Dementia has long been linked to the loss of cognitive capacities. Meanwhile, recent research has discovered a fascinating phenomenon: some people with particular types of dementia display startling bursts of creativity. Both scientists and artists are now examining the complex relationship between the two in light of the unexpected link between cognitive decline and creativity.

Memory loss and cognitive decline that determine a person’s identity have historically been seen as negative effects of dementia. Memory loss and cognitive impairment are two features that frequently characterize Alzheimer’s disease, the most prevalent type of dementia. Nonetheless, some people with Alzheimer’s disease and other dementias related to it have demonstrated artistic aptitude and creative talents that seem to get better as their cognitive functions decline. These new abilities appear to have emerged at the beginning of the disorder.

Formerly called Pick’s Disease, this dementia brings about changes in brain connections, which, according to researchers, may be the cause of this contradictory association between dementia and creativity. A novel and inventive concept may arise as certain neural routes fail, possibly opening up new, less common neural pathways. This may help to explain why some people who may not have previously shown an aptitude for the arts suddenly demonstrate it through their writing, singing, or other creative endeavors. The brain appears to respond to destruction in a manner unthought of previously, and it apparently releases new areas to work unlike before.

The famed abstract expressionist artist Willem de Kooning is one of the best-known examples of creativity coming back from dementia. In his later years, De Kooning received a diagnosis of Alzheimer’s disease, but he still created amazing works of art despite his cognitive impairment. Similar instances of people with dementia making complex visual art, composing music, and recounting stories on the spot have been reported.

Vincent van Gogh may have been afflicted with this form of dementia, and here the speculation about age, dementia, and creativity merge if not sufficiently, to raise our curiosity. The protective factor of creativity is one of the more interesting aspects of how the brain might react to some intrusion bringing about mental change. It is a gain of function in a time of neurodegeneration, and that seems more than unusual.

Another example of this type of dementia-driven creativity can be found in the work of Ravel. One melodic clause appears again in his piece “Boléro,” which lasts fifteen minutes. This repetitive behavior may be a sign of FTD patients’ tendency toward obsessive repetition.

First discovered by Bruce Miller at a VA in California, the disease is related to which side of the brain is being attacked and its abilities diminished. In one study of people with FTD, the left temporal lobe had gotten worse, but at the same time, areas of the brain involved in processing visual information had become overactive. Researchers are now beginning to study this unusual creativity of dementia and the normal brains of creative people.

The complexity of the human brain can be better understood by understanding this phenomenon, which also has implications for treatment methods. Participating in artistic activities with people who have dementia may improve their quality of life by giving them a way to express themselves and a way to cope with the frustrations of cognitive loss. Sometimes, this creative ability may appear when speech is lost as in the case of the biologist Anne Adams. To activate these dormant creative capacities, dementia care has already investigated art therapy and other creative approaches.

The surprisingly high level of creativity linked to some forms of dementia has shown the complex link between cognitive decline and artistic expression. By highlighting the potential for creative growth even in the context of neurological diseases, this phenomenon contradicts traditional ideas of dementia as only a degenerative condition.

Investigating this link advances our knowledge of the human brain and creates opportunities for cutting-edge therapeutic strategies. We are still wandering in the vast and highly secretive forest of the brain, and, thus far, the roads we have found have revealed unexpected opportunities for treatments far afield from what we usually prescribe.

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In the classic rat sleep deprivation trials, total sleep deprivation ended up killing the rats in 11-32 days. When the researchers deprived the rats of REM sleep, or commonly known as “dreaming sleep,” the rats also died, although they did survive for a longer time period, 16-54 days. Nevertheless, sleep deprivation is very detrimental, and when I was training as a sleep specialist, I learned about myriad health problems when people become sleep deprived.

So, when patients are admitted to the hospital, why do we wake them up in the early morning to draw blood tests? Yale University researchers studied this, and they found that nearly 40% of laboratory studies occurred between 4:00 AM and 6:59 AM:

The traditional thinking behind this is that, by the time the physicians and APPs come in to see their patients in the morning, usually at 7:00 AM, the blood tests are ready for them, and they can act on the findings of those blood tests to help care for the patients.

Yet, this begs the question: do we really need to get blood tests that early in the morning? Would care suffer significantly if those blood tests were drawn at, say, 8:00 AM? There should be enough time to act on any abnormal test results in the morning and before morning rounds. At my hospital, we round at 10:00 AM, and so if blood tests were drawn at 8:00 AM, they should be back by the time I round with the rest of the team.

As far as I can remember – and into today – “AM Labs” are usually drawn at 4:00 or 5:00 AM by default or even tradition. Unless the patient is comatose in the ICU, getting a blood test at 4:00 or 5:00 AM can disrupt the sleep of our patients, which can be very detrimental and can hinder their recovery from illness.

It can also precipitate delirium in our patients due to the sleep deprivation, the effects of which can also be very detrimental to the recovery of our patients. Moreover, it can also disrupt the sleep of the clinicians caring for those patients at night, who have to be awakened also at 4:30 or 5:00 AM to receive notification of critical results and act on them. This sleep disruption can also affect clinician well-being and burnout.

Good sleep is often the elusive treasure of a hospital stay. Many clinicians chuckle when they hear this, but it really is no laughing matter. It may be time to rethink the necessity of getting blood tests so early in the morning, so that our patients can actually get a good night’s sleep and be well on their way to a good recovery from illness.

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When I was a teenager, I became horribly sick after sleeping in front of a fan for hours on end (it was summertime and very hot). I also remember reading – way back in medical school – that respiratory viruses are able to attach better to the nasal mucosa in cold air. New research has elucidated the possible mechanism behind this. It turns out that our nasal mucosa has inherent, innate anti-viral properties.

There are things called “nasal epithelium-derived extracellular vesicles in innate Toll-like receptors” that line our nasal epithelium, or the lining of our noses. According to this research, these extracellular vesicles induce “a swarm-like increase in the secretion of nasal epithelial EVs via the TLR3 signaling,” and this helps prevent viral infections from happening.

Cold air, it turns out, seems to disrupt this process:

And so this may help explain why colds are more common in the winter months.

Now, it is true that there is also increased influenza in the winter months, even in warmer climates such as the Southern part of the U.S. And COVID did not stop during the summer, although it was definitely less prevalent than in the winter. Still, this may help explain part of the reason why respiratory viral infections are more common during the cold winter months.

Therefore…there seems to be a scientific case for a scarf: the scarf can help keep the upper airway nice and warm, so this innate antiviral defense system can stay as intact as possible. The same is true with a…dare I say it…mask (or balaclava) in the cold as well. It should be able to do the same thing: keep the ambient air in the upper airway warm.

Is this fool-proof? Of course not. But it is one possible extra arrow in the quiver to fight against respiratory viral infections in the winter. It is relatively inexpensive, does not involve drugs or medicines, and can be fashionable as well! And, with how annoying – and potentially deadly – some of these respiratory viruses can be, we need all the defenses we can muster.

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Many have postulated that secondary bacterial infections may be one culprit. Indeed, as much as we try to avoid it, many patients suffering from COVID-19 do in fact get bacterial infections in the lungs and other organs. Are these infections – and the sepsis they may cause – the reason why some COVID-19 patients die? New research just published in Nature Microbiology challenges this assertion.

Researchers from New York studied samples from the lungs of 142 patients who underwent clinically indicated bronchoscopies (cameras tests in the lungs) during their course of treatment of COVID-19. They found that – in those patients who ultimately died – the amount of virus in the lungs, known as the viral load, was significantly higher than those that survived. Moreover, the immune response in the lungs themselves was also weaker in those patients who died as well.

They did not find bacterial infection to be associated with mortality, interestingly. And the researchers did extensive analysis on the bronchoscopic samples. These findings make sense.

The more virus you have in the lung, the more viral replication occurs, and the more virus-induced destruction of lung tissue occurs. This helps explain why many patients with severe COVID-19 develop collapse of the lung requiring chest tube placement. What surprised me was the fact that it was not an exaggerated immune response that did the destroying, but the immune response was actually not strong enough in those patients that ended up dying from COVID-19.

What are the implications of these findings?

First, does this mean that suppressing the immune response may be counterproductive? Yet, steroids are recommended as first-line therapy for COVID-19 pneumonia causing hypoxia, or low oxygen levels. And the anti-inflammatory drug tociluzimab has also been shown to provide beneficial outcomes as well. Why the disconnect?

Second, if there are fewer antibodies in the lungs of those who died from COVID-19, should be we giving them antibodies – either with monoclonal antibodies or convalescent plasma – to help the immune system along? Yet, when this very thing was studied, patients who were critically ill actually did worse, and these therapies are not recommended. Again, why the disconnect?

It remains unclear. Still, these findings are very important, and they help explain why some patients succumb to this horrible illness: there is so much virus in the lungs, and all that virus overwhelms the immune response and causes extensive, and ultimately irreversible, destruction in the lungs. Several other studies have also shown that mortality corresponds to viral load, and the current investigation is further confirmation of this.

The other major takeaways of this stud for me are that, first, we need to get vaccinated against COVID-19. The patients in this study were infected early on in the pandemic, before the vaccines were available. Now, we have no excuse. Vaccines are free and widely available, and they are extremely effective at preventing the very thing from which these study patients suffered: death and/or severe illness.

Second, wear a mask. A mask helps reduce viral particles that get into your upper airway (which is why leaving the nose uncovered is counterproductive). This is especially true if everyone is masked. With less viral particles, the chance of severe infection – or perhaps even any infection – goes down.

The science on SARS CoV-2 and COVID-19 is forever changing. We are constantly learning new things about this virus and the scourge it is causing. This is ultimately a good thing. Knowledge is power, and the more we know, the more we can learn about what this virus does and how we can effectively fight against it.

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Enter a new study into the mix, published in the journal Nature. Scientists studied sixty-three individuals who recovered from COVID-19 12 months later. Most of them had mild infections, and only 10% were hospitalized. 41% of them received a mRNA (Pfizer or Moderna) vaccine prior to being studied.

Powerful immunity

The researchers found that – at 12 months – there was still a significant amount of immunity against SARS CoV-2 in those patients with natural infection. Yet, in those individuals who recovered from COVID and also got vaccinated, the immunity was much greater – orders of magnitude greater. What’s more, this immunity crossed over to many of the variants of concern, and as can be seen in the graphic below, having natural infection and vaccination increased the levels of antibodies dramatically:

In addition, they found that those individuals who were vaccinated had 8.6 times the number of circulating SARS CoV-2 specific B-cells.

This is good news. The lead researcher, Michel Nussenzweig, MD PhD, told JAMA that he is not sure how long immunity lasts in those individuals who were vaccinated alone, without also having been infected by SARS CoV-2. He speculated that these people may need a booster shot at some point, but it is not clear when that booster will be needed.

But, he also told JAMA that – based on the findings of this research – he thinks the variants will not cause serious illness in most people who have recovered from COVID-19. That’s also great news. In addition, he recommends people get vaccinated after recovering from COVID because, according to Dr. Nussenzweig, “they become bulletproof when they do so.”

So what are the implications of this research?

First, it is becoming more and more apparent that immunity after natural infection probably lasts a long time. Only time – and further research – will tell whether immunity will ever wane completely. And only time – and further research – will tell whether booster shots for SARS CoV-2 will be needed, if ever.

Second, vaccination is crucial, even in those who have recovered from natural infection by SARS CoV-2. Vaccination, even by itself, induces a very powerful immune response in most people, and this response does a great job in protecting against variants of concern. Furthermore, this research shows that, in those who already got COVID and recovered, the vaccine greatly boosts the immune response to the point where – in the words of the lead researcher – it makes one “bulletproof” from reinfection.

This research further solidifies the fact that vaccination is the only way to safely get us out of this pandemic. Simply “letting the virus rip” through communities is not an effective strategy. First of all, even mild infections can cause long-term symptoms, which can be devastating (ask anyone who still can’t smell after recovering from Covid).

More importantly, more infections will inevitably increase the number of hospitalizations and deaths. And each death is an absolute tragedy – not only for the one who has died, but also for the extended circle of family and friends who have been affected by this death. And, given how really safe and effective these vaccines are, the rare side effects notwithstanding, each illness and death in the unvaccinated is such a senseless tragedy. And as the data show, the vast majority of those who are dying from COVID now are unvaccinated.

Bottom line is this: get. the. vaccine. It is safe. It is effective. The vaccine protects you from the emerging variants. And vaccination is the only way we can most safely return to our normal lives.

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But what if a person who has clinically recovered from Covid still tests positive? Is that person infectious? A new, large cohort study of the 2020 NBA season in Orlando helps shed light on the answer to this question, and it is good news.

3648 NBA players, staff, and vendors participated in the NBA’s regular and postseason occupational health program in Orlando for the 2020 season. Of these participants, 36 got COVID and clinically recovered, but persistently tested positive after recovery. They were monitored up to 100 days, and these people had repeated unmasked interactions. There were no cases of transmission of the virus.

This is a great study because of its size and real world setting. It further supports ending isolation after 10 days from symptom onset or first positive test. Further, it shows that those who have recovered from COVID but are still testing positive are likely not infectious.

Questions remain, however, and the authors allude to this at the end of the paper:

“Our results support the safety of the time-based CDC public health recommendations regarding discontinuation of isolation precautions. As the pandemic progresses, and particularly if the number of reported reinfection cases increases, interpretation of subsequent positive SARS-CoV-2 RT-PCR test results in recovered individuals will become increasingly challenging.”

If someone tests positive again after recovering, is that a reinfection? Given these data, if someone has recovered from Covid, do they even need to test again, especially if they have no symptoms? More research is needed.

Still, this study gives further support — and adds further data — to the recommendation of a time-based, rather than testing-based, isolation for those who contract SARS CoV-2. It is nice to know that the CDC got it right with this 10-day recommendation.

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The new variant is being called, BV-1, referring to its origin in the Brazos Valley. Although only one case has been identified, scientists are watching closely as this new strain shows signs of resistance to immune system antibodies. A potentially vaccine-resistant Covid-19 variant creates new challenges for public health workers.

According to the press release, a Texas A&M student tested positive for Covid-19 on March 5th. Most labs reserve genetic sequencing for severe cases of Covid-19, but the research scientists at Texas A&M have taken a different approach by sequencing Covid strains from severe, mild, and asymptomatic infections.

Genetic sequencing provides public policymakers with more information to better guide health policy. This comprehensive approach enables the early detection of new health threats as the research team closely monitors the coronavirus circulating strains in Texas.

Testing has slowed in Texas but remains a critical element of our fight against the pandemic. Testing allows us to diagnose and treat those who have Covid-19. Testing enables health workers to do contact tracing and find others who may have been exposed. Testing with genetic sequencing provides information to the public health system to track trends in specific communities.

The CDC tracks the various coronavirus strains and categorizes them into lineages. The viral groups are then categorized as variants of concern (VOC) or variants of interest (VOI). At this point, BV-1 is uncategorized. The Uk strain, B.1.1.7, is the dominant strain in most states, including Texas. The B.1.1.7 variant accounts for 44.7% of the cases load in Texas.

SARS-CoV-2 Variants Circulating in the United States

Scientists track the emerging variants to better understand how easily they might be transmitted. They also monitor the variants response to our currently FDA-approved vaccines.

The B.1.1.7 variant first emerged in the UK during September 2020 but quickly became a dominant variant worldwide. It has a specific mutation in the receptor-binding domain (RBD) of the SARS-CoV-2 spike protein. This mutation makes it easier to spread. The UK reported evidence that the B.1.1.7 variant may be associated with an increased risk of death in January. Other early reports found no evidence that the B.1.1.7 variant impacted the severity of the disease. These reports also showed our vaccines are effective against B.1.1.7.

One case of Covid BV-1 may seem like no big deal. The discovery of the new variant raised eyebrows because Covid BV-1 may be resistant to antibodies. BV-1 has some genetic similarities to the B.1.1.7 variant (UK strain), which has proven to more contagious and potentially more dangerous. BV-1 also shares genetic markers with other coronavirus strains that can bypass neutralizing antibodies.

Sharing the discovery of the BV-1 variant is essential because of its genetic similarity to other coronavirus strains that can evade the immune system antibodies.

Antibodies are present in our bodies after natural infection or after vaccination. To reach herd immunity, enough people must have antibodies to prevent a virus from spreading. Data shows Covid-19 survivors generated antibodies after natural infection, and patients with a mild disease lose this protection faster than those who had a severe illness.

The Texas A&M University researchers provide large amounts of data to help Texas public health officials and the CDC monitor potential threats to our community. This data will be critically important as we move into the next phase of the pandemic and address the growing needs of those with post-Covid conditions.

A recent report shows one out of three Covid-19 survivors continue to have symptoms after their initial infection resolves. Stories about “Covid long haulers” are popping up worldwide.

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Immunologists have determined the process driving life-threatening inflammation, lung damage and organ failure in patients with COVID-19, sepsis and other inflammatory disorders suggesting possible treatment using existing drugs.

Date of Release: Nov. 18, 2020

MEMPHIS, Tenn /PRNewswire/ — The COVID-19 pandemic continues to cause significant illness and death while treatment options remain limited. St. Jude Children’s Research Hospital scientists have discovered a potential strategy to prevent life-threatening inflammation, lung damage, and organ failure in patients with COVID-19. The research appeared online in the journal Cell.

The scientists identified the drugs after discovering that the hyperinflammatory immune response associated with COVID-19 leads to tissue damage and multi-organ failure in mice by triggering inflammatory cell death pathways. The researchers detailed how the inflammatory cell death signaling pathway worked, which led to potential therapies to disrupt the process.

“Understanding the pathways and mechanism driving this inflammation is critical to develop effective treatment strategies,” said corresponding author Thirumala-Devi Kanneganti, Ph.D., vice chair of the St. Jude Department of Immunology. “This research provides that understanding. We also identified the specific cytokines that activate inflammatory cell death pathways and have considerable potential for treatment of COVID-19 and other highly fatal diseases, including sepsis.”

COVID-19, cytokines, and inflammatory cell death

COVID-19 is caused by the SARS-CoV-2 virus. The infection has killed more than 1.2 million people in less than one year and sickened millions more.

The infection is marked by increased blood levels of multiple cytokines. These small proteins are secreted primarily by immune cells to ensure a rapid response to restrict the virus. Some cytokines also trigger inflammation.

The phrase cytokine storm has been used to describe the dramatically elevated cytokine levels in the blood and other immune changes that have also been observed in COVID-19, sepsis and inflammatory disorders such as hemophagocytic lymphohistiocytosis (HLH). But the specific pathways that initiate the cytokine storm and the subsequent inflammation, lung damage and organ failure in COVID-19 and the other disorders was unclear. The cellular and molecular mechanisms that comprehensively define cytokine storm was also lacking.

Kanneganti’s team focused on a select set of the most elevated cytokines in COVID-19 patients. The scientists showed that no single cytokine induced cell death in innate immune cells.

The St. Jude investigators then tried 28 cytokine combinations and found just one duo that, working together, induced a form of inflammatory cell death previously described by Kanneganti as PANoptosis. The cytokines are tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma. PANoptosis is a unique type of cell death that features coordination of three different cell death pathways—pyroptosis, apoptosis and necroptosis. PANoptosis fuels inflammation through cell death, resulting in the release of more cytokines and inflammatory molecules.

The investigators showed that blocking individual cell death pathways was ineffective in stopping cell death caused by TNF-alpha and IFN-gamma. A closer look at proteins that make up the pathways identified several, including caspase-8 and STAT1, that were essential for PANoptosis in response to these cytokines. Deleting those proteins blocked PANoptosis in innate immune cells called macrophages.

Potential for repurposing TNF-alpha and IFN-gamma blockers to treat COVID-19

Because TNF-alpha and IFN-gamma are produced during COVID-19 and cause inflammatory cell death, the investigators questioned whether these cytokines were responsible for the clinical manifestations and deadly effects of the disease. They found that the TNF-alpha and IFN-gamma combination triggered tissue damage and inflammation that mirror the symptoms of COVID-19 along with rapid death.

Neutralizing antibodies against TNF-alpha and IFN-gamma are currently used to treat inflammatory diseases in the clinic. The investigators found that treatment with these antibodies protected mice from death associated with SARS-CoV-2 infection, sepsis, HLH and cytokine shock.

“The findings link inflammatory cell death induced by TNF-alpha and IFN-gamma to COVID-19,” Kanneganti said. “The results also suggest that therapies that target this cytokine combination are candidates for rapid clinical trials for treatment of not only COVID-19, but several other often fatal disorders associated with cytokine storm.”

Added co-first author Rajendra Karki, Ph.D., a scientist in the Kanneganti laboratory: “We were excited to connect these dots to understand how TNF-alpha and IFN-gamma trigger PANoptosis.” Co-first author Bhesh Raj Sharma, Ph.D., a scientist in the Kanneganti laboratory, added: “Indeed, understanding how PANoptosis contributes to disease and mortality is critical for identifying therapies.”

Redefining cytokine storm

Based on this fundamental research, Kanneganti and her colleagues have proposed a definition of cytokine storm that puts the cytokine-mediated inflammatory cell death via PANoptosis at the center of the process. The researchers noted that PANoptosis results in the release of more cytokines and inflammatory molecules, which intensifies systemic inflammation.

“We have solved a major piece of the cytokine storm mystery by characterizing critical factors responsible for initiating this process, and thereby identifying a unique combination therapy using existing drugs that can be applied in the clinic to save lives,” Kanneganti said.

The other authors are Shraddha Tuladhar, Parimal Samir, Min Zheng, Balamurugan Sundaram, Balaji Banoth, R. K. Subbarao Malireddi, Patrick Schreiner, Geoffrey Neale, Peter Vogel and Richard Webby, of St. Jude; and Evan Peter Williams, Lillian Zalduondo and Colleen Beth Jonsson, of the University of Tennessee Health Science Center.

The research was supported in part by grants (AI101935, AI124346, AR056296, CA253095) from the National Institutes of Health; and ALSAC, the awareness and fundraising organization of St. Jude.

St. Jude Children’s Research Hospital

St. Jude Children’s Research Hospital is leading the way the world understands, treats and cures childhood cancer and other life-threatening diseases. It is the only National Cancer Institute-designated Comprehensive Cancer Center devoted solely to children. Treatments developed at St. Jude have helped push the overall childhood cancer survival rate from 20% to 80% since the hospital opened more than 50 years ago. St. Jude freely shares the breakthroughs it makes, and every child saved at St. Jude means doctors and scientists worldwide can use that knowledge to save thousands more children. Families never receive a bill from St. Jude for treatment, travel, housing and food — because all a family should worry about is helping their child live. To learn more, visit stjude.org or follow St. Jude on social media at @stjuderesearch.

SOURCE St. Jude Children’s Research Hospital

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