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An exploding white dwarf star blasted itself out of its orbit with another star in a 'partial supernova' and is now hurtling across our galaxy, according to a new study from the University of Warwick.

It opens up the possibility of many more survivors of supernovae travelling undiscovered through the Milky Way, as well as other types of supernovae occurring in other galaxies that astronomers have never seen before.

Reported today (15 July) in Monthly Notices of the Royal Astronomical Society the research, funded by the Leverhulme Trust and Science and Technology Facilities Council (STFC), analysed a white dwarf that was previously found to have an unusual atmospheric composition. It reveals that the star was most likely a binary star that survived its supernova explosion, which sent it and its companion flying through the Milky Way in opposite directions.

White dwarfs are the remaining cores of red giants after these huge stars have died and shed their outer layers, cooling over the course of billions of years. The majority of white dwarfs have atmospheres composed almost entirely of hydrogen or helium, with occasional evidence of carbon or oxygen dredged up from the star's core.

This star, designated SDSS J1240+6710 and discovered in 2015, seemed to contain neither hydrogen nor helium, composed instead of an unusual mix of oxygen, neon, magnesium and silicon. Using the Hubble Space Telescope, the scientists also identified carbon, sodium, and aluminium in the star's atmosphere, all of which are produced in the first thermonuclear reactions of a supernova.

However, there is a clear absence of what is known as the 'iron group' of elements, iron, nickel, chromium and manganese. These heavier elements are normally cooked up from the lighter ones, and make up the defining features of thermonuclear supernovae. The lack of iron group elements in SDSSJ1240+6710 suggests that the star only went through a partial supernova before the nuclear burning died out.

The scientists were able to measure the white dwarf's velocity and found that it is travelling at 900,000 kilometres per hour. It also has a particularly low mass for a white dwarf - only 40% the mass of our Sun - which would be consistent with the loss of mass from a partial supernova.

Lead author Professor Boris Gaensicke from the Department of Physics at the University of Warwick said: "This star is unique because it has all the key features of a white dwarf but it has this very high velocity and unusual abundances that make no sense when combined with its low mass.

"It has a chemical composition which is the fingerprint of nuclear burning, a low mass and a very high velocity: all of these facts imply that it must have come from some kind of close binary system and it must have undergone thermonuclear ignition. It would have been a type of supernova, but of a kind that that we haven't seen before."

The scientists theorise that the supernova disrupted the white dwarf's orbit with its partner star when it very abruptly ejected a large proportion of its mass. Both stars would have been carried off in opposite directions at their orbital velocities in a kind of slingshot manoeuvre. That would account for the star's high velocity.

Professor Gaensicke adds: "If it was a tight binary and it underwent thermonuclear ignition, ejecting quite a lot of its mass, you have the conditions to produce a low mass white dwarf and have it fly away with its orbital velocity."

The best studied thermonuclear supernovae are the "Type Ia", which led to the discovery of dark energy, and are now routinely used to map the structure of the Universe. But there is growing evidence that thermonuclear supernovae can happen under very different conditions.

SDSSJ1240+6710 may be the survivor of a type of supernova that hasn't yet been "caught in the act". Without the radioactive nickel that powers the long-lasting afterglow of the Type Ia supernovae, the explosion that sent SDSS1240+6710 hurtling across our Galaxy would have been a brief flash of light that would have been difficult to discover.

Professor Gaensicke adds: "The study of thermonuclear supernovae is a huge field and there's a vast amount of observational effort into finding supernovae in other galaxies. The difficulty is that you see the star when it explodes but it's very difficult to know the properties of the star before it exploded.

"We are now discovering that there are different types of white dwarf that survive supernovae under different conditions and using the compositions, masses and velocities that they have, we can figure out what type of supernova they have undergone. There is clearly a whole zoo out there. Studying the survivors of supernovae in our Milky Way will help us to understand the myriads of supernovae that we see going off in other galaxies."

Professor S.O. Kepler of Universidade Federal do Rio Grande do Sul, Brazil, and who originally discovered this star, said: "The fact that such a low mass white dwarf went through carbon burning is a testimony of the effects of interacting binary evolution and its effect on the chemical evolution of the Universe."

Dr Roberto Raddi of Universitat Politècnica de Catalunya, Spain, who carried out the kinematic analysis, said: "Once again, the synergy between very precise Gaia astrometry and spectroscopic analysis have helped to constrain the striking properties of a unique white dwarf, which probably formed in a thermonuclear supernova and was ejected at high velocity as consequence of the explosion."

World's population likely to shrink after mid-century, forecasting major shifts in global population and economic power - new analysis, published in The Lancet forecasts global, regional, and national populations, mortality, fertility, and migration for 195 countries worldwide.

The USA is projected to have population growth until just after mid-century (364 million in 2062), followed by a moderate decline of less than 10% to 336 million by 2100--the world's fourth most populous country.

The USA's total fertility rate--which represents the average number of children a woman delivers over her lifetime--is predicted to steadily decline from 1.8 in 2017 to 1.5 in 2100; well below the minimum birth rate (2.1) considered necessary to maintain existing population levels long-term without immigration.

In 2100, the USA is forecasted to have the fourth largest working-age population in the world (around 181 million), after India, Nigeria, and China (figure 8)--with immigration likely sustaining the US workforce, with the largest net immigration in absolute numbers (more than half a million more people are estimated to immigrate to the USA in 2100 than will emigrate out). However, the researchers warn that US liberal immigration policies have faced a political backlash in recent years, threatening the country's potential to sustain population and economic growth.

The forecasting model predicts that while the USA had the largest economy in 2017, China is set to replace it in 2035, but the USA is forecasted to once again become the largest economy in 2098--bolstered by immigration (figure 9). Among the 10 countries with the largest populations in 2017 or 2100, the USA is predicted to have the fifth highest life expectancy in 2100 (82.3 years), up from 78.4 in 2017 (appendix 2, section 3).

Please find below: 1) Media release, 2) Access to the Article + linked Comments 3) Country data 4) Infographics. For further information, please contact The Lancet press office (pressoffice@lancet.com)

By 2100, projected fertility rates in 183 of 195 countries will not be high enough to maintain current populations without liberal immigration policies.

World population forecasted to peak in 2064 at around 9.7 billion people and fall to 8.8 billion by century's end, with 23 countries seeing populations shrink by more than 50%, including Japan, Thailand, Italy, and Spain.

Dramatic declines in working age-populations are predicted in countries such as India and China, which will hamper economic growth and lead to shifts in global powers.

Liberal immigration policies could help maintain population size and economic growth even as fertility falls.

Authors warn response to population decline must not compromise progress on women's freedom and reproductive rights.

Improvements in access to modern contraception and the education of girls and women are generating widespread, sustained declines in fertility, and world population will likely peak in 2064 at around 9.7 billion, and then decline to about 8.8 billion by 2100--about 2 billion lower than some previous estimates [1], according to a new study published in The Lancet.

The modelling research uses data from the Global Burden of Disease Study 2017 to project future global, regional, and national population. Using novel methods for forecasting mortality, fertility, and migration, the researchers from the Institute for Health Metrics and Evaluation (IHME) at the University of Washington's School of Medicine estimate that by 2100, 183 of 195 countries will have total fertility rates (TFR), which represent the average number of children a woman delivers over her lifetime, below replacement level of 2.1 births per woman. This means that in these countries populations will decline unless low fertility is compensated by immigration.

The new population forecasts contrast to projections of 'continuing global growth' by the United Nations Population Division [1], and highlight the huge challenges to economic growth of a shrinking workforce, the high burden on health and social support systems of an ageing population, and the impact on global power linked to shifts in world population.

The new study also predicts huge shifts in the global age structure, with an estimated 2.37 billion individuals over 65 years globally in 2100, compared with 1.7 billion under 20 years, underscoring the need for liberal immigration policies in countries with significantly declining working age populations.

"Continued global population growth through the century is no longer the most likely trajectory for the world's population", says IHME Director Dr. Christopher Murray, who led the research. "This study provides governments of all countries an opportunity to start rethinking their policies on migration, workforces and economic development to address the challenges presented by demographic change." [2]

IHME Professor Stein Emil Vollset, first author of the paper, continues, "The societal, economic, and geopolitical power implications of our predictions are substantial. In particular, our findings suggest that the decline in the numbers of working-age adults alone will reduce GDP growth rates that could result in major shifts in global economic power by the century's end. Responding to population decline is likely to become an overriding policy concern in many nations, but must not compromise efforts to enhance women's reproductive health or progress on women's rights." [2]

Dr Richard Horton, Editor-in-Chief, The Lancet, adds: "This important research charts a future we need to be planning for urgently. It offers a vision for radical shifts in geopolitical power, challenges myths about immigration, and underlines the importance of protecting and strengthening the sexual and reproductive rights of women. The 21st century will see a revolution in the story of our human civilisation. Africa and the Arab World will shape our future, while Europe and Asia will recede in their influence. By the end of the century, the world will be multipolar, with India, Nigeria, China, and the US the dominant powers. This will truly be a new world, one we should be preparing for today." [2]

Accelerating decline in fertility worldwide

The global TFR is predicted to steadily decline, from 2.37 in 2017 to 1.66 in 2100--well below the minimum rate (2.1) considered necessary to maintain population numbers (replacement level)-- with rates falling to around 1.2 in Italy and Spain, and as low as 1.17 in Poland.

Even slight changes in TFR translate into large differences in population size in countries below the replacement level--increasing TFR by as little as 0.1 births per woman is equivalent to around 500 million more individuals on the planet in 2100.

Much of the anticipated fertility decline is predicted in high-fertility countries, particularly those in sub-Saharan Africa where rates are expected to fall below the replacement level for the first time--from an average 4.6 births per woman in 2017 to just 1.7 by 2100. In Niger, where the fertility rate was the highest in the world in 2017--with women giving birth to an average of seven children--the rate is projected to decline to around 1.8 by 2100.

Nevertheless, the population of sub-Saharan Africa is forecast to triple over the course of the century, from an estimated 1.03 billion in 2017 to 3.07 billion in 2100--as death rates decline and an increasing number of women enter reproductive age. North Africa and the Middle East is the only other region predicted to have a larger population in 2100 (978 million) than in 2017 (600 million).

Many of the fastest-shrinking populations will be in Asia and central and eastern Europe. Populations are expected to more than halve in 23 countries and territories, including Japan (from around 128 million people in 2017 to 60 million in 2100), Thailand (71 to 35 million), Spain (46 to 23 million), Italy (61 to 31 million), Portugal (11 to 5 million), and South Korea (53 to 27 million). An additional 34 countries are expected to have population declines of 25 to 50%, including China (1.4 billion in 2017 to 732 million in 2100; see table).

Huge shifts in global age structure - with over 80s outnumbering under 5s two to one

As fertility falls and life expectancy increases worldwide, the number of children under 5 years old is forecasted to decline by 41% from 681 million in 2017 to 401 million in 2100, whilst the number of individuals older than 80 years is projected to increase six fold, from 141 million to 866 million. Similarly, the global ratio of adults over 80 years to each person aged 15 years or younger is projected to rise from 0.16 in 2017 to 1.50 in 2100, in countries with a population decline of more than 25%.

Furthermore, the global ratio of non-working adults to workers was around 0.8 in 2017, but is projected to increase to 1.16 in 2100 if labour force participation by age and sex does not change.

"While population decline is potentially good news for reducing carbon emissions and stress on food systems, with more old people and fewer young people, economic challenges will arise as societies struggle to grow with fewer workers and taxpayers, and countries' abilities to generate the wealth needed to fund social support and health care for the elderly are reduced", says Vollset. [2]

Declining working-age populations could see major shifts in size of economies

The study also examined the economic impact of fewer working-age adults for all countries in 2017. While China is set to replace the USA in 2035 with the largest total gross domestic product (GDP) globally, rapid population decline from 2050 onward will curtail economic growth. As a result, the USA is expected to reclaim the top spot by 2098, if immigration continues to sustain the US workforce (figure 9).

Although numbers of working-age adults in India are projected to fall from 762 million in 2017 to around 578 million in 2100, it is expected to be one of the few – if only – major power in Asia to protect its working-age population over the century. It is expected to surpass China’s workforce population in the mid-2020s (where numbers of workers are estimated to decline from 950 million in 2017 to 357 million in 2100)—rising up the GDP rankings from 7th to 3rd (figure 8).

Sub-Saharan Africa is likely to become an increasingly powerful continent on the geopolitical stage as its population rises. Nigeria is projected to be the only country among the world’s 10 most populated nations to see its working-age population grow over the course of the century (from 86 million in 2017 to 458 million in 2100), supporting rapid economic growth and its rise in GDP rankings from 23rd place in 2017 to 9th place in 2100 (figure 8).

While the UK, Germany, and France are expected to remain in the top 10 for largest GDP worldwide at the turn of the century, Italy (from rank 9th in 2017 to 25th in 2100) and Spain (from 13th to 28th) are projected to fall down the rankings, reflecting much greater population decline (figure 9).

Liberal immigration could help sustain population size and economic growth

The study also suggests that population decline could be offset by immigration, with countries that promote liberal immigration better able to maintain their population size and support economic growth, even in the face of declining fertility rates.

The model predicts that some countries with fertility lower than replacement level, such as the USA, Australia, and Canada, will probably maintain their working-age populations through net immigration (see appendix 2 section 4). Although the authors note that there is considerable uncertainty about these future trends.

"For high-income countries with below-replacement fertility rates, the best solutions for sustaining current population levels, economic growth, and geopolitical security are open immigration policies and social policies supportive of families having their desired number of children", Murray says. "However, a very real danger exists that, in the face of declining population, some countries might consider policies that restrict access to reproductive health services, with potentially devastating consequences. It is imperative that women's freedom and rights are at the top of every government's development agenda." [2]

The authors note some important limitations, including that while the study uses the best available data, predictions are constrained by the quantity and quality of past data. They also note that past trends are not always predictive of what will happen in the future, and that some factors not included in the model could change the pace of fertility, mortality, or migration. For example, the COVID-19 pandemic has affected local and national health systems throughout the world, and caused over half a million deaths. However, the authors believe the excess deaths caused by the pandemic are unlikely to significantly alter longer term forecasting trends of global population.

Writing in a linked Comment, Professor Ibrahim Abubakar, University College London (UCL), UK, and Chair of Lancet Migration (who was not involved in the study) [3], says:"Migration can be a potential solution to the predicted shortage of working-age populations. While demographers continue to debate the long-term implications of migration as a remedy for declining TFR, for it to be successful, we need a fundamental rethink of global politics. Greater multilateralism and a new global leadership should enable both migrant sending and migrant-receiving countries to benefit, while protecting the rights of individuals. Nations would need to cooperate at levels that have eluded us to date to strategically support and fund the development of excess skilled human capital in countries that are a source of migrants. An equitable change in global migration policy will need the voice of rich and poor countries. The projected changes in the sizes of national economies and the consequent change in military power might force these discussions."

He adds: "Ultimately, if Murray and colleagues' predictions are even half accurate, migration will become a necessity for all nations and not an option. The positive impacts of migration on health and economies are known globally. The choice that we face is whether we improve health and wealth by allowing planned population movement or if we end up with an underclass of imported labour and unstable societies. The Anthropocene has created many challenges such as climate change and greater global migration. The distribution of working-age populations will be crucial to whether humanity prospers or withers."

WASHINGTON (July 14, 2020)--Silver strands and graying hair is a sign of aging in humans, but things aren't so simple for our closest ape relatives--the chimpanzee. A new study published today in the journal PLOS ONE by researchers at the George Washington University found graying hair is not indicative of a chimpanzee's age.

This research calls into question the significance of the graying phenotype in wild non-human species. While graying is among the most salient traits a chimpanzee has--the world's most famous chimpanzee was named David Greybeard--there is significant pigmentation variation among individuals. Graying occurs until a chimpanzee reaches midlife and then plateaus as they continue to age, according to Elizabeth Tapanes, a Ph.D. candidate in the GW Department of Anthropology and lead author of the study.

"With humans, the pattern is pretty linear, and it's progressive. You gray more as you age. With chimps that's really not the pattern we found at all," Tapanes said. "Chimps reach this point where they're just a little salt and peppery, but they're never fully gray so you can't use it as a marker to age them."

The researchers gathered photos of two subspecies of wild and captive chimpanzees from their collaborators in the field to test this observation. They visually examined photos of the primates, evaluated how much visible gray hair they had and rated them accordingly. The researchers then analyzed that data, comparing it to the age of the individual chimpanzees at the time the photos were taken.

The researchers hypothesize there could be several reasons why chimpanzees did not evolve graying hair patterns similar to humans. Their signature dark pigmentation might be critical for thermoregulation or helping individuals identify one another.

Dr. Brenda Bradley, an associate professor of anthropology, is the senior author on the paper. This research dates back to an observation Dr. Bradley made while visiting a field site in Uganda five years ago. As she was learning the names of various wild chimpanzees, she found herself making assumptions about how old they were based on their pigmentation. On-site researchers told her that chimps did not go gray the same way humans do. Dr. Bradley was curious to learn if that observation could be quantified.

There has been little previous research on pigmentation loss in chimpanzees or any wild mammals, Dr. Bradley said. Most existing research on human graying is oriented around the cosmetic industry and clinical dermatology.

"There's a lot of work done on trying to understand physiology and maybe how to override it," Dr. Bradley said. "But very little work done on an evolutionary framework for why is this something that seems to be so prevalent in humans."

The researchers plan to build on their findings by looking at the pattern of gene expression in individual chimpanzee hairs. This will help determine whether changes are taking place at the genetic level that match changes the eye can see.

This study comes ahead of World Chimpanzee Day on July 14. GW's faculty and student researchers make contributions to our global understanding of chimpanzees and primates as part of the GW Center for the Advanced Study of Human Paleobiology. Through various labs, investigators study the evolution of social behavior in the chimpanzees and bonobos, the evolution of primate brain structure, and lead on-the-ground projects at the Gombe Stream Research Center in Tanzania. Dr. Bradley's lab is also currently working on research about color vision and hair variation in lemurs.

UTICA, NY-- Nearly 20% of all COVID-19-associated deaths are from cardiac complications, yet the mechanisms from which these complications arise have remained a topic of debate in the cardiology community. One hypothesis centers on the infection of the heart itself, but the understanding of which cells may be infected is unclear. To address this, MMRI Assistant Professor Dr. Nathan Tucker, in collaboration with the Broad Institute, the University of Pennsylvania, and Bayer US, report the distribution of the SARS-CoV-2 receptor in a manuscript titled, "Myocyte upregulation of ACE2 in cardiovascular disease" published in the journal, Circulation.

COVID-19 (SARS-CoV-2) infects cells through a particular cellular molecule, termed ACE2. To assess levels of this molecule in different patient populations and in response to common hypertension medications (ACE inhibitors), the group applied state-of-the-art single nucleus sequencing technologies in human heart samples. From these studies, they were able to conclude that the amount of the viral receptor is increased in patients with pre-existing cardiac conditions, but only in the beating cells of the heart, termed cardiomyocytes. Additionally, they found that the effect of anti-hypertension medications, termed ACE inhibitors, do not appreciably affect the levels of ACE2 in a way that would support any changes in clinical use of these medications.

"This is but an early step in our understanding of cardiac pathology in people who contract COVID-19," said Tucker, the first author of the manuscript. "There's much more work to do. As an example, we are already working to establish direct evidence of cardiac infection, while also examining receptor distributions in other populations and through other approaches. We hope to provide more information as soon as we are able."

While just a piece in a very complex puzzle, this study offers a potential explanation as to why patients with pre-existing heart disease are more likely to suffer severe cardiac symptoms from COVID-19 infection. Importantly, it also provides data on the effects of anti-hypertensive medications, supporting the previous statements urging continued use of ACE inhibitors from the American Heart Association, American College of Cardiology, and European Society of Cardiology with additional human-derived data.

Volume 11, Issue 28 of Oncotarget features "Lipid and protein tumor markers for head and neck squamous cell carcinoma identified by imaging mass spectrometry" by Schmidt et, al. which reported that the authors used MALDI imaging mass spectrometry and immunohistochemistry to seek tumor-specific expression of proteins and lipids in HNSCC samples.

Among low molecular weight proteins visualized, S100A8 and S100A9 were found to be expressed in the regions of tumor tissue but not in the surrounding healthy stroma of a post-operative microdissected tissue.

Furthermore, the marker potential of lysophospholipids was supported by elevated expression levels of the lysophospholipid degrading enzyme lysophospholipase A1 in the tumor regions of paraffin-embedded HNSCC samples.

Finally, experimental evidence of 3D cell spheroid tests showed that LPC facilitates HNSCC invasion, implying that HNSCC progression in vivo may be dependent on lysophospholipid supply.

Altogether, a series of novel proteins and lipid species were identified by IMS and IHC screening, which may serve as potential molecular markers for tumor diagnosis, prognosis, and may pave the way to better understand HNSCC pathophysiology.

Dr. Zsolt Balogi and Dr. László Márk from The University of Pécs said, "Head and neck squamous cell carcinoma (HNSCC) includes a family of tumors arising from multiple locations (mouth, throat, larynx, sinuses and salivary glands) and is currently the sixth most common cancer worldwide."

Improving treatment success rates would require earlier and more precise diagnosis as well as clinically applicable specific molecular markers of the tumor with prognostic value.

To date, molecular marker candidates of HNSCC include HPV, EGFR mutations, chemokine receptors, methylation markers, interleukins, which are mostly related to a subgroup of cases and also fail to provide a basis for specific and sensitive tumor identification.

Therefore, seeking molecular markers for early and precise diagnosis, reliable prediction of treatment results, and recurrence rate remain a major goal in fighting HNSCC. Receptor mutations or changes in protein expression levels and localization have long been in the focus of tumor marker discovery, and recently lipidomic and metabolomic patterns have been outlining a molecular signature that may be of diagnostic and prognostic value.

Screening for tumor-associated LMW protein and lipid changes in HNSCC tissue, here the authors identify S100A8, S100A9 and specific phospholipids to accumulate and lysophosphatidylcholine to be depleted in the tumor.

The Balogi/Márk Research Team concluded in their Oncotarget Research Paper that elevated expression of S100A8 and S100A9, upregulation of LYPLA1, and concomitant depletion of specific lysophospholipids, paralleled with an accumulation of specific phospholipids were identified as potential tumor markers via imaging mass spectrometry and immunohistochemistry-based screening of HNSCC specimens.

Given that S100A8/9 supports CD36-mediated fatty acid uptake we propose that a set of molecular changes identified in this study may represent a fingerprint of fatty acid and lipid dependence of HNSCC pathophysiology.

"Given that S100A8/9 supports CD36-mediated fatty acid uptake we propose that a set of molecular changes identified in this study may represent a fingerprint of fatty acid and lipid dependence of HNSCC pathophysiology."

Together with serum and blood sample information, this molecular signature of HNSCC tumors might be used as future possible pre- or post-operative diagnostic and prognostic tools.

A research team led by Cardiff University scientists say they are closer to understanding how a supermassive black hole (SMBH) is born thanks to a new technique that has enabled them to zoom in on one of these enigmatic cosmic objects in unprecedented detail.

Scientists are unsure as to whether SMBHs were formed in the extreme conditions shortly after the big bang, in a process dubbed a 'direct collapse', or were grown much later from 'seed' black holes resulting from the death of massive stars.

If the former method were true, SMBHs would be born with extremely large masses - hundreds of thousands to millions of times more massive than our Sun - and would have a fixed minimum size.

If the latter were true then SMBHs would start out relatively small, around 100 times the mass of our Sun, and start to grow larger over time by feeding on the stars and gas clouds that live around them.

Astronomers have long been striving to find the lowest mass SMBHs, which are the missing links needed to decipher this problem.

In a study published today, the Cardiff-led team has pushed the boundaries, revealing one of the lowest-mass SMBHs ever observed at the centre of a nearby galaxy, weighing less than one million times the mass of our sun.

The SMBH lives in a galaxy that is familiarly known as "Mirach's Ghost", due to its close proximity to a very bright star called Mirach, giving it a ghostly shadow.

The findings were made using a new technique with the Atacama Large Millimeter/submillimeter Array (ALMA), a state-of-the-art telescope situated high on the Chajnantor plateau in the Chilean Andes that is used to study light from some of the coldest objects in the Universe.

"The SMBH in Mirach's Ghost appears to have a mass within the range predicted by 'direct collapse' models," said Dr Tim Davis from Cardiff University's School of Physics and Astronomy.

"We know it is currently active and swallowing gas, so some of the more extreme 'direct collapse' models that only make very massive SMBHs cannot be true.

"This on its own is not enough to definitively tell the difference between the 'seed' picture and 'direct collapse' - we need to understand the statistics for that - but this is a massive step in the right direction."

Black holes are objects that have collapsed under the weight of gravity, leaving behind small but incredibly dense regions of space from which nothing can escape, not even light.

An SMBH is the largest type of black hole that can be hundreds of thousands, if not billions, of times the mass of the Sun.

It is believed that nearly all large galaxies, such as our own Milky Way, contain an SMBH located at its centre.

"SMBHs have also been found in very distant galaxies as they appeared just a few hundred million years after the big bang", said Dr Marc Sarzi, a member of Dr. Davis' team from the Armagh Observatory & Planetarium.

"This suggest that at least some SMBHs could have grown very massive in a very short time, which is hard to explain according to models for the formation and evolution of galaxies."

"All black holes grow as they swallow gas clouds and disrupt stars that venture too close to them, but some have more active lives than others."

"Looking for the smallest SMBHs in nearby galaxies could therefore help us reveal how SMBHs start off," continued Dr. Sarzi.

In their study, the international team used brand new techniques to zoom further into the heart of a small nearby galaxy, called NGC404, than ever before, allowing them to observe the swirling gas clouds that surrounded the SMBH at its centre.

The ALMA telescope enabled the team to resolve the gas clouds in the heart of the galaxy, revealing details only 1.5 light years across, making this one of the highest resolution maps of gas ever made of another galaxy.

Being able to observe this galaxy with such high resolution enabled the team to overcome a decade's worth of conflicting results and reveal the true nature of the SMBH at the galaxy's centre.

"Our study demonstrates that with this new technique we can really begin to explore both the properties and origins of these mysterious objects," continued Dr Davis.

"If there is a minimum mass for a supermassive black hole, we haven't found it yet."

By studying fifty COVID-19 patients, researchers in France identified a unique signature - a combination of deficiency in a response of a particular interferon, as well as exacerbated inflammation - in the most critically ill. They propose this signature, which may be a hallmark of severe COVID-19, provides a rationale for therapeutic approaches that combine interferon supplementation with neutralization of inflammatory signaling. COVID-19 is characterized by distinct patterns of disease progression depending on the patient, which implies patients exhibit different immune responses to the SARS-Cov-2 virus. So far, studies suggest some 5-10% of patients progress to severe or critical disease. However, little is known about the immunological features involved in COVID-19 severity. To help to fill this gap, Jérome Hadjadj and colleagues analyzed immune cells of COVID-19 patients with symptoms ranging from mild to critical. The critical patients exhibited a distinctive dual signature involving a deficiency in responses of type I interferons, proteins that help fight viral infections, as well as exacerbated proinflammatory signaling. While recent work to investigate the role of interferon signaling in COVID-19 patients has shown that local interferon signaling may be important to mitigate disease progression, the results of Hadjadj et al. suggest broader production of interferons may in fact be beneficial. The work of these studies collectively reinforces a growing hypothesis that the location, timing, and duration of interferon exposure are critical parameters underlying the success of therapeutics for SARS-CoV-2 infections. Hadjadj et al. also suggest severely ill COVID-19 patients could be treated with a combined approach focused on interferon administration and adapted anti-inflammatory therapies, "a hypothesis worth cautious testing," they say.

LA JOLLA, CA--A team led by scientists at Scripps Research has discovered a common molecular feature found in many of the human antibodies that neutralize SARS-CoV-2, the coronavirus that causes COVID-19.

The scientists, whose study appears July 13 in Science, reviewed data on nearly 300 anti-SARS-CoV-2 antibodies that their labs and others have found in convalescent COVID-19 patients over the past few months. They noted that a subset of these antibodies is particularly powerful at neutralizing the virus--and these potent antibodies are all encoded, in part, by the same antibody gene, IGHV3-53.

The scientists used a powerful tool known as X-ray crystallography to image two of these antibodies attached to their target site on SARS-CoV-2. The resulting atomic-structure details of this interaction should be useful to vaccine designers, as well as to scientists hoping to develop antiviral drugs targeting the same site on SARS-CoV-2.

Prior research suggests that antibodies encoded by IGHV3-53 are generally present, at least in small numbers, in healthy people's blood. The results therefore offer hope that using a vaccine to boost levels of these ever-present antibodies will protect adequately against the virus.

"This type of antibody has been isolated frequently in studies of COVID-19 patients, and we can now understand the structural basis for its interaction with SARS-CoV-2," says the study's senior author Ian Wilson, DPhil, Hansen Professor of Structural Biology and Chair of the Department of Integrative Structural and Computational Biology at Scripps Research.

"This study provides important inspiration for effective COVID-19 vaccine design," says co-author Dennis Burton, PhD, professor and co-chair of the Department of Immunology and Microbiology at Scripps Research.

The research was a collaboration chiefly involving the Wilson and Burton labs, and the Scripps Research-based Neutralizing Antibody Center of IAVI, a prominent non-profit vaccine research organization.

SARS-CoV-2 so far has infected more than 12 million people around the world and killed more than 500,000, in addition to causing widespread socioeconomic disruption and damage. Developing an effective vaccine to stop the pandemic is currently the world's top public health priority.

Although several potential vaccines are already in clinical trials, scientists don't yet have a full understanding of the molecular features that would define a protective antibody response. In the new study, the scientists took a big step toward that goal.

The team started by analyzing 294 different SARS-CoV-2-neutralizing antibodies isolated from COVID-19 patients' blood over the past few months. Antibodies are Y-shaped proteins made in immune cells called B-cells. Each B-cell makes a specific antibody type, or clone, which is encoded by a unique combination of antibody genes in the cell. The scientists found that an antibody gene called IGHV3-53 was the most common of the genes for the 294 antibodies, encoding about 10 percent of them.

The scientists also noted that the IGHV3-53-encoded antibodies in their study contain an unusually short variant of the CDR H3 loop, normally a key target-binding element. These antibodies are nevertheless very potent against SARS-CoV-2 when compared to other antibodies not encoded by IGHV3-53.

A powerful response right off the bat

The IGHV3-53 antibodies had yet another property suggesting that boosting their numbers would be a good and achievable aim for a SARS-CoV-2 vaccine: They appeared to have mutated only minimally from the original versions that would be circulating, initially in small numbers, in the blood of healthy people.

Normally, when activated by an encounter with a virus to which they fit, B-cells will start proliferating and also mutating parts of their antibody genes, in order to generate new B-cells whose antibodies fit the viral target even better. The more mutations needed for this "affinity maturation" process to generate virus-neutralizing antibodies, the harder it can be to induce this same process with a vaccine.

Fortunately, the IGHV3-53 antibodies found in the study seemed to have undergone little or no affinity maturation and yet were already very potent at neutralizing the virus--which hints that a vaccine may be able to induce a protective response from these potent neutralizers relatively easily.

"Coronaviruses have been around for hundreds to thousands of years, and one can imagine that our immune system has evolved in such a way that we carry antibodies like these that can make a powerful response right off the bat, so to speak" Wilson says.

Map for vaccine-makers, gauge for clinical trials

Wilson's team used high-resolution X-ray crystallography to image two different IGHV3-53 antibodies bound to their target on SARS-CoV-2. This target, known as the receptor binding site, is a crucial structure on the viral "spike" protein that normally connects to a receptor on human cells to begin the process of cell infection. Many of the antibodies that neutralize SARS-CoV-2 appear to do so by blocking this virus-receptor connection.

"We were able to reveal unique structural features of these IGHV3-53-encoded antibodies--features that facilitate their high binding affinity and their specificity for the SARS-CoV-2 receptor binding site," says co-first author Meng Yuan, PhD, a postdoctoral research associate in the Wilson lab.

The detailed atomic-scale structural data should be of interest to vaccine designers and drug developers. Moreover, the researchers say, the identification of IGHV3-53-encoded antibodies as key elements of the immune response to COVID-19 suggests that levels of these antibodies might be useful as an indirect marker of success in ongoing and future vaccine trials.

An analysis of nearly 300 recently identified human SARS-CoV-2 antibodies uncovered a gene frequently used in antibodies that most effectively target the virus. The results contribute to growing structural insight that will be needed for successful vaccine development against SARS-CoV-2. As the global COVID-19 pandemic continues, multiple vaccine candidates have entered clinical trials. Yet, the molecular features that contribute to the most effective antibody response remain unclear. The spike protein of SARS-CoV-2 uses its receptor binding domain (RBD) to infect the host receptor, ACE2, on human cells. Antibodies that could target RBD and block binding to ACE2 are highly sought, and a number have been discovered. Here, Yuan Meng and colleagues compiled a list of 294 such RBD-targeting antibodies. By analyzing them, they found that a gene in the IGHV gene family, known as IGHV3-53, is the most frequently used IGHV gene for targeting the RBD of the virus spike protein. IGHV3-53 antibodies, the authors say, not only have lower mutation rates but are also more potent. By studying the crystal structures of two IGHV3-53 antibodies bound to the RBD, the researchers identified the features that lead them to be so effective at binding and so highly potent, features that make them promising for vaccine design. This detailed insight into IGHV-53 neutralizing antibodies should facilitate design of vaccine antigens that elicit this type of neutralizing antibody response, the authors say. "As IGHV3-53 is found at a reasonable frequency in healthy individuals, this particular antibody response could be commonly elicited during vaccination," they write.

Antibodies derived from llamas have been shown to neutralise the SARS-CoV-2 virus in lab tests, UK researchers announced today.

The team involves researchers from the Rosalind Franklin Institute, Oxford University, Diamond Light Source and Public Health England. They hope the antibodies - known as nanobodies due to their small size - could eventually be developed as a treatment for patients with severe COVID-19. The peer reviewed findings are published in Nature Structural & Molecular Biology.

Llamas, camels and alpacas naturally produce quantities of small antibodies with a simpler structure, that can be turned into nanobodies. The team engineered their new nanobodies using a collection of antibodies taken from llama blood cells. They have shown that the nanobodies bind tightly to the spike protein of the SARS-CoV-2 virus, blocking it from entering human cells and stopping infection.

Using advanced imaging with X-rays and electrons at Diamond Light Source and Oxford University, the team also identified that the nanobodies bind to the spike protein in a new and different way to other antibodies already discovered.

There is currently no cure or vaccine for COVID-19. However, transfusion of critically ill patients with serum from convalesced individuals, which contain human antibodies against the virus, has been shown to greatly improve clinical outcome. This process, known as passive immunisation, has been used for over 100 years, but it is not straightforward to identify the right individuals with the right antibodies and to give such a blood product safely. A lab-based product which can be made on demand would have considerable advantages and could be used earlier in the disease where it is likely to be more effective.

Professor James Naismith, Director of The Rosalind Franklin Institute and Professor of Structural Biology at Oxford University said: "These nanobodies have the potential to be used in a similar way to convalescent serum, effectively stopping progression of the virus in patients who are ill. We were able to combine one of the nanobodies with a human antibody and show the combination was even more powerful than either alone. Combinations are particularly useful since the virus has to change multiple things at the same time to escape; this is very hard for the virus to do. The nanobodies also have potential as a powerful diagnostic."

Professor Ray Owens from Oxford University, who leads the nanobody program at the Franklin, said: "This research is a great example of team work in science, as we have created, analysed and tested the nanobodies in 12 weeks. This has seen the team carry out experiments in just a few days, that would typically take months to complete. We are hopeful that we can push this breakthrough on into pre-clinical trials."

Professor David Stuart, from Diamond Light Source and Oxford University said: "The electron microscopy structures showed us that the three nanobodies can bind to the virus spike, essentially covering up the portions that the virus uses to enter human cells."

The team started from a lab-based library of llama antibodies. They are now screening antibodies from Fifi, one of the 'Franklin llamas' based at the University of Reading, taken after she was immunised with harmless purified virus proteins.

The team are investigating preliminary results which show that Fifi's immune system has produced different antibodies from those already identified, which will enable cocktails of nanobodies to be tested against the virus.

The Rosalind Franklin Institute is a new research institute funded through UK Research and Innovation's Engineering and Physical Sciences Research Council. The Franklin is leading the UK's work in the innovative field of nanobodies, whose tiny size and specificity make them perfect tools for scientific research, usually used to stabilise proteins for imaging.
The Institute is named for the researcher Rosalind Franklin, who was born 100 years ago this year. Although famous for her contribution to the discovery of DNA, Franklin's later career turned to imaging virus structures, including polio.

Professor Naismith said: "2020 marks the centenary of Franklin's birth. As an institute named for a pioneer of biological imaging, we are proud to follow in her footsteps and continue her work in viruses, applied here to an unprecedented global pandemic. Franklin's work transformed biology, and our projects aspire to that same transformational effect."

New research confirms the high impact of PSMA PET/CT in the detection and management of recurrent disease in prostate cancer patients. In initial results from a multicenter trial assessing the impact of 18F-DCFPyL prostate-specific membrane antigen positron emission tomography/computed tomography (PSMA PET/CT), a PET-directed change in management was observed in two-thirds of patients. The research was presented at the Society of Nuclear Medicine and Molecular Imaging's 2020 Virtual Annual Meeting.

Prostate cancer is the second most common cancer in men in the United States. According to the American Cancer Society, an estimated one in nine men will receive a prostate cancer diagnosis in his lifetime, and more than 191,000 men will be diagnosed with prostate cancer this year. Approximately 30 to 40 percent of men experience a biochemical recurrence of prostate cancer in which their prostate-specific antigen (PSA) levels rise after initial treatment.

DCFPyL (PSMA) PET/CT has been shown to be effective in diagnosing patients with prostate cancer. To assess its impact on the management of patients with suspected limited recurrent prostate cancer after primary therapy, researchers conducted a prospective, large-scale multicenter trial. The study included 410 men who had biochemical failure after primary therapy, had either no or limited disease on conventional imaging (CT and bone scintigraphy), and had undergone one of several prostate cancer treatments.

PSMA PET/CT identified disease in more than half of the men in whom CT and bone scan scintigraphy was negative. Additional sites of disease were observed in nearly two-thirds of patients in whom limited metastases were detected prior to PET. PSMA PET-directed management changes were recorded in 66 percent of the patients. The most common changes were conversion from observation or systemic therapy to surgery or radiation, or the addition of nodal-directed therapy to salvage surgery or radiation.

"The identification of extent of recurrence and specific sites of recurrence is crucial in determining the most appropriate mode of therapy for these men," noted Ur Metser, MD, professor of radiology at the University of Toronto in Ontario, Canada. "Findings from this study add to the body of evidence on the utility of PSMA PET in the management of prostate cancer patients."

He continued, "At this time, PSMA PET remains investigational in North American jurisdictions. Evidence generated from this study will help in seeking regulatory approvals to make molecular imaging with 18F-DCFPyL widely available and will pave the way for clinical studies that incorporate PSMA PET as a treatment planning tool to assess ultimate impact on patient outcomes."

The individual mix of microorganisms in the human gastrointestinal tract provides vital clues as to how any future incidence of type 2 diabetes can be predicted, prevented and treated. This is demonstrated in a population study led from the University of Gothenburg. Sweden.

That a person's gut microbiota can contribute to type 2 diabetes has been shown in previous research, led by Fredrik Bäckhed, Professor of Molecular Medicine at Sahlgrenska Academy, University of Gothenburg.

The present study, now published in the journal Cell Metabolism, describes newly discovered clues in the microbiota to how bacteria may contribute to type 2 diabetes and potentially predict who will develop disease based individual's gut microbiota.

By studying people who have not yet developed type 2 diabetes, the researchers were able to rule out the possibility that the gut microbiota was affected by the disease or its treatment. The majority of previous studies in this field have compared healthy individuals with patients.

What has emerged is that in individuals with raised fasting blood glucose levels or reduced glucose tolerance, a condition known as prediabetes, as well as in people with untreated type 2 diabetes, the gut microbiota is changed. Accordingly, the findings show that the gut microbiota can be used to identify individuals with diabetes.

The study also shows that, in the gut microbiota of study participants with prediabetes or who had developed type 2 diabetes, the potential to produce butyrate (a fatty acid that promotes hormone production in the gastrointestinal tract and controls inflammation) was reduced. This substance is formed mainly by beneficial bacteria in intestines as they digest dietary fibers. One possible implication is that altering individuals fiber intake and perhaps matching fiber types to specific microbiota, or development of next generation probiotics to add missing bacteria, may enable the development of novel diabetes prevention or therapeutics.

"Our study shows clearly that the composition of the gut microbiota may have a great potential for helping us to understand the risks of developing type 2 diabetes, and therefore improve our chances of detecting, preventing and treating the disease," Bäckhed says.

The results confirm the picture that the gut microbiota interacts with the body's functions and internal conditions. The intestinal tract contains more than a kilogram of bacteria that are important for our health, and the kinds of gut bacteria found in people with type 2 diabetes seem to differ from those in healthy people.

"We hope to find patterns and identify which components of the gut microbiota identify individuals whose risk of developing type 2 diabetes is elevated. In the future, perhaps we'll be able to prescribe individualized dietary changes, or develop new types of probiotic that can prevent or perhaps even treat the disease," Bäckhed says.

The research now published builds on a population-based study that has been underway at the University of Gothenburg and Sahlgrenska University Hospital since 2013. It covered some 5,000 randomly selected people who were invited to take part in the study, and its purpose was to investigate which factors may entail an increased risk of type 2 diabetes. To confirm and verify the findings, the researchers also analyzed samples collected from the Swedish Cardiopulmonary Bioimage Study (SCAPIS), a nation-wide population study.

Netflix, which provides an online streaming service around the world, has 42 million videos and about 160 million subscribers in total. It takes just a few seconds to download a 30-minute video clip and you can watch a show within 15 minutes after it airs. As distribution and transmission of high-quality contents are growing rapidly, it is critical to develop reliable and stable semiconductor memories.

To this end, POSTECH research team has developed a memory device using a two-dimensional layered-structure material, unlocking the possibility of commercializing the next-generation memory device that can be stably operated at a low power.

POSTECH research team consisting of Professor Jang-Sik Lee of the Department of Materials Science and Engineering, Professor Donghwa Lee of the Division of Advanced Materials Science, Youngjun Park, and Seong Hun Kim in the PhD course succeeded in designing an optimal halide perovskite material (CsPb2Br5) that can be applied to a ReRAM*1 device by applying the first-principles calculation*2 based on quantum mechanics. The findings were published in Advanced Science.

The ideal next-generation memory device should process information at high speeds, store large amounts of information with non-volatile characteristics where the information does not disappear when power is off, and operate at low power for mobile devices.

The recent discovery of the resistive switching property in halide perovskite materials has led to worldwide active research to apply them to ReRAM devices. However, the poor stability of halide perovskite materials when they are exposed to the atmosphere have been raised as an issue.

The research team compared the relative stability and properties of halide perovskites with various structures using the first principles calculation2. DFT calculations predicted that CsPb2Br5, a two-dimensional layered structure in the form of AB2X5, may have better stability than the three-dimensional structure of ABX3 or other structures (A3B2X7, A2BX4), and that this structure could show improved performance in memory devices.

To verify this result, CsPb2Br5, an inorganic perovskite material with a two-dimensional layered structure, was synthesized and applied to memory devices for the first time. The memory devices with a three-dimensional structure of CsPbBr3 lost their memory characteristics at temperatures higher than 100 °C. However, the memory devices using a two-dimensional layered-structure of CsPb2Br5 maintained their memory characteristics over 140 °C and could be operated at voltages lower than 1V.

Professor Jang-Sik Lee who led the research commented, "Using this materials-designing technique based on the first-principles screening and experimental verification, the development of memory devices can be accelerated by reducing the time spent on searching for new materials. By designing an optimal new material for memory devices through computer calculations and applying it to actually producing them, the material can be applied to memory devices of various electronic devices such as mobile devices that require low power consumption or servers that require reliable operation. This is expected to accelerate the commercialization of next-generation data storage devices."

Cystic fibrosis, one of the most common genetic diseases in Switzerland, causes severe respiratory and digestive disorders. Despite considerable therapeutic advances, this disease still reduces life expectancy, in particular due to life-threatening respiratory infections. Scientists from the University of Geneva (UNIGE) have discovered the reason for this large number of lung infections: a protein, Vav3, promotes these infections by creating a "bacterial docking station" on airways' surface. Inhibiting this protein might prevent bacteria from docking on airways' surface and causing recurrent infections. These results, to be read in the journal Cell Reports, pave the way of interesting therapeutic prospects for limiting respiratory complications in people with cystic fibrosis.

Cystic fibrosis, affecting more than 700,000 people worldwide, is one of the most common genetic diseases in Switzerland. It stems from mutations in the gene responsible for a protein that participates in the secretion of mucus, making it abnormally thick. The alteration of this single gene leads to severe respiratory and digestive problems and limits both life quality and life expectancy of those affected. In lungs for example, hyperviscous mucus stagnates and obstructs airways.

Recurrent infections

Mucus accumulation does not only obstruct airways, it also promotes persistent lung infections. Despite major therapeutic advances, these lung infections remain frequent and serious. They are mostly due to a bacterium known for its resistance to antibiotics, Pseudomonas aeruginosa. "While it is known that mucus viscosity plays a role in trapping bacteria, the reason why they anchor so easily to airways was unknown," explains Marc Chanson, Professor at the Department of Cell Physiology and Metabolism of the Faculty of Medicine of the UNIGE. "Anchoring of Pseudomonas aeruginosa to airways' cells is the starting point for these often fatal infections. Understanding this process could help preventing their occurrence."

A bacterial docking station

UNIGE researchers compared airway cells from sick people with healthy cells. "The whole project began when we found that the protein Vav3, which had not been shown to be involved in this disease until now, was over-expressed in sick cells," enthuses Mehdi Badaoui, researcher in Prof. Marc Chanson's team and first author of this work. After numerous in vitro analyses, scientists discovered the key role of this protein: it directs the construction of a true bacterial docking station. In concrete terms, Vav3 forces two other proteins, fibronectin and integrin b1, to associate with it on cell surface and create a complex that promotes Pseudomonas aeruginosa infections. "This is the first time that a mechanism creating a favourable microenvironment for a bacterium before it even arrives has been observed," says Marc Chanson. "This might explain the high number of chronic lung infections in people with cystic fibrosis."

Inhibiting Vav3 to limit respiratory infections

How to build on this mechanism to develop therapeutic options? By inhibiting Vav3 in sick cells, scientists succeeded in preventing the expression of the two other proteins that make up the docking station. "And, indeed, the absence of this structure limits the adhesion of Pseudomonas aeruginosa", adds Mehdi Badaoui. Although the exact link between the protein Vav3 and the genetic defect that causes cystic fibrosis has yet to be determined, this discovery is a promising therapeutic target for limiting respiratory complications.

This work has been made possible, in particular, thanks to the support of the Swiss National Science Foundation (SNSF) and the Swiss Society for Cystic Fibrosis.

Apathy offers an important early warning sign of dementia in individuals with cerebrovascular disease, but depression does not, new research led by the University of Cambridge suggests.

Depression is often thought to be a risk factor for dementia but this may be because some depression scales used by clinicians and researchers partially assess apathy, say scientists from the universities of Cambridge, King's College London, Radboud and Oxford.

The study, published on 11 July in the Journal of Neurology, Neurosurgery & Psychiatry is the first to examine the relationships between apathy, depression, and dementia in individuals with cerebral small vessel disease (SVD). SVD may occur in one out of three elderly individuals, causes about a quarter of all strokes, and is the most common cause of vascular dementia.

The team studied two independent cohorts of SVD patients, one from the UK and the other from the Netherlands.* Across both cohorts, they found that individuals with higher baseline apathy, as well as those with increasing apathy over time, had a greater risk of dementia. In contrast, neither baseline depression nor change in depression had any detectable influence on dementia risk.

These findings were consistent despite variation in the severity of participants' symptoms, suggesting that they could be generalised across a broad spectrum of SVD cases. The relationship between apathy and dementia remained after controlling for other well-established risk factors for dementia including age, education, and cognition.

Lead author, Jonathan Tay, from Cambridge's Department of Clinical Neurosciences said: "There has been a lot of conflicting research on the association between late-life depression and dementia. Our study suggests that may partially be due to common clinical depression scales not distinguishing between depression and apathy."

Apathy, defined as a reduction in 'goal-directed behaviour', is a common neuropsychiatric symptom in SVD, and is distinct from depression, which is another symptom in SVD. Although there is some symptomatic overlap between the two, previous MRI research linked apathy, but not depression, with white matter network damage in SVD.

Jonathan Tay said: "Continued monitoring of apathy may be used to assess changes in dementia risk and inform diagnosis. Individuals identified as having high apathy, or increasing apathy over time, could be sent for more detailed clinical examinations, or be recommended for treatment."

Over 450 participants - all with MRI-confirmed SVD - recruited from three hospitals in South London and Radboud University's Neurology Department in the Netherlands, were assessed for apathy, depression and dementia over several years.

In the UK cohort, nearly 20% of participants developed dementia, while 11% in the Netherlands cohort did, likely due to the more severe burden of SVD in the UK cohort. In both datasets, patients who later developed dementia showed higher apathy, but similar levels of depression at baseline, compared to patients who did not.

The study provides the basis for further research, including the mechanisms that link apathy, vascular cognitive impairment, and dementia. Recent MRI work suggests that similar white matter networks underlie motivation and cognitive function in SVD. Cerebrovascular disease, which can be caused by hypertension and diabetes, can lead to network damage, resulting in an early form of dementia, presenting with apathy and cognitive deficits. Over time, SVD-related pathology increases, which is paralleled by increasing cognitive and motivational impairment, eventually becoming severe enough to meet criteria for a dementia state.

Jonathan Tay says: "This implies that apathy is not a risk factor for dementia per se, but rather an early symptom of white matter network damage. Understanding these relationships better could have major implications for the diagnosis and treatment of patients in the future."