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Radiation treatment may alleviate symptoms of severe Alzheimer’s disease

Radiation treatment may alleviate symptoms of severe Alzheimer’s disease

  • A pilot study showed that treatment with a low dose of radiation in people with severe Alzheimer’s disease could improve quality of life.
  • The low dose of radiation causes a small amount of damage to molecules, which stimulates a cellular protective response that involves antioxidant production and damage repair.
  • Further studies are needed to determine the optimal range of radiation efficacy.

Alzheimer’s disease (AD) is a progressive neurodegenerative disease that involves damage in the brain’s nerve cells, leading to memory loss and disruption of cognitive functioning. In the United States, AD is one of the leading causes of death in older populations, making up 60–80% of dementia cases.

There is no cure to prevent or treat AD, although there are therapies to relieve and slow the progression of some of its symptoms.

Key symptoms of AD include memory loss, confusion, and the loss of other cognitive abilities such as reasoning and decision-making. Health experts characterize late-stage, severe AD as an inability to communicate as well as impaired movement.

Case study of people with severe AD

A recent pilot study — conducted by scientists at the Baycrest and Sunnybrook Health Centres in Toronto, and Cuttler & Associates in Vaughan, Canada — showed that administering low doses of radiation, such as from a CT scan, may improve quality of life in severe AD patients.

The study appears in the Journal of Alzheimer’s Disease.

Dr. Sean Symons, a scientist at the Sunnybrook Research Institute and author of the study, provided additional comments for this article.

The team wanted to determine if they could observe similar results from a 2015 case study. According to this research, a patient with severe AD who received low doses of radiation displayed significant improvement in cognitive abilities, speech, and movement to the point where they were able to transfer out from a hospice into a care home.

Oxidative stress, which can cause DNA and cellular damage, can contribute to the development of Alzheimer’s disease and other neurodegenerative diseases.

The authors of the study hypothesized that low-dose ionizing radiation (LDIR) stimulates the mechanisms that offer protection from the damaging effects of oxidative stress, alleviating some of the symptoms of AD.

Four participants between the ages of 81 to 90 years, with severe AD, received a total of three low-dose radiation treatments through normal CT brain scans, 2 weeks apart. The first treatment consisted of two scans with a total of 80 milligrays (mGy) of radiation, while the latter two treatments were 40 mGy each.

The study analyzed both quantitative measures — measuring cognitive, behavioral, and functional abilities — and qualitative measures, meaning observations and reports of interactions with family members and caretakers, to determine improvements in quality of life.

Increased alertness, awareness, and recognition

The quantitative measures displayed minor differences, while the authors noted these measures were not sufficient to observe significant changes in severe AD patients.

However, the researchers saw the most significant changes through the qualitative measures. For three of the four participants, their family or caretakers reported increased alertness, awareness of surroundings, and recognition within a day after their first treatment.

One of the participants “was able to get into his wheelchair easily and put his feet on the footrests when asked to do so. At a concert, he sang to the rhythm and applauded appropriately.”

Another participant’s family member noted, “He was excited to see me — he spoke to me right away and gave me multiple kisses — real kisses like years ago. He was clapping his hands to the music. My mom agreed [it’d] been years since he has done this.”

One of the participants showed no changes or improvements in qualitative or quantitative measures. However, in all participants, there was no evidence to suggest worsened conditions or symptoms after radiation.

Rejuvenating' the Alzheimer's brain

Rejuvenating’ the Alzheimer’s brain

Rejuvenating' the Alzheimer's brain

Alzheimer’s disease is the main cause of dementia and current therapeutic strategies cannot prevent, slow down or cure the pathology. The disease is characterized by memory loss, caused by the degeneration and death of neuronal cells in several regions of the brain, including the hippocampus, which is where memories are initially formed. Researchers from the Netherlands Institute for Neuroscience (NIN) have identified a small molecule that can be used to rejuvenate the brain and counteract the memory loss.

New cells in old brains

The presence of adult-born cells in the hippocampus of old people was recently demonstrated in scientific studies. It suggests that, generally speaking, the so-called process of adult neurogenesis is sustained throughout adulthood. Adult neurogenesis is linked to several aspects of cognition and memory in both animal models and humans, and it was reported to sharply decrease in the brains of patients with Alzheimer’s disease. Researchers also found that higher levels of adult neurogenesis in these patients seem to correlate with better cognitive performance before death. “This could suggest that the adult-born neurons in our brain may contribute to a sort of cognitive reserve that could later on provide higher resilience to memory loss”, says Evgenia Salta, group leader at the NIN. Therefore, researchers from the NIN investigated if giving a boost to adult neurogenesis could help prevent or improve dementia in Alzheimer’s disease.

A small molecule with big potential

Salta: “Seven years ago, while studying a small RNA molecule that is expressed in our brain, called microRNA-132, we came across a rather unexpected observation. This molecule, which we had previously found to be decreased in the brain of Alzheimer’s patients, seemed to regulate homeostasis of neural stem cells in the central nervous system”. Back then, Alzheimer’s was thought to be a disease affecting only mature neuronal cells, so at first glance this finding did not seem to explain a possible role of microRNA-132 in the progression of Alzheimer’s.

In this study, the researchers set out to address whether microRNA-132 can regulate adult hippocampal neurogenesis in healthy and Alzheimer’s brains. Using distinct Alzheimer’s mouse models, cultured human neural stem cells and post-mortem human brain tissue, they discovered that this RNA molecule is required for the neurogenic process in the adult hippocampus. “Decreasing the levels of microRNA-132 in the adult mouse brain or in human neural stem cells in a dish impairs the generation of new neurons. However, restoring the levels of microRNA-132 in Alzheimer’s mice rescues neurogenic deficits and counteracts memory impairment related to adult neurogenesis”, Sarah Snoeck, technician in the group of Salta, explains.

These results provide a proof-of-concept regarding the putative therapeutic potential of bringing about adult neurogenesis in Alzheimer’s. Salta: “Our next goal is to systematically assess the efficacy and safety of targeting microRNA-132 as a therapeutic strategy in Alzheimer’s disease”.

 

Source: EurekAlert

BioNTech and Moderna set their sights on treating cancer

BioNTech and Moderna set their sights on treating cancer

COVID-19 vaccines launched BioNTech and Moderna into the limelight, making these once little-known companies prominent companies. But neither wants to be pigeonholed as a COVID-19 vaccine company.

BioNTech cofounder Özlem Türeci stressed in a recent interview with AP that the mRNA vaccine technology that is its focus could be a powerful weapon against cancer. “We have several different cancer vaccines based on mRNA,” said Türeci, BioNTech’s chief medical officer.

Such therapy could be available to people within a “couple of years,” Türeci said, stressing that it is difficult to predict regulatory timelines involving emerging therapies. 

BioNTech is currently working on several novel immunotherapies for oncology targeting melanoma, prostate cancer and cancers associated with human papillomavirus. 

Moderna is also exploring the possibility of using its mRNA vaccines for treating cancer. The company has Phase 2 studies underway investigating melanoma and ovarian cancer. 

Moderna is also testing mRNA vaccines’ potential to revascularize heart tissue post-heart attack. 

Its pipeline also includes a vaccine for cytomegalovirus (CMV), which is a frequent cause of birth defects. Roughly one out of every 200 babies is born with congenital CMV, according to CDC

Source: DrugDiscoveryTrends

Prototype app for mobile devices could screen children at risk for autism spectrum disorder

Prototype app for mobile devices could screen children at risk for autism spectrum disorder

NIH-funded research project develops app to track eye movements in response to videos.

A mobile app was successful at distinguishing toddlers diagnosed with autism spectrum disorder (ASD) from typically developing toddlers based on their eye movements while watching videos, according to a study funded by the National Institutes of Health. The findings suggest that the app could one day screen infants and toddlers for ASD and refer them for early intervention when chances for treatment success are greatest.

The study appears in JAMA Pediatrics and was conducted by Geraldine Dawson, Ph.D., director of the NIH Autism Center of Excellence at Duke University, and colleagues. Funding was provided by NIH’s Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) and National Institute of Mental Health.

Studies have found that the human brain is hard-wired for social cues, with a person’s gaze automatically focusing on social signals. In ASD, attention to social stimuli is reduced, and researchers have sought to screen for ASD in young children by tracking their eye movements while they view social stimuli. However, equipment used for visual tracking is expensive and requires specially trained personnel, limiting its use outside of laboratory settings.

The current study enrolled 933 toddlers ages 16 to 38 months during a well-child primary care visit. Of these children, 40 were later diagnosed with ASD. They viewed on a mobile device short videos of people smiling and making eye contact or engaging in conversation. Researchers recorded the children’s gaze patterns with the device’s camera and measured them using computer vision and machine learning analysis. Children with ASD were much less likely than typically developing children to focus on social cues and visually track the conversations in the videos.

Pending confirmation by larger studies, the authors concluded that this eye-tracking app featuring specially designed videos and computer vision analysis could be a viable method for identifying young children with ASD.

Source: nih.gov 

Study links structural brain changes to behavioral problems in children who snore

Study links structural brain changes to behavioral problems in children who snore

A large study of children has uncovered evidence that behavioral problems in children who snore may be associated with changes in the structure of their brain’s frontal lobe. The findings support the early evaluation of children with habitual snoring (snoring three or more nights a week). The research, published in Nature Communications, was supported by the National Institute on Drug Abuse (NIDA) and nine other Institutes, Centers, and Offices of the National Institutes of Health.

Large, population-based studies have established a clear link between snoring and behavioral problems, such as inattention or hyperactivity, but the exact nature of this relationship is not fully understood. While a few small studies have reported a correlation between sleep apnea—when pauses in breathing are prolonged—and certain brain changes, little is known about whether these changes contribute to the behaviors seen in some children with obstructive sleep-disordered breathing (oSDB), a group of conditions commonly associated with snoring that are characterized by resistance to breathing during sleep.

To address this knowledge gap, researchers led by Amal Isaiah, M.D., D.Phil., of the University of Maryland School of Medicine, capitalized on the large and diverse dataset provided by the Adolescent Brain Cognitive Development (ABCD) Study(link is external), a long-term study of child health and brain development in the United States. The team of researchers mined this wealth of data from more than 11,000 9- and 10-year-old children to examine the relationships among snoring, brain structure, and behavioral problems.

Confirming the results of previous work, their statistical analysis revealed a positive correlation between habitual snoring and behavioral problems, with the children who most frequently snored generally exhibiting worse behavior according to an assessment completed by parents. The findings further showed that snoring is linked to smaller volumes of multiple regions of the brain’s frontal lobe, an area involved in cognitive functions such as problem solving, impulse control, and social interactions. The statistical analysis also suggested that the brain differences seen in children who snore may contribute to behavioral problems, but additional work on how snoring, brain structure, and behavioral problems change over time is needed to confirm a causal link.

This study’s findings point to oSDB as a potential reversible cause of behavioral problems, suggesting that children routinely be screened for snoring. Children who habitually snore may then be referred for follow-up care. Such care may include assessment and treatment for conditions that contribute to oSDB, such as obesity, or evaluation for surgical removal of the adenoids and tonsils.

The ABCD Study, the largest of its kind in the United States, is tracking nearly 12,000 youth as they grow into young adults. Investigators regularly measure participants’ brain structure and activity using magnetic resonance imaging (MRI) machines, and collect psychological, environmental, and cognitive information, as well as biological samples. The goal of the study is to define standards for normal brain and cognitive development and to identify factors that can enhance or disrupt a young person’s life trajectory.

The Adolescent Brain Cognitive Development Study and ABCD Study are service marks and registered trademarks, respectively, of the U.S. Department of Health and Human Services.

Source: nih.gov

Large-Scale Genetics Study Sheds Light on Developmental Origins of Autism

Large-Scale Genetics Study Sheds Light on Developmental Origins of Autism

Autism spectrum disorder (ASD) is a complex developmental disorder that encompasses a range of symptoms. Scientific evidence suggests that there are likely many factors that contribute to the disorder – certain genetic variations have been associated with ASD, but the way these variations shape the development and function of the brain remains unclear. Groundbreaking NIMH-funded research is helping to unravel this neurodevelopmental knot by examining the human exome.

The exome includes all of the exons, DNA components that provide instructions for making proteins, in a person’s genome. Although exons make up an estimated 1 to 1.5% of a person’s entire genetic code, they are typically where disease-causing mutations are found for single-gene disorders. Sequencing the whole exome can provide an efficient method for identifying genetic mutations that may be associated with certain conditions or disorders.

To tease apart the genetic underpinnings of ASD, Joseph D. Buxbaum, Ph.D., and colleagues in the Autism Sequencing Consortium conducted a large-scale exome sequencing study, comparing the exomes of individuals with and without ASD. By making this comprehensive comparison, they hoped to illuminate genetic contributions to developmental and physiological alterations in ASD.

Using biological samples and other data shared via the Autism Sequencing Consortium, the international research team analyzed data from 35,584 people, including 11,986 people with ASD. The data included information from families (individuals with ASD, siblings without ASD, and both parents) and from matched pairs of individuals with and without ASD. Importantly, the unprecedented size and scope of the study allowed the scientists to identify different types of rare genetic variations associated with ASD.

The results provided very strong evidence linking ASD with 26 genes and strong evidence linking ASD with 76 additional genes, a marked increase in the number of associated genes identified in previous studies. Of the 102 total genes, 60 had not been linked with ASD before, and 30 had not been linked with any neurodevelopmental disorder.

These findings suggest that there are many more genetic variants associated with ASD than previously thought. Further analyses indicated that some variations may be more common in people who have both ASD and developmental delay, while others may be more common in people who only have an ASD diagnosis.

Looking at the range of genes identified, the researchers found that the types of genes comprised two functional groups: genes that play a role in switching other genes on or off and genes that play a role in building connections between neurons. Importantly, people who had variants of genes that are involved in turning other genes on and off also tended to have more significant developmental delays, including impaired cognitive, social, and motor skills.

Most of the 102 genes the researchers identified are often expressed at high levels in the brain’s cortex, the outer layer of the brain that is involved in complex functions and behaviors. The genes are expressed in both excitatory neurons, which increase the likelihood of neuronal firing, and inhibitory neurons, which decrease the likelihood of neuronal firing. The genes also tend to be expressed in early stages of brain development, which aligns with some of the differences in brain structure and function that have been associated with ASD.

Taken together, the findings suggest there are multiple genetic pathways that contribute to the core clinical features of ASD. Studying how and when those pathways converge will allow researchers to sketch a more detailed developmental picture—distinguishing the mechanisms that lead to social dysfunction and repetitive behaviors from those that lead to more general impairment.

Source: NIMH.NIH.gov

Is there a link between COVID-19 and Parkinson’s disease?

Is there a link between COVID-19 and Parkinson’s disease?

Although extremely rare, Parkinson’s-like symptoms have occurred in a few people with COVID-19. This phenomenon has researchers investigating whether there is a link between SARS-CoV-2 and Parkinson’s disease.

Since the start of the COVID-19 pandemic, scientists have continued to search for information about how SARS-CoV-2 affects the body.

At this point, researchers and healthcare professionals know that the effects extend beyond the respiratory system. SARS-CoV-2 can impact other organsTrusted Source, including the heartTrusted SourcebrainTrusted SourcekidneysTrusted Source, and skinTrusted Source.

In November 2020, an article published in The Lancet Neurology reported that up to 65%Trusted Source of people with COVID-19 has experienced hyposmia, a loss or change in their sense of smell, which is also a symptom of Parkinson’s disease.

The same article reported three cases of people experiencing Parkinson’s-like symptoms after a SARS-CoV-2 infection, though they had no known risk factors for the condition.

These incidents have scientists questioning whether there is a link between SARS-CoV-2 and Parkinson’s disease or Parkinson’s-like symptoms.

In this Special Feature, we take a closer look at this phenomenon to investigate what scientists know about the possible association between Parkinson’s disease and COVID-19

What is Parkinson’s disease?

Parkinson’s disease is a neurological condition. Its symptoms appear slowly and progress as time goes on. Symptoms include shaking or tremors, stiffness, and difficulties with balance, walking, talking, and coordination.

Because the disease affects the brain, people with Parkinson’s also experience behavioral changes, memory problems, sleep issues, and fatigue.

The condition results from the impairment of the nerve cells responsible for controlling movement. Other factors thought to contribute include low dopamine or norepinephrine levels and possibly the presence of Lewy bodies in the brain. According to scientists, genetic and environmental factors appear to set off these changes, causing the disease.

A distinct condition is called parkinsonism. People with parkinsonism have symptoms similar to those of Parkinson’s disease, but the symptoms are somewhat atypical.

This condition often accompanies another disorder, and there are different forms, including vascular parkinsonism and drug-induced parkinsonism.

Parkinsonism and viral infections: A possible link?

Reports of Parkinson’s-like symptoms in people with influenza have some scientists speculating whether there could be a viral cause of some types of parkinsonism.

To explore the possible connection, researchers have reviewed the reported instances of a viral illness leading to Parkinson’s-like symptoms. Their findings appear in the journal Frontiers in NeurologyTrusted Source.

The scientists evaluated data about viruses including influenza, herpes simplex virus 1, Epstein-Barr, varicella zoster, hepatitis C, Japanese encephalitis, West Nile virus, and HIV.

The team also noted that parkinsonism had developed in some people during the 1918 influenza pandemic. Although these two events are temporally coincidental, a direct cause between influenza and parkinsonism has not been established.

Since then, some symptoms of parkinsonism, including tremors and walking disturbances, have been reported in people with influenza, most often within the first few weeks of the infection. Scientists are particularly interested in the role that influenza A may playTrusted Source in contributing to Parkinson’s-like symptoms.

Researchers speculate that parkinsonism may, rarely, occur in severe influenza infections because of the inflammatory process associated with the body’s immune response to viral threats.

This leads some to believe that there could be a link between parkinsonism and infections with other viruses, including SARS-CoV-2.

 
 

Parkinson’s-like symptoms in COVID-19

According to the most recent data, published in The Lancet NeurologyTrusted Source on November 27, 2020, three people with COVID-19 have also experienced Parkinson’s-like symptoms.

Two men, aged 45 and 58 years, and one woman, aged 35 years, reported slowness of movement accompanied by muscle stiffness, muscle spasms, irregular eye movement, and tremor.

All three showed the reduced function of the brain’s dopamine pathway system on imaging tests. Two of the three responded positively to medication and one recovered spontaneously.

None had a family history or clinical signs of Parkinson’s disease before their illness.

 

Why would Parkinson’s-like symptoms occur with COVID-19?

Scientists have developed three theories about mechanisms that could be involved in the appearance of parkinsonism following a SARS-CoV-2 infection. They describe their hypotheses in the journal Trends in Neurosciences.

First, SARS-CoV-2 is known to cause vascular complications in the brain and other organs, and scientists suggest that this process could harm brain pathways. This damage is similar to what happens during the progression of vascular parkinsonism.

Second, because there is a known association between inflammation and an increased risk of Parkinson’s disease, inflammation caused by the immune response to a SARS-CoV-2 infection could potentially trigger parkinsonism.

Studies have also shown that some people with COVID-19 have elevated levels of interleukin-6, an immune system protein, as well as disruptions in the kynurenine pathwayTrusted Source. Both are mechanisms associated with Parkinson’s disease.

In addition, the neuroinvasive nature of SARS-CoV-2 may contribute to a possible association between COVID-19 and parkinsonism. Researchers have discovered viral RNA in the brain tissue of people who have died from COVID-19, indicating that the virus may invade brain cells and pathways.

Meanwhile, some research suggests that the progression of Parkinson’s disease may begin in the olfactory system, where the sense of smell originates. Because COVID-19 can present with a loss of smell and taste, scientists wonder whether SARS-CoV-2 can gain access to the same brain pathways associated with Parkinson’s disease.

Researchers also hypothesize that a SARS-CoV-2 infection may reveal Parkinson’s disease that has not yet become symptomatic. Alternately, the infection might initiate the progression of the disease in people who are genetically prone to it.

Closely following further developments

While experiencing parkinsonism during a SARS-CoV-2 infection is currently quite rare, scientists say that the appearance of these symptoms in relation to COVID-19 merits further exploration.

They recommend close monitoring for Parkinson’s-like symptoms in a large cohort of people with COVID-19. Determining whether a link between parkinsonism and COVID-19 exists could help scientists better understand both health issues and develop more effective treatments.

At present, there is still much to learn about a possible connection between COVID-19 and parkinsonism, and scientists are just beginning to investigate this rare and poorly understood phenomenon.

Source: MedicalNewsToday

Can genetics predict bothersome hot flashes?

Can genetics predict bothersome hot flashes?

New study suggests that some of the same genetic variants that help to predict reproductive aging are associated with frequency and severity of hot flashes

CLEVELAND, Ohio (April 28, 2021)–Hot flashes are a hallmark of the menopause transition. Yet, they don’t strike with the same frequency or severity for all women. A new study suggests that some of the same genetic factors that affect a woman’s reproductive life cycle may also help predict her likelihood of having bothersome hot flashes. Study results are published online today in Menopause, the journal of The North American Menopause Society (NAMS).

Despite multiple studies on the subject, questions still remain as to why some women are more affected than others by hot flashes and night sweats during the menopause transition. Genetics may be one reason, because black women have more problems with hot flashes than white women do, and Chinese and Japanese women seem to suffer the least with symptoms. Prior studies have also attempted to address why some women experience hot flashes much earlier in the menopause transition than other women who have more frequent hot flashes postmenopause. Still there are others who consistently experience hot flashes for more than a decade.

In this study involving more than 1,200 women of various ethnicities, researchers concluded that some of the same genetic factors that predict reproductive aging may also be associated with hot flashes, thus suggesting that genetics may play a role in predicting the severity and frequency of a woman’s hot flashes.

Factors shown to affect reproductive aging and likely to influence a woman’s experience with hot flashes include the age at menarche and the age at menopause. Some studies have also previously suggested an association between body mass index and the frequency and severity of hot flashes, although this relationship is described as complex and dependent on the stage of reproductive aging. Lower estrogen levels have also been associated with more prevalent and frequent hot flashes. Although a number of these studies provided evidence of some overlap in genes associated with age at menarche and age at natural menopause, no prior studies focused on how these factors affected hot flashes.

Researchers believe that understanding the effect of genetic variants is critical to identifying future treatments for managing bothersome hot flashes. They created a video highlighting their results that can be found at https://links.lww.com/MENO/A761.

Results are published in the article “Genetic variants predictive of reproductive aging are associated with vasomotor symptoms in a multiracial/ethnic cohort.”

“This study found that genetic factors associated with aging of the reproductive system may be linked to vasomotor symptoms during the menopause transition and differ across racial/ethnic groups. These findings move us one step closer to being able to predict a woman’s experience with menopause symptoms and, subsequently, to provide management recommendations based, in part, on her genetics. In addition, researchers may be able to use these specific genetic variations as targets for the development of new drugs to alleviate vasomotor symptoms,” says Dr. Stephanie Faubion, NAMS medical director.

Source:  EurekAlert