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A new highly selective PET imaging agent can detect the presence of overexpressed monoamine oxidase-B (MAO-B) in cognitively unimpaired individuals with high beta amyloid (Ab) — one of the earliest signs of Alzheimer’s disease — according to research published in the October issue of The Journal of Nuclear Medicine. The radiotracer, 18F-SMBT-1, allows for a better understanding of the role of inflammation in Alzheimer’s disease, which can enable more accurate staging and prognosis at earlier stages.
Brain inflammation that accompanies Alzheimer’s disease involves reactive astrocytes, which are cells that overexpress MAO-B. The newly developed 18F-SMBT-1 radiotracer is highly selective for MAO-B and as a result has increased binding to reactive astrocytes. “This increased binding suggests that 18F-SMBT-1 can potentially be used as a surrogate marker to detect reactive astrogliosis in Alzheimer’s disease,” noted Victor Villemagne, MD, professor of psychiatry at the University of Pittsburgh in Pittsburgh, Pennsylvania.
The study aimed to characterize 18F-SMBT-1 binding to reactive astrocytes across the Alzheimer’s disease continuum. Study participants included three clinical groups: 57 cognitively unimpaired controls, 12 subjects meeting criteria for mild cognitive impairment (MCI), and eight subjects meeting criteria for Alzheimer’s disease.
Participants underwent several types of imaging, including 18F-SMBT-1 PET, Ab PET, tau PET, and MRI. Images were normalized and statistical analyses conducted to assess 18F-SMBT-1 binding in relation to Ab and tau pathology burden. 18F-SMBT-1 was found to be highly correlated with Ab burden, and much less with tau burden.
The three clinical groups were then classified based on their Ab status (either as Ab+ or Ab-). No significant differences in 18F-SMBT-1 binding were found among Ab- participants in the control and MCI groups. In the Ab+ subjects with Alzheimer’s disease, 18F-SMBT-1 binding was significantly higher. Most importantly, 18F-SMBT-1 binding was significantly higher in the Ab+ control group as compared to Ab- control group.
“It’s of note that the brain regions where we saw this higher 18F-SMBT-1 binding in the control group are regions known for early Ab deposition. This suggests that reactive astrocytes are associated with early Ab deposition at the preclinical stages of Alzheimer’s disease and likely play a role over clinical progression,” said Villemagne.
He continued, “Implementation of 18F-SMBT-1 will clarify the role of reactive astrogliosis in neurodegenerative conditions, not just Alzheimer’s disease and its potential independent and/or synergistic effects on pathology, neurodegeneration, cognition, and disease progression. This has the potential to define and refine the diagnostic, staging and prognostic roles of reactive astrogliosis in these conditions.”
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A newly developed mathematical model incorporates the influence of social interactions on community exercise trends, suggesting that interacting with moderately active people could influence sedentary people to become more active. Ensela Mema of Kean University in Union, New Jersey, and colleagues present these findings in the open-access journal PLOS ONE on October 19, 2022.
In 2018, the U.S. Department of Health and Human Services published evidence-based guidelines outlining recommended types and amounts of physical activity to promote health benefits for different populations of Americans. However, national population-level trends suggest that there has been little improvement in meeting these recommendations.
To help address this issue, Mema and colleagues drew on previous research showing that social interactions with peers can play a key role in boosting physical activity within a community. In line with that knowledge, they developed a mathematical model that simulates how social interactions can affect a population’s exercise trends over time. The model incorporates data from the U.S. Military Academy.
The model simulations showed that, in the absence of social interactions, populations experienced a long-term decrease in physically active individuals, and sedentary behavior began to dominate. However, when the simulations included social interactions between sedentary and moderately active people, sedentary populations became more physically active in the long term. Still, in simulations where moderately active people became more sedentary over time, overall physical activity trends plummeted.
While these simulations were not validated with real-world data, the researchers say they provide new insights that could inform public health efforts to boost community physical activity levels. The researchers outline a number of recommendations for such efforts, such as social activities designed to boost interactions between sedentary and moderately active people.
These simulations could also inform efforts to maintain physical fitness in the U.S. military, the researchers note. However, they say, more research will be needed to better understand the balance between encouraging exercise among sedentary people while retaining activity levels in moderately active people.
The authors add: “We have traditionally directed physical activity interventions by engaging sedentary individuals to become more active. Our model suggests that focusing on the moderately active population to sustain their activity and increasing their interactions with sedentary people could stimulate higher levels of overall physical activity in the population.”
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Scientists at Scripps Research have developed a new tool to monitor brain plasticity — the way our brains remodel and physically adapt as we learn and experience things, from watching a movie to learning a new song or language. Their approach, which measures the proteins produced by individual types of brain cells, has the potential to both answer basic questions about how the brain works, and shed light on numerous brain diseases in which plasticity goes awry.
Prior experiments in several labs have already revealed how brain activity spurs changes in the gene expression in neurons, an early step in plasticity. The team’s experiments, described in Journal of Neuroscience on September 7, focus on the next essential step in plasticity, translation of the genetic code into proteins.
“We still don’t understand all the mechanisms underlying how cells in our brain change in response to experiences, but this approach gives us a new window into the process,” says Hollis Cline, PhD, the Hahn Professor and Chair of Neuroscience at Scripps Research and senior author of the new work.
When you learn something new, two things happen: First, neurons immediately pass electrical signals along new routes in your brain. Then, over time, this leads to changes in the physical structure of cells and their connections in the brain. But scientists have long wondered what happens in between these two steps. How does this electrical activity in neurons ultimately coax the brain to change in more lasting ways? Even further, how and why does this plasticity decrease with age and certain diseases?
Previously, researchers have studied how genes in neurons turn on and off in response to brain activity, hoping to get insight into plasticity. With the advent of high-throughput gene sequencing technologies, tracking genes in this way has become relatively easy. But most of those genes encode proteins — the real workhorses of cells, the levels of which are more difficult to monitor. But Cline, in close collaboration with Scripps professor John Yates III, PhD, and associate professor Anton Maximov, PhD, wanted to look directly at how proteins in the brain change.
“We wanted to jump into the deep end of the pool and see what proteins are important to brain plasticity,” says Cline.

About 60% of healthcare workers participating in an optional rapid antigen testing program at UCLA tested positive at day five, and about 50% were positive at day seven after initially testing positive for COVID-19 with a PCR test. The results indicated those with positive tests were more likely to be infectious and were not allowed to return to work until after 10 days of isolation.
A surge in COVID cases in December 2021 led to a shortage of healthcare workers across the U.S. While the isolation period to reduce transmission has changed during the pandemic based on various factors, the U.S. Centers for Disease Control and Prevention (CDC) on Dec. 23 had shortened the isolation period’s length to five days from symptom onset, with or without a negative COVID test, during times of critical staffing shortages. This prompted the researchers to undertake this study. The CDC recently changed the healthcare return-to-work guidance.
PCR tests detect viral nucleic acids (RNA) and are used for diagnosing COVID. Those nucleic acids can, however, continue to be detected beyond the point when someone is still infectious. The antigen test detects proteins from the actual virus, which is typically only present when infectious virus remains, making them a better proxy than the PCR test for indicating infectiousness.
From Dec. 25, 2021 to Feb. 4, 2022, UCLA Health ran an optional program in which 870 healthcare workers with COVID and were asymptomatic or mildly symptomatic with improving symptoms could return to work after five days of isolation if a subsequent antigen test for SARS-CoV-2 was negative. They underwent the rapid antigen test five or more days after their initial positive COVID PCR test.
Some limitations to the findings include an inability to perform viral cultures or repeat PCR tests and a lack of data on infections that may have occurred during work hours, though that risk was likely low due to masking and the fact that workers were allowed to return only after a negative test. Also, only about 37% of the 2,316 UCLA healthcare workers who had positive PCR tests during the period volunteered for the optional antigen testing program.
The findings demonstrate how the rapid antigen test can be used to triage healthcare workers for returning to work during periods of acute staffing shortages during COVID surges. They also show that a majority of health care workers remain antigen positive five to seven days following COVID-19 infection. Other healthcare systems can also look to these findings as they implement their own return-to-work testing programs.
“Antigen tests correlate well with being infectious, so these tests were able to identify healthcare workers who might have still been infectious following a COVID infection,” said lead author Dr. Paul Adamson, assistant professor of medicine, division of infectious diseases, at the David Geffen School of Medicine at UCLA “The antigen test positivity was higher than we initially expected following the isolation period.”
Study co-authors are Dr. Judith Currier, Dr. Daniel Uslan, and Omai Garner of UCLA.
The study is published in Open Forum Infectious Diseases.
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Research led by doctors and scientists at UCLA Jonsson Comprehensive Cancer Center and the UCLA Jane & Terry Semel Institute for Neuroscience & Human Behavior have identified a gene that may provide a therapeutic target for the deadly, treatment-resistant brain cancer glioblastoma multiforme (GBM).
The gene, P300, enables GBM cells that have been damaged by radiation therapy to recover by rearranging DNA, and initiating a molecular mechanism that refortifies tumor cells for growth and survival. Blocking P300 disrupted its ability to set this process in motion, according to the researchers, who conducted their studies in mouse models and in human GBM cells. Their results appear online in Nature Communications.
Although glioblastoma is considered rare — about 13,000 new cases are expected to be diagnosed in the United States this year, according to the National Brain Tumor Society — it is the most common primary brain tumor in adults. There is no known cure, and the average length of survival is measured in months. GBM cells and their precursors, glioma stem cells (GSC), quickly adapt and recover from injury, so chemotherapy and radiation therapy, which may initially slow a tumor’s progress, can ultimately contribute to growth and recurrence..
By performing single-cell transcriptomic sequencing, which can identify molecular changes in cancerous cells, the UCLA-led research team showed that radiation therapy-induced stress promotes phenotypic conversion of glioma stem cells to resemble two types of cells that are normally found in blood vessels (vascular endothelial-like cells and pericyte-like cells). They found that these converted cells promoted tumor growth and post-treatment recurrence. The conversion was brought about by changes within specific vascular gene regions in a process mediated by the gene P300, or P300 HAT (histone acetyltransferase).
“Our findings show at the single-cell level that ‘radiation-stress’ alters the functional states of glioma cells, but instead of reconstituting the vascular system to carry blood supply, as has sometimes been theorized, these converted cells provide trophic support that enables the cancer cells to survive and grow under the hostile conditions created by radiation,” said senior author Harley Kornblum, M.D., Ph.D., a researcher at the UCLA Jonsson Comprehensive Cancer Center and the UCLA Brain Research Institute.
“Just as P300 plays a key role in changing the molecular landscape of glioma stem cells, inhibiting the gene’s function appears to block the phenotypic conversion. This suggests that small molecules that inhibit P300 HAT activity may be useful in preventing tumor growth and adaptive resistance of GBM,” said Dr. Sree Deepthi Muthukrishnan, Assistant Project Scientist and the first author of the study.
While the authors were able to identify some candidate factors expressed by the vascular-like cells and their experiments show those factors’ potential role in promoting proliferation of radiated tumor cells, they say that further studies will be needed to fully uncover the underlying mechanisms at play. Importantly though, the factors that mediate the trophic actions of radiation-induced vascular-like cells would likely be targets for potential therapeutic intervention to prevent GBM relapse.
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People who gain or lose weight soon after being diagnosed with Parkinson’s disease may be more likely to have changes in their thinking skills than people who maintain their weight, according to a study published in the October 19, 2022, online issue of Neurology®, the medical journal of the American Academy of Neurology.
“Early weight loss is a common symptom in people with Parkinson’s disease,” said study author Jin-Sun Jun, MD, of Kangnam Sacred Heart Hospital in Seoul, Republic of Korea. “It could serve as a sign that people are at risk of cognitive decline.”
The study involved 358 people who were recently diagnosed with Parkinson’s disease and had not yet started taking Parkinson’s medications. They were an average age of 61 and had been diagnosed an average of two years earlier. They were compared to 174 people who did not have Parkinson’s disease.
Weight gain or loss was defined as a change of more than 3% of body weight during the first year of the study. Weight maintenance was defined as no change or change of no more than 3%. A total of 98 people had weight loss, 59 had weight gain and 201 maintained their weight.
Participants took tests of thinking skills at the beginning of the study and then every year for up to eight years. They also took tests for other non-motor symptoms that can occur in people with Parkinson’s disease, such as depression, anxiety and sleep disorders.
The people with Parkinson’s who lost weight had a faster decline in their overall thinking scores compared to those with Parkinson’s who maintained their weight. Both groups started with average scores of 27 on the test. The scores of those who lost weight declined 0.19 points faster per year than those of those who maintained their weight. The thinking skills with the steepest declines were related to verbal fluency skills, which are a measure of executive function.

Pancreatic cancer often lurks as a silent disease. With no known symptoms, it can progress undetected and spread to other organs.
According to the National Cancer Institute, more than 60,000 Americans will be diagnosed with pancreatic cancer this year, and only about 1 in 10 of those diagnosed will survive the next five years. The disease ranks as the third leading cause of cancer deaths in the U.S. because it is rarely detected in the early stages when treatment options are most effective.
Pancreatic cancer’s stealth-like nature has the attention of University of Florida scientists, who have discovered a way to reverse a key cellular process involved in its progression.
UF researchers identified two small molecules that inhibit precancerous cell progression. The molecules also reversed a process known as acinar ductal metaplasia, or ADM, which precedes pancreatic cancer.
“To our knowledge, this is the first time researchers have been able to pharmacologically reverse ADM,” said Tom Schmittgen, Ph.D., the study’s senior author and chair of the department of pharmaceutics in the UF College of Pharmacy, part of UF Health, the university’s academic health center. “With these compounds, we could potentially treat a pancreatic cancer patient at an earlier stage of the disease and hopefully improve the treatment options available.”
ADM often occurs when inflammation is present. It is a defense mechanism to avoid having the pancreas make too many digestive enzymes and destroy itself. During ADM, stable, enzyme-making acinar cells turn into protective ductal cells that line the pancreatic duct. If certain genes mutate during the transition, then the cells can become precancerous and eventually develop into cancer.
To study ADM, UF scientists built a laboratory model using animal cells with pancreatic cancer and tissue from a healthy human. They introduced the cells to two compounds — one of which was developed by Chenglong Li, Ph.D., the Nicholas Bodor Professor in Drug Discovery in the UF College of Pharmacy. The ductal cells responded by changing back to acinar cells. Pancreatic cancer can be prevented when acinar cells are maintained in their natural state.
“The findings are significant because we have now demonstrated that ADM can be reversed using drugs,” said Schmittgen, who also serves as the V. Ravi Chandran Professor of Pharmaceutical Sciences in the UF College of Pharmacy. “This research may lead to developing treatments for patients who are at a high risk for pancreatic cancer development.”
Schmittgen hopes this discovery will encourage scientists to think about new ways to treat pancreatic cancer by manipulating ADM. Future research will involve testing other compounds in collaboration with Hendrik Luesch, Ph.D., a co-author of the study and a professor and chair of medicinal chemistry and the Debbie and Sylvia DeSantis Chair in Natural Products Drug Discovery and Development in the UF College of Pharmacy. These compounds may prove to be more effective, as scientists seek new treatments for a disease with very few treatment options.
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Materials provided by University of Florida. Original written by Matthew Splett. Note: Content may be edited for style and length.

In medieval Norway, high status individuals tended to be taller and to have stronger bones, possibly as a result of a favorable lifestyle, according to a study published October 19, 2022 in the open-access journal PLOS ONE by Elin Brødholt of the University of Oslo and colleagues.
Throughout modern history, socioeconomic status has been linked to health and longevity, a relationship that can potentially be detected even in the skeletal remains of past cultures. Medieval Norway was a period characterized by notable levels of social stratification and poverty and is therefore a valuable case study in identifying correlations between social status and individual health.
The authors examined the remains of 227 individuals from five burial sites spanning the 11th through 16th centuries AD. Two of the sites, a royal church and a Dominican monastery, yielded the remains of high-status individuals, while the other three sites represented parish populations. For each individual, the researchers measured patterns of bone mineral density as well as stature and found significant skeletal differences between the socioeconomic groups.
In general, high-status individuals were taller and had higher bone mineral density compared with the parish populations. This pattern likely reflects differences in nutrition, activity level, and susceptibility to disease brought on by differing lifestyles between high-class and low-class individuals. These results were also influenced by other factors. For example, women showed more marked differences in skeletal traits between the socioeconomic groups as compared to men, possibly indicating that women in medieval Norway experienced a particularly high degree of lifestyle differences influenced by social class. These data are valuable in understanding the complex ways in which socioeconomic status has influenced health over the centuries.
The authors add: “Bone mineral density (BMD) has varied notably between archaeological populations and time periods in Scandinavia, and these exciting results demonstrate the effect of social inequality on skeletal BMD. By combining DXA-scanning and osteological analysis, we were able to elucidate new facts about life according to socioeconomic status in the medieval society of Norway.”
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Published19 minutes agoSharecloseShare pageCopy linkAbout sharingImage source, Getty ImagesBy Annabel RackhamBBC NewsSocial interaction could be key to kick-starting a fitness regime, US research suggests.After analysing data, including from the US Military Academy, scientists at Kean University recommended social activities that boosted interactions between less- and more-active people.When the less active interacted with those who exercised regularly, they felt encouraged, the researchers found.But those who were less social ended up exercising less.Regular exercise has already been cited as something that improves mental health significantly, with many finding group activity helpful.There are many ways to combine socialising and exercising, such as:walking with friendsplaying five-a-side taking a fitness class’It gives you accountability’ Exercising with a friend requires commitment and accountability, Andre Bates, of Barry’s Bootcamp, which holds group exercise classes across the UK, says.”It’s very easy not to go and exercise when you’re relying on yourself – but with a friend, you can use each other for motivation to make sure you stick at what you set out to do,” he says.Regular exercise ‘best for mental health”How football changed our mental health and lives'”You can make friends in a group exercise environment – and then if you’re not there for your usual 06:00 class on a Monday or Tuesday, they might ask, ‘Where are you?’ so there’s that little bit of guilt that makes sure you’re there next time.”Image source, Andre BatesAnd although some might be at a different level of fitness to others, everyone is trying to achieve the same thing.”Everyone is on their own individual journey,” Andre says. “Rather than looking at someone as competition, look at them as a benchmark of what you want to be and don’t be afraid to ask them about it and see how they got there.”We’re all pushing for the same purpose, whether it’s mental improvement, physical improvement, fitness or performance – everyone is here to improve.” ‘Really changed my life’ Kai Hunter, 25, who lives in Cardiff, started exercising regularly six months ago – after finding motivation from his group of friends. “Because I work from home, I didn’t really get out much – so I started to put on weight and wanted to do something about it as it was affecting my confidence quite a lot,” he tells BBC News.”I asked a few people in my social circle who were into fitness already how they had got into it – and asked for workout routines.”Kai also gained a lot of motivation sharing progress with friends in a group chat. Image source, Kai Hunter”All the people around me were always supporting me,” he says. “It was good to have that around me and to feel the results myself.”Kai’s friends have also helped him gain confidence going to the gym, which he used to “really struggle with doing”.”I’ve done a couple of leg-day workout routines with friends and have been shown how to use the different machines,” he says.”It’s really changed my life and helped a lot with my self-confidence and anxiety.”I wouldn’t ever have thought about stepping into a gym – whether with someone or not – and now I’m almost looking forward to it.”More on this storyRegular exercise ‘best for mental health’9 August 2018’How football changed our mental health and lives’10 OctoberDepression, anxiety, OCD – running helped us beat them4 August 2018

Using bacteria of the Bartonella henselae species, researchers from Goethe University, Frankfurt University Hospital, the Paul Ehrlich Federal Institute for Vaccines and Biomedicines in Langen, and the University of Oslo demonstrated for the first time that antibodies can prevent certain surface proteins of bacterial pathogens from entering host cells. The findings are important for the development of new drugs against highly resistant infectious agents.
Infections, especially those with highly resistant pathogens, pose a significant threat to human health. It is dangerous when pathogens manage to colonize the organism and subsequently cause severe infections. The first step in such an infection always consists of the pathogens attaching themselves to the host cells’ surface. From here, the infections spread, resulting, for example, in infections of deeper tissue layers and organs.
A group of scientists surrounding Prof. Volkhard Kempf from Frankfurt University Hospital’s Institute of Microbiology and Hospital Hygiene has now succeeded in blocking this adhesion mechanism in a bacterium, thereby preventing the infection of host cells. For this purpose, the researchers examined the pathogen Bartonella henselae, usually causing cat scratch disease. Transmitted by cats, the disease mainly affects young children, whose symptoms include swollen and hardened lymph nodes around the site of infection — usually following a scratch or bite injury caused by infected cats.
Bartonella bacteria infect so-called endothelial cells, which line the blood vessels. Via their surface protein Bartonella adhesin A (BadA), they attach themselves to a protein (fibronectin) of the so-called “extracellular matrix,” a network of protein fibers that lie on top of the endothelial cells.
To determine which parts of the BadA protein are important in the bacterial adhesion process, the researchers equipped Bartonella bacteria with various genetically modified BadA variants, among others, and then analyzed the extent to which these variants were still able to bind fibronectin. Once it was clear which BadA segments were responsible for the binding, the team produced antibodies against them, using cell culture experiments to show for the first time that such antibodies can prevent infection by such bacteria.
Prof. Volkhard Kempf explains: “Bartonella henselae is not a very dangerous pathogen, and in most cases, cat scratch disease does not require any specific medical treatment. However, for us Bartonella henselae is a very important model organism for far more dangerous pathogens such as Acinetobacter baumannii, a serious pathogen that usually causes wound infection or pneumonia and often shows resistance to several last-choice antibiotics. The BadA protein of Bartonella henselae belongs to the so-called ‘trimeric autotransporter adhesins’, which are also responsible for adhesion to human cells in Acinetobacter and a number of other pathogens. A drug-induced blocking of these adhesins is therefore a promising novel and future approach to combat dangerous bacterial infections.”
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