Will Reduction in Tau Protein Protect Against Parkinson’s and Lewy Body Dementias? (Neuroscience)

New results suggest the answer is no, implying that the role of tau in the pathogenesis of Lewy body dementias is distinct from Alzheimer’s disease.

Will a reduction in tau protein in brain neurons protect against Parkinson’s disease and Lewy body dementias? 

A new study, published in the journal eNeuro, suggests the answer is no. If this is borne out, that result differs from Alzheimer’s disease, where reducing endogenous tau levels in brain neurons is protective for multiple models of the disease — which further suggests that the role of tau in the pathogenesis of Lewy body dementias is distinct from Alzheimer’s disease.

Both Parkinson’s disease dementia and Lewy body dementia are characterized by intracellular aggregates of misfolded alpha-synuclein protein in brain neurons, and the two diseases together are the second most common cause of neurodegenerative dementia after Alzheimer’s.

University of Alabama at Birmingham researchers, led by Laura Volpicelli-Daley, Ph.D., associate professor of neurology, used a Parkinson’s disease model she developed 11 years ago. Volpicelli-Daley applies very low concentrations of altered alpha-synuclein, which has taken on a pathologic conformation, to either in vitro or in vivo neurons. The nerve cells take up some of the fibrils. Inside the cells, the altered alpha-synuclein acts as a seed to attract the soluble alpha-synuclein that is naturally present in neurons. This transforms soluble alpha-synuclein into pathological, insoluble aggregates that impair neuron function and lead to cell death. These modified alpha-synuclein inclusions share morphology with those found in the Parkinson’s disease brains after death.

This disease model — termed templated alpha-synuclein inclusion formation — was used to compare neurons that produce the normal amount of tau protein, against mutant neurons that lack one or both genes for tau, and thus have less or no tau protein. If endogenous tau contributes to disease progression, the heterozygous or knockout tau mutants were expected to show protection. However, the UAB researchers found no difference from the wild-type control.

In their results, the researchers first showed that there was indeed an interaction between tau and alpha-synuclein in the cells — both proteins localized in presynaptic terminals of primary culture neurons, and in the cortex of the mouse brain, which is consistent with previous findings from preparations of human brains, and with several in vitro studies showing that the two proteins interact with each other.

However, the reduction or complete absence of tau did not prevent fibril-induced alpha-synuclein inclusion formation in primary hippocampal neurons growing in vitro. In mice, reduction or absence of tau also did not prevent fibril-induced alpha-synuclein formation in the motor control or limbic areas of the brain, including the cortex, amygdala, hippocampus and the substantia nigra pars compacta, as measured six weeks or six months after fibril injections.

Laura Volpicelli-Daley, Ph.D., associate professor of neurology (Photo by: Lexi Coon)
Laura Volpicelli-Daley, Ph.D., associate professor of neurology (Photo by: Lexi Coon)

Finally, while the alpha-synuclein fibrils in the mouse model caused the death of half of the wild-type neurons that produce the neurotransmitter dopamine, the dopaminergic neurons in tau-heterozygous or tau-knockout mice showed the same amount of neuron death, which meant no protection. In addition, reducing tau did not have any major impact on behavioral phenotypes of mice with fibril-induced α-synuclein inclusions.

“Here, we have shown that reduction of endogenous tau did not influence formation of templated alpha-synuclein inclusion formation or the loss of dopamine neurons,” Volpicelli-Daley said. “This suggests that therapeutics directed to tau for Parkinson’s disease may be more complicated than tau reduction. This is unlike Alzheimer’s disease, where tau reduction has been suggested as a possible therapy.”

Co-authors with Volpicelli-Daley of the study, “Templated alpha-synuclein inclusion formation is independent of endogenous tau,” are Lindsay E. Stoyka, Casey L. Mahoney, Drake R. Thrasher, Drèson L. Russell, Anna K. Cook, Anner T. Harris, Ashwin Narayanan, Tiara P. Janado, David G. Standaert and Erik D. Roberson, UAB Center for Neurodegeneration and Experimental Therapeutics.

Support came from the Department of Defense Parkinson’s Research Program grant PD15032, and from National Institutes of Health grants NS102257, NS075487, NS108675, AG058458 and GM008361.


Reference: Lindsay E. Stoyka, Casey L. Mahoney, Drake R. Thrasher, Drèson L. Russell, Anna K. Cook, Anner T. Harris, Ashwin Narayanan, Tiara P. Janado, David G. Standaert, Erik D. Roberson and Laura A. Volpicelli-Daley, “Templated α-Synuclein Inclusion Formation Is Independent of Endogenous Tau”, eNeuro 10 May 2021, 8 (3) ENEURO.0458-20.2021; DOI: https://doi.org/10.1523/ENEURO.0458-20.2021


Provided by UAB

Common Antibiotic Found Useful in Accelerating Recovery in Tuberculosis Patients (Medicine)

Trial in 30 patients shows that doxycycline, in combination with tuberculosis treatment, reduced lung cavity size and increased other markers of recovery

Globally, an estimated 10 million people develop tuberculosis (TB) each year and the disease remains a leading cause of death from a single infectious agent. Standard short-course anti-TB treatment still requires a regimen of at least six months of antimicrobial drugs, and drug-resistant TB is an increasing public health threat. Even after the traces of TB disease are quashed, patients often suffer from significant sequelae, such as lung scarring. TB survivors have approximately three to four times greater mortality than their local population.

In pulmonary TB, the most common form of active TB disease, the Mycobacterium tuberculosis bacteria causes the formation of sites of high bacterial load, known as cavities. These cavities are poorly penetrated by TB drugs. After TB treatment is complete, there is likely to be tissue damage within the lungs that can lead to further lung problems such as permanent respiratory dysfunction leading to difficulty in breathing, stiffness in the lungs and bronchiectasis, which can make people cough up blood.

Researchers from NUS Yong Loo Lin School of Medicine’s Infectious Diseases Translational Research Programme have discovered that the use of a common antibiotic, doxycycline, in combination with TB drug treatment, reduces the size of lung cavities and accelerates markers of lung recovery.

In the Phase 2 double-blind trial conducted at the National University Hospital and TB Control Unit, the treatment was found to be safe, with side effects similar to patients on placebo pills. The study shows promise in delivering a new standard-of-care which can potentially prevent long term complications and the study team is seeking funds for a fully-powered larger scale Phase 3 trial to verify these findings.

“Pulmonary TB patients tend to suffer from lung damage after TB, which is associated with mortality, and poorer quality of life. Doxycycline is a cheap and widely available antibiotic that can decrease lung damage, and potentially improve quality of life for these patients,” said Assistant Professor Catherine Ong, Principal Investigator of the study and member of the Infectious Diseases Translational Research Programme (TRP) at NUS Medicine. The study findings were published in the Journal of Clinical Investigation.

Professor Paul Tambyah, who was also involved in the study and is Deputy Director of the Infectious Diseases TRP commented, “While we have been able to successfully treat most cases of TB for the last few decades, we have seen many people suffer the complications of the lung damage from the original TB infection. If this common drug, doxycycline, can help prevent the complications of “Long TB” (to use a term currently in vogue), this will really help a lot of patients in Singapore and worldwide.”

The Infectious Diseases TRP aims to provide a holistic, patient-centric approach to infectious diseases that are relevant to Singapore and the region. The Programme focuses on programmatic research areas including pathogen evolution and transmission, host-microbe interactions and vaccine and therapeutics development.

The study, “Doxycycline host-directed therapy in human pulmonary tuberculosis”, published in J Clin Invest. On June 2021. https://doi.org/10.1172/JCI141895.


Provided by National University of Singapore

The ‘Mozart Effect’ Shown To Reduce Epileptic Brain Activity, New Research Reveals (Neuroscience)

Music by Mozart has been shown to have an anti-epileptic effect on the brain and may be a possible treatment to prevent epileptic seizures, according to new research presented today at the 7th Congress of the European Academy of Neurology (EAN)

Music by Mozart has been shown to have an anti-epileptic effect on the brain and may be a possible treatment to prevent epileptic seizures, according to new research presented today at the 7th Congress of the European Academy of Neurology (EAN).

Researchers believe that the acoustic (physical) properties within the music are responsible for this effect.

Listening to the famous 18th century composer’s Sonata for Two Pianos K448 led to a 32% reduction in epileptiform discharges (EDs). These are electrical brain waves associated with epilepsy and can cause seizures or bursts of electrical activity that temporarily affect how the brain works.

A team led by Professor Ivan Rektor, from the Epilepsy Centre at the Hospital St Anne and CEITEC Masaryk University, Brno, Czech Republic, compared the effects of listening to Mozart’s Sonata for Two Pianos K448 with Haydn’s Symphony No 94. The effects on brain activity were measured by intracerebral electrodes that had been implanted in the brains of epilepsy patients prior to surgery.

“To our surprise, there were significant differences between the effects of listening to Mozart’s K448 and Haydn’s No 94”, commented Professor Rektor. “Listening to Mozart led to a 32% decrease in EDs, but listening to Haydn’s No 94 caused a 45% increase.”

“In the second part of our study, we set out to explain the ‘Mozart effect’ in epilepsy”, furthered Professor Rektor. The study found that men and women responded differently to the two pieces of music. Listening to Haydn’s music led to suppressed epileptiform discharges only in women; in the men, there was an increase of epileptiform discharges. The acoustic properties, such as the rhythm, dynamics and tone, showed that the acoustic features of music composition have a different effect on men and women.

“We believe the physical ‘acoustic’ features of the Mozart music affect brain oscillations – or brain waves – which is responsible for reducing EDs”.

Researchers have previously hypothesised that the Mozart effect in epilepsy was connected to the emotional effects of music, as dopamine (the main neurotransmitters of the brain’s reward system) is released when listening to music. Still, there is no direct proof of the mechanism.

“We found that the reduction in EDs was larger in the lateral temporal lobe, which the part of the brain which participates in translating acoustic signals, rather than in the mesiotemporal limbic region, which plays an important role in the emotional response to music.”

“The effects of listening to music on epilepsy cannot be explained by the effect of dopamine released by the reward system”, explained Professor Rektor. “Our patients were not music connoisseurs and said they were emotionally indifferent to the two pieces of music. There was, therefore, no reason to believe that K448 evoked more pleasure than No. 94.”

Experts believe the study’s findings could pave the way for individualised music therapies to be developed to prevent and control epileptic seizures in the future and have called for more research into the effects of music on the brain. Epilepsy affects 6 million people in Europe, and 15 million Europeans have one seizure at some time in their lives.

“Based on our research, we suggest studying the use of musical pieces with well-defined acoustic properties as a non-invasive method to reduce epileptic activity in patients with epilepsy”, concluded Professor Rektor.


References:

1. K Stillova et al. Mozart effect in epilepsy: Why is Mozart better than Haydn? Acoustic quality-based analysis of stereo electroencephalography. 2. World Health Organisation: https://www.who.int/mental_health/neurology/epilepsy/euro_report.pdf


Provided by Spink Health

Researchers Find Losartan is Not Effective in Reducing Hospitalization From Mild COVID-19 (Medicine)

The common blood pressure medication also does not appear to have any significant harmful side effects on patients with COVID-19

University of Minnesota Medical School researchers determined that the common blood pressure medication, losartan, is not effective in reducing hospitalization for mildly-ill COVID-19 outpatients.

In the multicenter, randomized, double-blinded clinical trial, non-hospitalized patients recently diagnosed with COVID-19 were given either losartan or a placebo and monitored for 15 days. The study’s results, which were published in EClinicalMedicine, showed that although losartan does not reduce the likelihood of hospitalization, the medication does not appear to worsen symptoms of COVID-19 or have any significant or harmful side effects on patients with mild COVID-19.

“Based on our results, there is no benefit to starting losartan for newly diagnosed outpatients with COVID-19, but those who are already taking the medication for pre-existing health conditions should feel safe continuing it,” said Michael Puskarich, MD, an associate professor in the Department of Emergency Medicine at the U of M Medical School and co-principal investigator of this study. He is also an emergency physician at Hennepin Healthcare.

Conflicting hypotheses since the start of the pandemic led this research team to investigate losartan as a potential treatment option. While some experts believed drugs like losartan may reduce inflammation and help those infected recover, others worried that the drug could worsen COVID-19 symptoms.

“Given SARS-CoV-2 binding with ACE2 there has been significant research interest into the utility of ACE and AT1R blocking agents to combat COVID-19. This study provides insight that for patients with mild COVID-19, who do not require hospital admission, that there is no benefit or harm from such agents,” said co-principal investigator Christopher Tignanelli, MD, MS, an assistant professor in the Department of Surgery at the U of M Medical School and critical care surgeon with M Health Fairview.

The same team has been working on another trial for inpatients to evaluate if losartan prevents lung injury in hospitalized patients with COVID-19 pneumonia. They have completed enrollment and are currently analyzing the data.

The study, “A multi-center phase II randomized clinical trial of losartan on symptomatic outpatients with COVID-19”, published in Lancet on June 17, 2021. DOI: https://doi.org/10.1016/j.eclinm.2021.100957


Provided by University of Minnesota Medical School

Study Reveals New Therapeutic Target For C. Difficile Infection (Medicine)

A new study paves the way for the development of next generation therapeutics for the prevention and treatment of Clostridioides difficile infection (CDI), the most frequent cause of healthcare-acquired gastrointestinal infections and death in developed countries.

Published today in Nature Communications, the study reveals the first 3D structure of the Clostridioides difficile toxin B (TcdB) in complex with chondroitin sulfate proteoglycan 4 (CSPG4), a human receptor.  The study was co-led by senior author Rongsheng Jin, PhD, a professor in the Department of Physiology & Biophysics at the University of California, Irvine, School of Medicine, and Min Dong, PhD, an associate professor at Harvard Medical School.

“TcdB is one of two homologous C. difficile exotoxins, which are major virulence factors responsible for the spread of C. difficile infections,” explained Jin.  “TcdB alone is capable of causing the full-spectrum of diseases associated with CDI in humans.”

Previous studies had identified CSPG4 as a potential receptor for TcdB, however the pathophysiological relevance and molecular details were unknown.  Results from this new study reveal a unique binding site involving TcdB and CSPG4, and also show that CSPG4-binding residues are highly conserved across most TcdB variants known to date.

CDI has become the most common cause of antibiotic-associated diarrhea and gastroenteritis-associated death in developed countries, accounting for approximately 223,900 infections, 12,800 deaths, and $1 billion in healthcare costs in the United States in 2017.  It is classified as one of the top five “urgent threats” by CDC. There is also growing global concern surrounding the emergence of rapidly spreading hypervirulent C. difficile strains, reminiscent of the current COVID pandemic.

“What these new findings tell us is that a rationally designed CSPG4-mimicking decoy could neutralize major TcdB variants, providing a unique therapeutic avenue for combating some of the hypervirulent C. difficile strains,” said Jin. In contrast, researchers also revealed that the therapeutic mechanism for bezlotoxumab, the only FDA approved anti-TcdB antibody, is sensitive to escaping mutations in some bacterial strains.

The current standard of care for CDI involves treatments using broad spectrum antibiotics, which often lead to frequent disease recurrence. While bezlotoxumab could reduce the recurrence rate of CDI in some patients, results from this and some earlier studies indicate it has weaker potency against some TcdB variants.

“We have designed a CSPG4-mimicking decoy based on the 3D structure we observed, which could neutralize major TcdB variants and is superior to bezlotoxumab on a major TcdB variant from a hypervirulent strain (TcdB2) in our studies. As a highly conserved cellular receptor of TcdB, a CSPG4 decoy molecule would be difficult for TcdB to escape, since any mutations that disrupt toxin binding to the decoy would also disrupt binding to its native receptors,” said Jin.

The team of researchers has also developed a family of recombinant protein therapeutics based on these new findings, as well as on an earlier discovery on how TcdB recognizes another human receptor Frizzled (FZD).

“We are now examining the therapeutic features of these novel antitoxin molecules, and we believe they could provide broad-spectrum protection and neutralization against most known TcdB variants, thus improving existing antibody therapeutics for CDI,” said Jin, whose team has filed a patent on these neutralizing molecules. 

This work was supported by part by the National Institutes of Health, Niedersächsisches Vorab, Deutsche Forschungsgemeinschaft, and the Burroughs Wellcome Fund.

Featured image: Clostridioides difficile (C. difficile) is classified as an urgent antibiotic resistance threat by the CDC. The 3-D structure shows how a key C. difficile toxin, TcdB (grey surface model), engages the human receptor CSPG4 (shown in green) for cell entry, and how an FDA-approved therapeutic antibody bezlotoxumab (shown in blue and purple) recognize two epitopes on TcdB. Some C. difficile hypervirulent strains evolve mutations in the bezlotoxumab-binding sites (blue and purple surface, while the mutated amino acids are colored red) that weaken the antibody potency. In contrast, the CSPG4-binding site on TcdB (gold surface) is highly conserved, suggesting a strategy to develop broad-spectrum therapeutics against TcdB. © UCI School of Medicine


Reference: Chen, P., Zeng, J., Liu, Z. et al. Structural basis for CSPG4 as a receptor for TcdB and a therapeutic target in Clostridioides difficile infection. Nat Commun 12, 3748 (2021). https://doi.org/10.1038/s41467-021-23878-3


Provided by UCI School of Medicine

How Protein Filaments Interact? (Chemistry)

University of Göttingen research team investigate microtubules

Just as the skeleton and muscles move the human body and hold its shape, all the cells of the body are stabilised and moved by a cellular skeleton. Unlike our skeleton, this cellular skeleton is a very dynamic structure, constantly changing and renewing itself. It consists of different types of protein filaments, which include intermediate filaments and microtubules. Now, a research team from the University of Göttingen is the first to succeed in observing a direct interaction between microtubules and intermediate filaments outside the cell, and also in quantitatively measuring this interaction. The results of the study were published in Nature Communications.

Microtubules are dynamic filaments that constantly grow and shrink again and, in this way, are responsible for many important processes in cells. The research team observed that intermediate filaments stabilise microtubules: when intermediate filaments are added to microtubules, shrinkage is suppressed and thus the lifespan of the microtubules is extended. To investigate whether this is actually due to direct interactions between the two filaments, a single microtubule was positioned crossed with a single intermediate filament.

Dr Laura Schaedel, who shares first authorship of the publication with Charlotta Lorenz (PhD student at the Institute for X-ray Physics at the University of Göttingen), explains: “The intermediate filament was ‘pulled’ over the microtubule like a bow over a violin string.” Lorenz adds, “This allows the two filaments to bind to each other. However, this bond is broken again shortly afterwards due to the pulling. The process of ‘tearing apart’ provides information about the strength of the bond.” Professor Stefan Klumpp from the Institute for the Dynamics of Complex Systems at Göttingen University, who led the project together with Professor Sarah Köster from the Institute for X-ray Physics, says, “In addition, we used models and simulations to show that the direct interaction leads to stabilisation.” The stabilisation of dynamic microtubules can be an important issue for biological cells, for example to regulate their local stability. “The interactions that we observed are important because they enable better understanding of cellular processes,” says Köster.

These results are in turn relevant for understanding many other processes, such as those involved in diseased cells. The new method to take direct measurements of the actual interaction of two different biopolymers can also be applied to other protein filaments, as well as to non-biological fibres.


Original publication: Laura Schaedel*, Charlotta Lorenz*, Anna V. Schepers, Stefan Klumpp#, and Sarah Köster#: Vimentin Intermediate Filaments Stabilize Dynamic Microtubules by Direct Interactions, Nat. Commun. 2021. Doi: 10.1038/s41467-021-23523-z . Text also available here: https://www.nature.com/articles/s41467-021-23523-z


Provided by University of Göttingen

New Study Uncovers Details Behind the Body’s Response to Stress (Medicine)

Findings could lead to new treatments for post-traumatic stress disorder and other conditions

The biological mechanisms behind stress-related psychiatric conditions, including major depressive disorder and post-traumatic stress disorder (PTSD), are poorly understood.

New research now details the interplay between proteins involved in controlling the body’s stress response and points to potential therapeutic targets when this response goes awry. The study, which was conducted by an international team led by investigators at McLean Hospital, appears in the journal Cell Reports.

Study Highlights

  • New research reveals how key proteins interact to regulate the body’s response to stress
  • Targeting these proteins may help treat or prevent stress-related psychiatric disorders

“A dysregulated stress response of the body can be damaging for the brain and promote susceptibility to mood and anxiety disorders,” said lead author Jakob Hartmann, PhD. Hartmann is an assistant neuroscientist in the Neurobiology of Fear Laboratory at McLean and an instructor in psychiatry at Harvard Medical School.

“A key brain region involved in the regulation of the stress response is the hippocampus,” said Hartmann. “The idea for this study occurred to us when we noticed interesting distinctions in hippocampal localization of three important stress-regulating proteins.”

The researchers’ experiments in non-human tissue and postmortem brain tissue revealed how these proteins—the glucocorticoid receptor (GR), the mineralocorticoid receptor (MR), and the FK506-binding protein 51 (FKBP5)—interact with each other.

Specifically, MRs, rather than GRs, control the production of FKBP5 under normal conditions. FKBP5 decreases GRs’ sensitivity to binding stress hormones during stressful situations. FKBP5 appears to fine-tune the stress response by acting as a mediator of the MR:GR balance in the hippocampus.

“Our findings suggest that therapeutic targeting of GR, MR, and FKBP5 may be complementary in manipulating central and peripheral regulation of stress,” said senior author Kerry J. Ressler, MD, PhD. Ressler is the chief scientific officer at McLean Hospital, chief of McLean’s Division of Depression and Anxiety Disorders, and a professor in psychiatry at Harvard Medical School.

“Moreover, our data further underline the important but largely unappreciated role of MR signaling in stress-related psychiatric disorders,” added Ressler. “The findings of this study will open new directions for future research.”

This study was supported by:

  • NARSAD Young Investigator Grant from the Brain & Behavior Research Foundation (awarded to Hartmann, grant no. 24774)
  • National Institutes of Health (R01MH108665, P50MH115874)
  • Intramural Research Program of the National Institute of Environmental Health Sciences, National Institutes of Health (Z01ES100221, awarded to Serena M. Dudek, PhD)
  • Research grants Q10 from NICHD (R21HD088931, R21HD097524), NIMH (R21MH117609), and ERA-Net Neuron (01EW2003), awarded to Torsten Klengel, MD, PhD

Provided by McLean Hospital

New Research Adds A Wrinkle to Our Understanding Of the Origins of Matter in the Milky Way (Cosmology)

New information about how different cosmic rays arrive at Earth hints at unique sources or propagation methods for different elements

New findings published this week in Physical Review Letters suggest that carbon, oxygen, and hydrogen cosmic rays travel through the galaxy toward Earth in a similar way, but, surprisingly, that iron arrives at Earth differently. Learning more about how cosmic rays move through the galaxy helps address a fundamental, lingering question in astrophysics: How is matter generated and distributed across the universe?

“So what does this finding mean?” asks John Krizmanic, a senior scientist with UMBC’s Center for Space Science and Technology (CSST). “These are indicators of something interesting happening. And what that something interesting is we’re going to have to see.”

Cosmic rays are atomic nuclei–atoms stripped of their electrons–that are constantly whizzing through space at nearly the speed of light. They enter Earth’s atmosphere at extremely high energies. Information about these cosmic rays can give scientists clues about where they came from in the galaxy and what kind of event generated them.

An instrument on the International Space Station (ISS) called the Calorimetric Electron Telescope (CALET) has been collecting data about cosmic rays since 2015. The data include details such as how many and what kinds of atoms are arriving, and how much energy they’re arriving with. The American, Italian, and Japanese teams that manage CALET, including UMBC’s Krizmanic and postdoc Nick Cannady, collaborated on the new research.

Iron on the move

Cosmic rays arrive at Earth from elsewhere in the galaxy at a huge range of energies–anywhere from 1 billion volts to 100 billion billion volts. The CALET instrument is one of extremely few in space that is able to deliver fine detail about the cosmic rays it detects. A graph called a cosmic ray spectrum shows how many cosmic rays are arriving at the detector at each energy level. The spectra for carbon, oxygen, and hydrogen cosmic rays are very similar, but the key finding from the new paper is that the spectrum for iron is significantly different.

There are several possibilities to explain the differences between iron and the three lighter elements. The cosmic rays could accelerate and travel through the galaxy differently, although scientists generally believe they understand the latter, Krizmanic says.

“Something that needs to be emphasized is that the way the elements get from the sources to us is different, but it may be that the sources are different as well,” adds Michael Cherry, physics professor emeritus at Louisiana State University (LSU) and a co-author on the new paper. Scientists generally believe that cosmic rays originate from exploding stars (supernovae), but neutron stars or very massive stars could be other potential sources.

Next-level precision

An instrument like CALET is important for answering questions about how cosmic rays accelerate and travel, and where they come from. Instruments on the ground or balloons flown high in Earth’s atmosphere were the main source of cosmic ray data in the past. But by the time cosmic rays reach those instruments, they have already interacted with Earth’s atmosphere and broken down into secondary particles. With Earth-based instruments, it is nearly impossible to identify precisely how many primary cosmic rays and which elements are arriving, plus their energies. But CALET, being on the ISS above the atmosphere, can measure the particles directly and distinguish individual elements precisely.

Iron is a particularly useful element to analyze, explains Cannady, a postdoc with CSST and a former Ph.D. student with Cherry at LSU. On their way to Earth, cosmic rays can break down into secondary particles, and it can be hard to distinguish between original particles ejected from a source (like a supernova) and secondary particles. That complicates deductions about where the particles originally came from.

“As things interact on their way to us, then you’ll get essentially conversions from one element to another,” Cannady says. “Iron is unique, in that being one of the heaviest things that can be synthesized in regular stellar evolution, we’re pretty certain that it is pretty much all primary cosmic rays. It’s the only pure primary cosmic ray, where with others you’ll have some secondary components feeding into that as well.”

“Made of stardust”

Measuring cosmic rays gives scientists a unique view into high-energy processes happening far, far away. The cosmic rays arriving at CALET represent “the stuff we’re made of. We are made of stardust,” Cherry says. “And energetic sources, things like supernovas, eject that material from their interiors, out into the galaxy, where it’s distributed, forms new planets, solar systems, and… us.”

“The study of cosmic rays is the study of how the universe generates and distributes matter, and how that affects the evolution of the galaxy,” Krizmanic adds. “So really it’s studying the astrophysics of this engine we call the Milky Way that’s throwing all these elements around.”

A global effort

The Japanese space agency launched CALET and today leads the mission in collaboration with the U.S. and Italian teams. In the U.S., the CALET team includes researchers from LSU; NASA Goddard Space Flight Center; UMBC; University of Maryland, College Park; University of Denver; and Washington University.The new paper is the fifth from this highly successful international collaboration published in PRL, one of the most prestigious physics journals.

CALET was optimized to detect cosmic ray electrons, because their spectrum can contain information about their sources. That’s especially true for sources that are relatively close to Earth in galactic terms: within less than one-thirtieth the distance across the Milky Way. But CALET also detects the atomic nuclei of cosmic rays very precisely. Now those nuclei are offering important insights about the sources of cosmic rays and how they got to Earth.

“We didn’t expect that the nuclei – the carbon, oxygen, protons, iron – would really start showing some of these detailed differences that are clearly pointing at things we don’t know,” Cherry says.

The latest finding creates more questions than it answers, emphasizing that there is still more to learn about how matter is generated and moves around the galaxy. “That’s a fundamental question: How do you make matter?” Krizmanic says. But, he adds, “That’s the whole point of why we went in this business, to try to understand more about how the universe works.”


Reference: O. Adriani et al. (CALET Collaboration), “Measurement of the Iron Spectrum in Cosmic Rays from 10  GeV/n to 2.0  TeV/n with the Calorimetric Electron Telescope on the International Space Station”, Phys. Rev. Lett. 126, 241101 – Published 14 June 2021. DOI: https://doi.org/10.1103/PhysRevLett.126.241101


Provided by UMBC

What Boosts Star Formation In Disk Galaxies? (Cosmology)

Jing Wang and colleagues investigated the impact of spiral structure on star formation using a sample of 2226 nearby bright disk galaxies. They found that, spiral arms help boost the star formation efficiency in disk galaxies and stronger arms are associated with higher specific star formation rate (SFR). Their study recently appeared in Arxiv.

Galaxy main sequence (or galactic main sequence or star formation main sequence or SF main sequence) is a term for the relationship between a galaxy’s star formation (SFR) and its stellar mass or you can say the relationship between SFR and stellar mass in star forming disk galaxies, displays a degree of regularity, which is often expressed as ‘Galaxy main sequence’.

Spiral arms are regions of stars that extend from the center of spiral and barred spiral galaxies. They may play an intertwined role with gas content and gas compression, and hence with the overall star formation process. Studying the interdependence of spiral structure on global star formation sheds light not only on the star formation process but also on how spiral arms evolve in disk galaxies.

“Recently, Yu & Ho analyze the spiral structure of a large, comprehensive sample of nearby galaxies. We use their catalog of spiral arm strength to study the impact of spiral structure on the global star formation process of disk galaxies.”

Examining the relationship between spiral arms, star formation rate (SFR), and stellar mass, they found that arm strength correlates well with the variation of SFR as a function of stellar mass. Arms are stronger above the star-forming galaxy main sequence (MS) and weaker below it: arm strength increases with higher log (SFR/SFRMS), where SFRMS is the SFR along the MS. Likewise, stronger arms are associated with higher specific SFR.

“This finding is confirmed for the full sample of 4378 disk galaxies using the u − r color index, showing that the position of spiral galaxies on the blue cloud depends systematically on their arm strength.”

They also found that, the dependence of log (SFR/SFRMS) on arm strength is independent of other galaxy structural parameters, such as bar strength, global stellar mass concentration (related to bulge dominance), and stellar mass surface density.

Figure 1: Systematic bias of spiral arm strength (log sarm) as a function of signal-to-noise ratio (SNR). The solid curve and shaded area mark the mean and scatter for a given SNR. © Jing Wang et al.

In addition, for the subset of galaxies with cold gas measurements, it has been found that spiral arm strength positively correlates with H I and H2 mass fraction, even after removing the mutual dependence of these quantities on log (SFR/SFRMS).

“We argue that the sensitivity of arm strength to gas content is in line with the notion that spiral arms are maintained by dynamical cooling provided by gas damping.”

Moreover, they showed that stronger arms lead to higher log (SFR/SFRMS) for a given gas fraction. This results in a trend of increasing arm strength with shorter gas depletion time, independent of stellar mass surface density. These correlations suggested that spiral arms enhance star formation efficiency, and that the relationship between spiral arms and star formation is driven only in part by gas fraction. Spiral arms and gas content play an intertwined role in disk galaxies.

“On the one hand, dissipation by gas damping maintains spiral structure, and on the other hand, spiral structure helps boost the star formation efficiency of the cold gas reservoir. This accounts for systematic variation of spiral arm strength on the star-forming MS.”


Reference: Si-Yue Yu, Luis C. Ho and Jing Wang, “Spiral Structure Boosts Star Formation In Disk Galaxies”, Arxiv, pp. 1-11, 2021. arXiv:2106.09715


Note for editors of other websites: To reuse this article fully or partially kindly give credit either to our author/editor S. Aman or provide a link of our article