out of early coronavirus hot spots like China, Italy, and New York City foretold that certain groups of people would be more vulnerable to Covid-19. The disease hit older people and people with underlying medical conditions the hardest. As early as February, diabetes had emerged as one of the conditions associated with the highest risk. In one large study out of China, people with diabetes were more than three times as likely to die of Covid-19 than the overall population.

But that’s not what brought four diabetes experts from Australia and the United Kingdom onto a Zoom call back in April. They were supposed to just be catching up—a virtual tea among friends. But talk soon turned to something strange that they’d been seeing in their own hospitals and hearing about through the grapevine. The weird thing was that people were showing up in Covid-19 wards, after having tested positive for the virus, with lots of sugar in their blood. These were people with no known history of diabetes. But you wouldn’t know it from their lab results.

After that call, the experts reached out to colleagues in other countries to see if they’d seen or heard of similar cases. They had. Acute viral infections of all sorts can stress the body, causing blood sugar levels to rise. So that in itself wasn’t unusual, says Francesco Rubino, a bariatric surgeon and diabetes researcher at King’s College in London, who was on that first Zoom call. “What we were seeing and hearing was a little bit different.”

Doctors around the world had described to him strange situations in which Covid-19 patients were showing symptoms of diabetes that didn’t fit the typical two-flavor manifestation of the disease. In most people with type 1 diabetes, their immune cells suddenly turn traitorous, destroying the cells in the pancreas that produce insulin—the hormone that allows glucose to exit the bloodstream and enter cells. People with type 2 diabetes have a different problem; their body slowly becomes resistant to the insulin it does produce. Rubino and his colleagues were seeing blended features of both types showing up spontaneously in people who’d recently been diagnosed with Covid-19.

That was the first clinical puzzle,” he says. For clues to an explanation, Rubino and his colleagues looked to ACE2, the protein receptor that SARS-CoV-2 uses to invade human cells. It appears in the airways, yes, but also in other organs involved in controlling blood sugar, including the gut. Doctors in China discovered copies of the coronavirus in the poop of their Covid-19 patients. And a meta-analysis found that gastrointestinal symptoms plague one out of 10 Covid-19 sufferers.

In the last few decades, scientists have discovered that the gut is not the passive digestive organ once thought. It actually is a major endocrine player—responsible for producing hormone signals that talk to the pancreas, telling it to make more insulin, and to the brain, ordering it to make its owner stop eating. If the coronavirus is messing with these signals, that could provide a biological basis for why Covid-19 would be associated with different forms of diabetes, including hybrid and previously unknown manifestations of the disease. Rubino is one of a growing number of researchers who think that the relationship between the coronavirus and diabetes is actually a two-way street. Having diabetes doesn’t just tip the odds toward contracting a worse case of Covid-19. In some people, the virus might actually trigger the onset of diabetes, and the potential for a lifetime of having to manage it.

Source: https://www.wired.com/

CRISPR Gene Editing Grows New Neurons In Diseased Brains

Transferring lab grown neurons into animal brains reduces the cells’ viability — their chances of integrating well into the tissue — and the efficiency with which they can restore function. So scientists at Shanghai Research Center for Brain Science and BrainInspired Intelligence fashioned a method to regenerate neurons inside the brain. The method is similar to how one would revive a dying plant: by nurturing it with the right conditions for it to grow new leaves.

Building up on a previous study, Haibo Zhou, a postdoctoral researcher in Hui Yang’s lab, and colleagues, set up a method to convert non neuronal brain cells called “glia” into neurons. They did this by turning down a gene called PTBP1 in glia of different parts of the mouse brain, using the gene-editing tool CRISPR. Depending on which brain region was targeted, the glia gave rise to different kinds of neurons.

Reducing PTBP1 levels presumably reverted glia to unspecified stem cells, which adopted varied neuronal identities based on which glia were targeted and the environmental signals they received. This was evident from the team’s successful attempts at restoring two different types of neurons and alleviating the symptoms associated with the loss of each.

Parkinson’s disease occurs due to loss of dopamine-producing neurons and manifests as tremors, stiffness, and loss of balance. To test their method in rejuvenating this group of neurons, the team first got rid of them using a toxic compound in mice. The authors then converted glia into dopamine-producing neurons, and the new cells showed the same activity as their original counterparts.

This rescue was not limited to just the neuron population. It also partially restored the normal motor behavior of the animal. This is a huge step forward from drug induced alleviation of symptoms because it puts forth a more permanent solution.

The team also tackled retinal diseases caused by death of retinal ganglion cells, or RGCs, which leads to permanent blindness. Turning down PTBP1 in glia of the retina transformed them into RGCs. Astoundingly, these renewed neurons not only responded to light independently, but also sent their projections to the visual cortex correctly, restoring circuit function. This led to a partial recovery of eyesight in the treated mice.

Source: https://www.salon.com/

New Electronic Skin Reacts To Pain Like Human Skin

Researchers have developed electronic artificial skin that reacts to pain just like real skin, opening the way to better prosthetics, smarter robotics and non-invasive alternatives to skin grafts. The prototype device developed by a team at RMIT University (Australia) can electronically replicate the way human skin senses pain. The device mimics the body’s near-instant feedback response and can react to painful sensations with the same lighting speed that nerve signals travel to the brain.

Lead researcher Professor Madhu Bhaskaran said the pain-sensing prototype was a significant advance towards next-generation biomedical technologies and intelligent robotics.

Skin is our body’s largest sensory organ, with complex features designed to send rapid-fire warning signals when anything hurts,” Bhaskaran said. “We’re sensing things all the time through the skin but our pain response only kicks in at a certain point, like when we touch something too hot or too sharp. No electronic technologies have been able to realistically mimic that very human feeling of pain – until now. “Our artificial skin reacts instantly when pressure, heat or cold reach a painful threshold. “It’s a critical step forward in the future development of the sophisticated feedback systems that we need to deliver truly smart prosthetics and intelligent robotics.”

As well as the pain-sensing prototype, the research team has also developed devices made with stretchable electronics that can sense and respond to changes in temperature and pressure. Bhaskaran, co-leader of the Functional Materials and Microsystems group at RMIT, said the three functional prototypes were designed to deliver key features of the skin’s sensing capability in electronic form.

With further development, the stretchable artificial skin could also be a future option for non-invasive skin grafts, where the traditional approach is not viable or not working. “We need further development to integrate this technology into biomedical applications but the fundamentals – biocompatibility, skin-like stretchability – are already there,” Bhaskaran added.

Source: https://www.rmit.edu.au/

Antibodies + Immunotherapy Result In Complete Elimination Of Tumors

Immunotherapy has revolutionized cancer treatment by stimulating the patient’s own immune system to attack cancer cells, yielding remarkably quick and complete remission in some cases. But such drugs work for less than a quarter of patients because tumors are notoriously adept at evading immune assault.

A new study in mice by researchers at Washington University School of Medicine in St. Louis has shown that the effects of a standard immunotherapy drug can be enhanced by blocking the protein TREM2, resulting in complete elimination of tumors. The findings, which are published in the journal Cell, point to a potential new way to unlock the power of immunotherapy for more cancer patients.

Immune cells infiltrate a human tumor in the four colorized images above. In a mouse study, researchers at Washington University School of Medicine in St. Louis have found that an antibody that targets the protein TREM2 empowers tumor-destroying immune cells and improves the effectiveness of cancer immunotherapy.

Essentially, we have found a new tool to enhance tumor immunotherapy,” said senior author Marco Colonna, MD, the Robert Rock Belliveau, MD, Professor of Pathology. “An antibody against TREM2 alone reduces the growth of certain tumors, and when we combine it with an immunotherapy drug, we see total rejection of the tumor. The nice thing is that some anti-TREM2 antibodies are already in clinical trials for another disease. We have to do more work in animal models to verify these results, but if those work, we’d be able to move into clinical trials fairly easily because there are already a number of antibodies available.”

T cells, a kind of immune cell, have the ability to detect and destroy tumor cells. To survive, tumors create a suppressive immune environment in and around themselves that keeps T cells subdued. A type of immunotherapy known as checkpoint inhibition wakes T cells from their quiescence so they can begin attacking the tumor. But if the tumor environment is still immunosuppressive, checkpoint inhibition alone may not be enough to eliminate the tumor.

An expert on the immune system, Colonna has long studied a protein called TREM2 in the context of Alzheimer’s disease, where it is associated with underperforming immune cells in the brain. Colonna and first author Martina Molgora, PhD, a postdoctoral researcher, realized that the same kind of immune cells, known as macrophages, also were found in tumors, where they produce TREM2 and promote an environment that suppresses the activity of T cells.

When we looked at where TREM2 is found in the body, we found that it is expressed at high levels inside the tumor and not outside of the tumor,” Colonna said. “So it’s actually an ideal target, because if you engage TREM2, you’ll have little effect on peripheral tissue.”

Colonna and Molgora — along with colleagues Robert D. Schreiber, PhD, the Andrew M. and Jane M. Bursky Distinguished Professor; and William Vermi, MD, an immunologist at the University of Brescia — set out to determine whether inhibiting TREM2 could reduce immunosuppression and boost the tumor-killing powers of T cells. As part of this study, the researchers injected cancerous cells into mice to induce the development of a sarcoma.

The mice were divided into four groups. In one group, the mice received an antibody that blocked TREM2; in another group, a checkpoint inhibitor; in the third group, both; and the fourth group, placebo. In the mice that received only placebo, the sarcomas grew steadily. In the mice that received the TREM2 antibody or the checkpoint inhibitor alone, the tumors grew more slowly and plateaued or, in a few cases, disappeared. But all of the mice that received both antibodies rejected the tumors completely. The researchers repeated the experiment using a colorectal cancer cell line with similarly impressive results.

Source: https://medicine.wustl.edu/

A Simple Blood Test To Find Early Signs Of Alzheimer’s

A new study found that a simple blood test can detect beta-amyloid protein buildup in a person’s brain years before Alzheimer’s disease symptoms appearHigh amounts of beta-amyloid can clump together and form plaques on the brain, which is strongly associated with Alzheimer’s disease. Other research has found that amyloid plaques can appear as early as 20 years before the first sign of Alzheimer’s symptoms, such as cognitive decline and memory loss.

In the study, 158 adults in their 60s and 70s — most of whom had normal cognitive function — underwent a PET scan to spot amyloid plaque in the brain, and a blood test to measure beta-amyloid in the body. The blood test looked for two forms of beta-amyloid protein: beta-amyloid 42 and beta-amyloid 40. When beta-amyloid begins to build up, the ratio between the two proteins changes, and the blood test detects this.

The researchers labeled each blood test result as either amyloid positive or negative. They then compared them with the PET scans. They found that the PET scans confirmed the blood test results  88% of the time. When other risk factors were included, such as age and the appearance of the gene variant ApoE4 (which also is linked to a higher risk for Alzheimer’s), the test’s accuracy rose to 94%.

While there is some debate as to whether amyloid plaque actually causes Alzheimer’s, a simple blood test that indicates you may be at a higher risk of the disease would be one more reason to adopt lifestyle changes. The researchers added that they expect the blood test to be available within a few years.

The results were published online Aug. 1, 2019, by the journal Neurology.

Source: https://www.health.harvard.edu/

Exercise Is The Most Powerful Technique To Keep Our Brain Sharp

Unfortunately, we can’t go hard forever. But in the future, that might not be a problem: New research has revealed how to harness the cognitive benefits of a workout — without the actual workout. Scientists think this help slow aging in the brain. A study published Thursday in Science suggests the benefits of exercise run in the blood and may be able to be transferred from one swoll organism to another, less-swoll one.

Researchers report that unexercised, aged mice who received blood plasma donations from exercised mice improved their performance on spatial memory tests and showed fewer markers of inflammation related to aging. The authors suggest that these improvements occurred because exercise releases a series of circulating factors (like proteins) into the bloodstream. Saul Villeda, the study’s senior author and an assistant professor of anatomy at The University of California San Francisco, said that one specific protein abundant in the liver appears to be especially important. It’s called Glpd and it sends a crucial message to the body.

I think it’s sort of signaling to your body: repair yourself or restore yourself,” Villeda explains.

The study builds upon the larger idea that aging in the brain isn’t inevitable, and that the basic lifestyle tools we have to stave it off can be further honed to keep brains sharp into old age. It’s possibly a step towards an exercise pill that’s intended to keep the brain swole, not the body — though Villeda cautions that this is far in the future.

Numerous studies have suggested that exercise can help slow cognitive decline. The mechanisms for that differ, but a working idea is that exercise triggers a series of changes in the body, including the release of certain blood factors that may confer benefits, the study notes. Villeda calls the blood a “conduit” for all the organs in the body to communicate with one another, which suggests that might help transfer exercise-related benefits from one creature to another. In the study, a group of aged mice (18 months old) was given access to a running wheel all the time. Another group of sedentary mice was provided with nesting materials (to promote more chilling and less running). Then, blood plasma (which is the white-ish part of blood that contains all the circulating cells and proteins) was taken from each group and injected into two additional groups over three weeks.

The mice with their fresh runner-blood injections then performed a water-based maze test — they had to find a platform to get to safety — and a fear conditioning test. These tests are designed to test spatial learning memory. If you’ve ever had a moment when you realize that you can’t find your car in the parking lot anymore, you’ve experienced a lapse in that type of memory, Villeda explains.

All of a sudden, you might see this older individual using their car alarm to try and find their car because they can’t quite remember where their car was,” he says. “Those are the types of impairments that already are occurring with just normal age before you get dementia or disease.

The mice who received blood plasma transfusions from the exercised mice were faster to learn the location of the dry platforms in the maze compared to those that got plasma from sedentary mice. In the fear-based test, the mice were quicker to freeze in response to a context clue – suggesting that they were faster to learn what might cause them harm. In mouse-years, you might think of these aged mice as 70-year-olds, Villeda says. The improvements seen in the mice who received plasma donation were the equivalent of turning back the clock decades, he explains:

We’re reversing it probably back to the late 30s, early 40s. But that’s a significant improvement for these animals.”

This study suggests that these transfusions may help to preserve memory functions that once existed in younger animals, Villeda says — his team found that they were able to reverse some of the animal’s cognitive impairments. What these transfusions can not do is boost memory — the goal is to prevent decline, not add benefits.

Source: https://science.sciencemag.org/
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https://www.inverse.com/

Biomarker detects Alzheimer’s decades before symptoms appear

Two new studies, published in the journal The Lancet Neurology, are suggesting increasing levels of a particular brain protein, detected in blood and spinal fluid, could be the earliest sign of neurodegenerative diseases such as Alzheimer’s and Huntington’sNeurofilament light chain (NfL) is a protein that is released as a result of brain cell damage. It is one of the most promising early-stage biomarkers for a variety of neurodegenerative diseases, including Parkinson’s disease, ALS and multiple sclerosis.

It is commonly suspected that the neurodegeneration associated with many of these devastating diseases begins years, or even decades, before clinical symptoms finally appear. And on the back of many failed drug trials, researchers are beginning to believe that once symptoms eventually appear much of the neurological damage could be irreversible. So finding ways to catch these diseases at the earliest possible point will be vital in delivering effective treatments.

Huntington’s disease is a heritable neurodegenerative disease with no cure. Clinical symptoms can begin appearing at any age, however, generally the condition doesn’t become apparent until middle-age, and once symptoms do appear a gradual decline to death takes place over about 20 years. Researchers have homed in on a number of clues, both behavioral and physiological, to detect the earliest stages of the disease but a new study from an international team of researchers is suggesting NfL levels in cerebrospinal fluid (CSF) could detect Huntington’s neurodegeneration up to 24 years before the clinical onset of the disease.

Other studies have found that subtle cognitive, motor and neuropsychiatric impairments can appear 10-15 years before disease onset,” explains co-first author on the study, Rachael Scahill. “We suspect that initiating treatment even earlier, just before any changes begin in the brain, could be ideal, but there may be a complex trade-off between the benefits of slowing the disease at that point and any negative effects of long-term treatment.

The new study presents the most detailed investigation ever conducted into early-stage Huntington’s disease biomarkers in a young cohort of patients. The study recruited 64 subjects, all carrying the Huntington’s gene mutation, and all estimated to be an average of 24 years ahead of the disease onset. The cohort was subjected to a large assortment of tests, with the researchers searching for an early sign of the disease. Elevated CSF NfL levels, compared to a control group, turned out to be the most prominent early sign of the disease. The researchers suggest this is the earliest sign of neuronal damage related to Huntington’s disease ever detected, and offers scientists a new biomarker to use to recruit subjects for clinical trials testing new preventative treatments.

We have found what could be the earliest Huntington’s-related changes, in a measure which could be used to monitor and gauge effectiveness of future treatments in gene carriers without symptoms,” says co-first author Paul Zeun. In the Huntington’s study it was primarily NfL levels in spinal fluid that presented as the most effective early diagnostic biomarker of the disease. However, another new study examining NfL levels in relation to Alzheimer’s disease, is suggesting a more simple blood test could be useful in detecting NfL changes for that particular neurodegenerative disease.

A study published early in 2019 suggested increasing NfL levels in blood samples could detect Alzheimer’s disease around a decade before clinical symptoms appear. Yakeel Quiroz, from Harvard Medical School, wondered how early this biomarker could indicate the neurodegenerative disease.

We wanted to determine the earliest age at which plasma NfL levels could distinguish individuals at high risk of Alzheimer’s,” says Quiroz, co-first author on the study.

The researchers examined more than 1,000 subjects with a particular familial genetic mutation that makes them at a high risk of developing Alzheimer’s disease. The cohort was aged between eight and 75 years, and the results remarkably revealed increasing NfL levels could be detected at the early age of 22. The estimated median age of onset for mild cognitive impairment associated with this form of familial Alzheimer’s disease is 44, so the researchers say the biomarker could indicate the very earliest stage of neurodegeneration linked to the disease, 22 years before symptoms appear.

Source: https://newatlas.com/

How To Prevent The Formation Of Alzheimer’s Plaques

People who are affected by Alzheimer’s disease have a specific type of plaque, made of self-assembled molecules called β-amyloid (Aβ) peptides, that build up in the brain over time. This buildup is thought to contribute to loss of neural connectivity and cell death. Researchers are studying ways to prevent the peptides from forming these dangerous plaques in order to halt development of Alzheimer’s disease in the brain.

In a multidisciplinary study, scientists at the U.S. Department of Energy’s (DOE) Argonne National Laboratory, along with collaborators from the Korean Institute of Science and Technology (KIST) and the Korea Advanced Institute of Science and Technology (KAIST), have developed an approach to prevent plaque formation by engineering a nano-sized device that captures the dangerous peptides before they can self-assemble.


Transmission Electron Microscopy (TEM) images of Aβ peptide samples in the presence of the Aβ nanodevices (scale bar: 200 nm). The lack of grains in the image indicates the effectiveness of the nanodevice in trapping the peptides

We’ve taken building blocks from nanotechnology and biology to engineer a high-capacity cage’ that traps the peptides and clears them from the brain.” — Elena Rozhkova, scientist, Center for Nanoscale Materials

The β-amyloid peptides arise from the breakdown of an amyloid precursor protein, a normal component of brain cells,” said Rosemarie Wilton, a molecular biologist in Argonne’s Biosciences division.In a healthy brain, these discarded peptides are eliminated.”

In brains prone to the development of Alzheimer’s, however, the brain does not eliminate the peptides, leaving them to conglomerate into the destructive plaques.

The idea is that, eventually, a slurry of our nanodevices could collect the peptides as they fall away from the cells — before they get a chance to aggregate,” added Elena Rozhkova, a scientist at Argonne’s Center for Nanoscale Materials (CNM), a DOE Office of Science User Facility.

Source: https://www.anl.gov/

VR game lets patients ‘shoot’ away their pain

The Frisian company Reducept (Netherlands) has developed VR glasses that allow patients to ‘shoot away’ pain in a game. Patients come into contact with their nervous system, where they have to fight the pain.

Reducept team has developed a virtual reality headset to combat chronic pain and has won the prestigious UN World Summit Award. Exactly how many people are suffering from chronic pain in the Netherlands is not known but their number runs into the thousands, medical experts say. Often the pain has no clear cause. The conventional treatment is painkillers but these are costly and don’t always work. The VR treatment tackles the pain by training the brain, said psychologist Louis Zantema, who founded Reducept.

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People with chronic pain are oversensitive to the pain signal sent by the body to the brain. The therapy helps the nervous system because the brain believes healing is taking place,’ he said. Shooting down the pain ‘When you put on the VR headset you travel into in your own nervous system. The painful spots show up as small red dots which you shoot at, as if you were playing a game,’ Zantema explained. After ‘shooting down’ the pain the next step is a mindfulness exercise focusing on the spinal cord. ‘There we are using a psychological trick which also works for people suffering from trauma. The patient does a complicated exercise which is alternated with an intensive focusing on the pain.’ Professor Harry van Goor tested the VR headset on 40 people all of whom experienced a reduction in pain symptoms. He says the treatment offers hope to many while saving money at the same time. ‘Chronic pain is causing depression and is putting a lot of pressure on the health system. The medication either doesn’t help or is addictive and waiting lists for the specialist pain clinics are very long,’ he added. The treatment is available at over 50 healthcare institutions but is not covered by health insurers. A session costs €15 apart from the cost of buying a VR headset.

Source: https://reducept.com/

Lifelong Antisocial Behaviour Linked To Brain Structure

People who engage in persistent antisocial behaviour long after adolescence have characteristic differences in brain structure, finds a new UCL-led study.

The study, published in The Lancet Psychiatry, identified brain differences between people who engage in antisocial behaviour – such as theft, aggression, violence, bullying, lying, or repeated failure to take care of work or school responsibilities – only during adolescence and those who persist throughout adulthood.

Our findings support the idea that, for the small proportion of individuals with life-course-persistent antisocial behaviour, there may be differences in their brain structure that make it difficult for them to develop social skills that prevent them from engaging in antisocial behaviour. These people could benefit from more support throughout their lives,” said lead author Dr Christina Carlisi (UCL Psychology & Language Sciences).

Most people who exhibit antisocial behaviour primarily do so only in adolescence, likely as a result of navigating socially difficult years, and these individuals do not display structural brain differences. It is also these individuals who are generally capable of reform and go on to become valuable members of society.”

Previous studies have found that antisocial behaviour is most prevalent in adolescence, before people mature into adulthood, while a smaller number of people will continue with antisocial behaviour over multiple decades.

Source: https://www.ucl.ac.uk/