How to Prevent Tooth Loss

Research headed by scientists at the National Institute of Dental and Craniofacial Research (NIDCR) has shown how blocking the function of the blood clotting protein, fibrin, prevents bone loss from periodontal (gum) disease in mice. Drawing on animal and human data, the study—headed by NIDCR investigators Niki Moutsopoulos, DDS, PhD, and Thomas Bugge, PhD, found that build-up of fibrin triggers an overactive immune response that damages the gums and underlying bone. The results suggest that suppressing abnormal fibrin activity could hold promise for preventing or treating periodontal disease, as well as other inflammatory disorders—including arthritis and multiple sclerosis—that are marked by fibrin buildup.

Severe periodontal disease can lead to tooth loss and remains a barrier to productivity and quality of life for far too many Americans, especially those lacking adequate access to dental care,” said NIDCR director Rena D’Souza, DDS, PhD. “By providing the most comprehensive picture yet of the underlying mechanisms of periodontal disease, this study brings us closer to more effective methods for prevention and treatment.”

Periodontal disease is a bacterial infection of the tissues supporting the teeth. The condition affects nearly half of people in the United States who are over the age 30, and 70% of those who are 65 years and older. In its early stages, periodontal disease causes redness and swelling (inflammation) of the gums. In advanced stages, called periodontitis, the underlying bone becomes damaged, leading to tooth loss. While scientists have known that periodontitis is driven in part by an exaggerated immune cell response, until now, it was unclear what triggered the response, and how it caused tissue and bone damage.

Moutsopoulos, Bugge, and colleagues reported their findings in Science, in a paper titled, “Fibrin is a critical regulator of neutrophil effector function at the oral mucosal barrier.”

 

Source: https://www.genengnews.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/

The Brain In Your Gut

From moods to memory, the brain in our guts has a big impact on the brain in our heads. Pioneering neuroscientist Associate Professor Elisa Hill-Yardin from RMIT in Australia has spent years delving deep into the gut-brain connection, an emerging field in health research. Here she shares the five critical things we should know about our “gut brain”.

The gut has similar types of neurons to the brain. The gut brain is a big nervous system, about the same size as the spinal cord, which controls the contractions of the gut and its secretions. There are very rare gene mutations that affect brain connectivity and we’ve learned that the vast majority of those gene mutations are also found in the gut. If those mutations change the wiring in the brain, they’re also likely to change the wiring and the action of the gut brain – the enteric nervous system. To date, we’ve only ever examined the effect of those mutations in the brain. Now we’re starting to look at them in our second brain, the gut.

We now know that microbes in the gut do change our mood and behaviour, and microbes even change brain activity. There’s a great study that looked at women, doing MRI brain scans and showing that if they ate yoghurt for a certain number of days their resting brain activity was different – which is amazing! But we also know from animal studies that microbes have an impact on mental health. You can breed mice that are germ free and we know that those mice show differences in their anxiety behaviours – in other words, they’re less anxious without the microbes. So you could say we’re being controlled by the microbes in our gut. They’re much more important to our feelings than we ever thought.

What’s come out in research in recent years, though it’s been known for a long time in the autism community, is that the majority of children with autism have serious gut problems. Now we don’t know the cause of autism but we do know that there are hundreds and hundreds of rare gene mutations that alter brain connectivity. And we now know that some of those mutated genes are also found in the gut. We’re also learning that diseases that affect cognition and memory, like dementia, may also have a gut component. Researchers are starting to look at traditional brain diseases like Alzheimer’s, Parkinson’s, Multiple Sclerosis, and finding difference in the microbes in the gut. So they’re starting to think about how we can make changes in our microbes to make changes to our brain health.

The Gut-Brain Axis team that I lead at RMIT is focused on understanding how the enteric nervous system is altered in neurological disorders such as autism. This includes researching how the gut nervous system interacts with microbes in the intestine and changes in inflammatory pathways. We’re trying to identify the basic mechanisms, examining the connections between the gastrointestinal tract and changes in mood and behaviour, including the impact of genetics on microbiota in the gut. The ultimate the aim is to find novel therapies that can improve daily life for people with autism, but our work also has broader application for other neurological disorders, such Parkinson’s disease.

Many of the great enteric physiologist pioneers are in Australia and they were the first to describe different types of neurons based on their activity and neurochemical content. This work has been done on animal models, due to the possibilities of emulating human genetic diseases in these models. So, a lot of basic anatomy and physiology has been studied. But what we need now is to move the field towards using the latest sophisticated techniques and capitalising on the recent interest in the gut-brain axis, which of course involves understanding how the gastrointestinal tract works in concert with the trillions of microbes that live inside it.

Professor Elisa Hill-Yardin has presented her work to the US Air Force Office of Scientific Research

Source: https://www.rmit.edu.au/

Man With Multiple Sclerosis Walks Again After Stem Cell Transplant

For a decade, Roy Palmer had no control of his legs. The man from Gloucester, England, had multiple sclerosis, or MS, which results in the body’s immune system eating away at the protective covering of nerves, disrupting communication between the brain and the body.  Palmer had no feeling in his legs and used a wheelchair. But last year, he received a life-changing treatment that restored his ability to walk — and dance — again,the BBC reports. The dad first heard of the treatment, called HSCT (hematopoietic stem cell transplantation), on the BBC program, “Panorama.”

Two people on that program went into Sheffield Hospital in wheelchairs and they both came out walking,” Palmer said. “As soon as we saw that, we both cried,” Palmer’s wife told the BBC. According to the National MS Society, HSCT still considered experimental, but Palmer decided it was worth a try.

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If they can have that done, on a trial, why can’t I have it done?” Palmer said. So last year, the 49-year-old started the grueling treatment, which is potentially risky, the BBC reports. HSCT doesn’t always work and there is a long-term risk of infection and infertility. “They take the stem cells out of your body. They give you chemotherapy to kill the rest of your immune system,” Palmer told the BBC. The stem cells are then used to reboot the immune system. “Let’s hope it works,” Palmer adds in a home video taken just before the treatment. It did. After HSCT, he regained feeling in his left leg within two days. “I haven’t felt that in 10 years,” comments Palmer. “It’s a miracle.” Eventually, he regained feeling in both of his legs and began to walk.

Source: https://www.cbsnews.com/