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Archive - 2021


February 3rd

New Work Reveals How Tau Protein “Tangles” Develop in Alzheimer’s Brain; Lysosomal Enzymes Permeabilize Membranes of Endosomes and of Tau-Containing Exosomes in Endolysosomes Releasing Tau into the Cytosol

University of Queensland (UQ) (Australia) researchers have discovered a new “seeding” process in brain cells that could be a cause of dementia and Alzheimer's disease. UQ’s Queensland Brain Institute ( dementia researcher Professor Jürgen Götz, PhD, said the study revealed that tangled neurons, a hallmark sign of dementia, form in part by a cellular process that has gone astray and allows a toxic protein, tau, to leak into healthy brain cells. “These leaks create a damaging seeding process that causes tau tangles and ultimately lead to memory loss and other impairments,” Professor Götz said. Professor Götz said, until now, researchers did not understand how tau seeds were able to escape after their uptake into healthy cells. “In people with Alzheimer’s disease, it seems the tiny sacs transporting messages within or outside the cells, called exosomes, trigger a reaction which punches holes in their own cell membrane and allows the toxic seeds to escape,” he said. "As more tau builds up in the brain, it eventually forms tangles, and together with abnormally configured proteins known as amyloid plaque, they form the key features of these neurological diseases." The new results are described in an article published online on January 8, 2021 in Acta Pathologica ( The open-access article is titled “Exosomes Induce Endolysosomal Permeabilization As a Gateway by Which Exosomal Tau Seeds Escape into the Cytosol.” In their abstract, the authors state the following.

How European Hibernating Bats Cope with White-Nose Syndrome, Which Kills Millions of North American Bats

Fungal diseases are a major threat to wildlife, sometimes resulting in significant population declines or even causing the extirpation of populations or species. White-nose syndrome, caused by the cold-loving fungus Pseudogymnoascus destructans, has become a major cause of death for hibernating bats in North America. European bats survive when infected by the same fungus during hibernation. What are the reasons for such a contrast in outcomes? A scientist team led by the Leibniz Institute for Zoo and Wildlife Research (Leibniz-IZW) has now analyzed the humoral innate immune defense of European greater mouse-eared bats to the fungus. In contrast to North American bats, European bats have sufficient baseline levels of key immune parameters and thus tolerate a certain level of infection throughout hibernation. The results were published online on January 18, 2021 in Developmental and Comparative Immunology. He article is titled “Determinants of Defence Strategies of a Hibernating European Bat Species Towards the Fungal Pathogen Pseudogymnoascus destructans.” During infections caused by the fungus P. destructans (Pd), the causative agent of white-nose syndrome, North American bats arouse frequently from hibernation to trigger a more elaborate immune response, whereas European bats remain in dormancy, owing, as the new results reveal, to their competent baseline immunity. Not being able to deal with the fungus by baseline immunity causes North American bats to deplete fat stores before the end of winter because of the need for additional and energetically expensive arousals, which ultimately leads to their starvation. European bats may also arouse once in a while when infected, but their strong baseline immunity allows them to balance the tight energy budget better during winter hibernation.

January 31st

Genetic Screening Before Prescribing Could Benefit Millions

Four million UK patients could benefit annually from genetic testing before being prescribed common medicines, according to new research from the University of East Anglia (UEA) in collaboration with Boots UK and Leiden University (Netherlands). The research results were published online on January 19, 2021 in the British Journal of Clinical Pharmacology. The open-access article is titled “'Estimating the Potential Impact of Implementing Pre-Emptive Pharmacogenetic Testing in Primary Care Across The UK.” Researchers looked through 2019 National Health Service (NHS) dispensing data across the UK to see how many patients are started on new prescriptions each year that could be potentially optimized by genetic testing. The scientists studied 56 medicines, including antidepressants, antibiotics, stomach ulcer treatments, and painkillers where there are known drug-gene interactions. And they found that in more than one in five occasions (21.1%) there was the potential for a doctor or pharmacist to take action under international pharmacogenetic guidelines. If this screening was applied to all new prescriptions, an estimated one in 11 (9.1%) would lead to a change of drug or dose, affecting over five million dispensed items. Depending on the results of individual pharmacogenetic tests, patients might receive either a higher or lower starting dose than normal or be more closely monitored during the early stages of treatment. Pharmacogenomic testing services already working in the Netherlands show that specially-trained general practitioners and pharmacists can carry out pre-prescribing tests and use the results to give advice on safer and more effective prescribing, delivering better patient outcomes.

Scientists Publish Blueprint to Apply Artificial Intelligence (AI) to Extend Human Longevity

On January 27, 2021, Deep Longevity, a fully-owned subsidiary of Regent Pacific (HKEX: 0575), specializing in the development and the application of next-generation artificial intelligence (AI) for aging and longevity research, announced the January 14, 2021 online publication of an open-access article in Nature Aging titled "Artificial Intelligence in Longevity Medicine” ( In the article, the authors describe a new field of study converging AI, basic research, and medicine referred to as Longevity Medicine. Another definition for Longevity Medicine is the preventative and restorative medicine enabled by the deep-aging clocks and artificial intelligence. The article was authored by Alex Zhavoronkov, PhD, the Founder and Chief Longevity Officer of Deep Longevity, a computer scientist with a doctoral degree in biophysics; Evelyne Yehudit Bischof, MD, MPH, a practicing medical doctor trained in the top European and the US medical schools actively engaged in aging research and gero-oncology at the University Hospital Basel in Switzerland, and at Shanghai University of Medicine and Health Sciences; and Kai-Fu Lee, PhD, one of the most prolific scientists and entrepreneurs in artificial intelligence, and Chairman and CEO of Sinovation Ventures ( The traditional approach to medicine is to treat diseases. However, scientists estimate (Cutler and Mattson, 2006) that complete elimination of cancer would result in only a 2.3-year increase in life expectancy in the US at birth and 1.3-year gain at age 65. Complete elimination of influenza and pneumonia would yield gains of 0.5 years and 0.2 years in life expectancy in general.

January 30th

Scientists Identify Protein (KIF18A) Key to Cancer Cells’ Ability to Replicate Despite Aneuploidy

An international research team, co-led by the Technische Universität Kaiserslautern (TUK), has identified a vulnerability in most cancer cells that could help lead to drugs that target tumors regardless of cancer type. Cancer cells with an abnormally high number of chromosomes appear to rely on a particular protein (KIF18A) for cell division and largely die when that protein is blocked, researchers in Germany, Israel, Italy, and the US report in an online publication on January 27,2021 in Nature ( The article is titled “Aneuploidy Renders Cancer Cells Vulnerable to Mitotic Checkpoint Inhibition.” Because more than 90 percent of tumors, regardless of tissue type, contain extra chromosomes, this protein could present an effective target for treating a wide range of cancers. “We think we have found a possible vulnerability of cancer cells with abnormal chromosome numbers,” says Zuzana Storchová, PhD, a Professor of Molecular Genetics at the Technische Universität Kaiserslautern (TUK) in Germany, and a co-senior author of the Nature article. Normal, healthy human cells have 46 chromosomes, but malignant tumors often consist of highly abnormal cancer cells that can have deviant chromosome numbers, usually ranging between 60 to 90 chromosomes. They are called aneuploid cancer cells. For a long time, researchers thought aneuploidy was a side-effect of cells turning cancerous, but in the last 15 years, more suspect this might be one of the driving forces of cancer. Finding a common feature associated with this aberrant number of chromosomes could be critical for targeting cancer, regardless of where it develops in the body. Dr. Storchová and collaborators conducted extensive experiments with nearly 1,000 cell lines from human cancer patients and model cancer cells cultured in the lab.

Scientists Gain New Insight into How Remdesivir Interacts with SARS-CoV-2 RNA Polymerase; Findings Could Be Basis for Developing Better Anti-Virals

More effective antiviral treatments could be on the way after research from The University of Texas at Austin (UT-Austin) sheds new light on the COVID-19 antiviral drug remdesivir, the only treatment of its kind currently approved in the U.S. for the coronavirus SARS-CoV-2. The study was published online on January 28, 2021 in Molecular Cell. The article is titled “Remdesivir Is a Delayed Translocation Inhibitor of SARS CoV-2 Replication.” Remdesivir targets a part of the coronavirus that allows it to make copies of itself and spread through the body. For the first time, scientists identified a critical mechanism that the drug uses and unearthed information that drug companies can use to develop new and improved antivirals to take advantage of the same trick. According to co-author Kenneth Johnson, PhD, Professor of Biochemistry at UT-Austin, the finding could also lead to more potent drugs, meaning a patient could take less of a dose, see fewer side effects, and experience faster relief. "Right now, it's a five-day regimen of taking quite a bit of remdesivir," said Dr. Johnson. "That's inconvenient and comes with side effects. What if you could take just one pill and that was all you needed to do? That would make a huge difference in terms of the here and now."Study co-author David Taylor, PhD, Assistant Professor of Molecular Biosciences at UT-Austin, likens the trick the team identified to a paper jam in the virus's photocopier. Remdesivir shuts down this photocopier--called an RNA polymerase--by preventing copying of the virus's genetic code and its ability to churn out duplicates and spread through the body. The team detected where the drug manages to gum up the gears, grinding the machine to a halt. "We were able to identify the point where that paper jam happens," said Dr. Taylor. "We know now exactly what's creating this block.

Parkinson’s Disease Risk & Severity Are Tied to Activity of Potassium Ion Channel in Lysosomes; Genetic Variations in TMEM175 Trans-Membrane Protein Are Associated With Both Increases & Reductions in Risk of This Neurodegenerative Disease

Many genetic mutations have been found to be associated with a person’s risk of developing Parkinson’s disease. Yet, for most of these variants, the mechanism through which they act remains unclear. Now a new study in Nature ( published online on January 27, 2021, and led by a team from the University of Pennsylvania (Penn), has revealed how two different variations—one that increases disease risk and leads to more severe disease in people who develop Parkinson’s and another that reduces risk—manifest in the body. The work, led by Dejian Ren (photo)(, PhD, Professor of Biology in the School of Arts & Sciences’ Department of Biology at Penn, showed that the variation that raises disease risk, which about 17% of people possess, causes a reduction in function of an ion channel in cellular organelles called lysosomes, also known as cells’ waste removal and recycling centers. Meanwhile, a different variation that reduces Parkinson’s disease risk by about 20% and is present in 7% of the general population enhances the activity of the same ion channel. The Nature article is titled “A growth-factor-activated lysosomal K+ channel regulates Parkinson’s pathology.” “We started with the basic biology, wanting to understand how these lysosomal channels are controlled,” says Dr. Ren. “But here we found this clear connection with Parkinson’s disease. To see that you can have a variation in an ion channel gene that can change the odds of developing Parkinson’s both ways—increasing and decreasing it—is highly novel.” The fact that the channel seems to play a crucial role in Parkinson’s also makes it an appealing potential target for a drug that could slow the disease’s progression, the researchers note.

January 28th

NK-Cell-Derived Exosomes, Harvested from On‐Chip Biogenesis, Exhibit Antitumor Activity Vs Non-Small-Cell Lung Cancer Cells

Building on the promise of emerging therapies to deploy the body’s “natural killer” immune cells to fight cancer, researchers at the University of Michigan (U-M) Rogel Cancer Center and U-M College of Engineering have gone one step further. They’ve developed what is believed to be the first systematic way to capture natural killer cells and get them to release cancer-killing exosomes. These nano-scale exosomes are thousands of times smaller than natural killer (NK) cells and thus better able to penetrate cancer cells’ defenses. A proof-of-concept study in blood samples from five patients with non-small cell lung cancer demonstrated that the approach was able to capture natural killer cells on a microfluidic chip and use them to release NK exosomes. The multidisciplinary team, which included U-M engineers and oncologists, further demonstrated that the exosomes could effectively kill circulating tumor cells in cell cultures, according to findings published online on January 28, 2021 in Advanced Science. The open-access article is titled “On‐Chip Biogenesis of Circulating NK Cell‐Derived Exosomes in Non‐Small Cell Lung Cancer Exhibits Antitumoral Activity.” “Exosomes are small sacs, of proteins and/or other molecules, that are naturally released by almost every type of cell in the body,” says Yoon-Tae Kang, PhD, a Research Fellow in Chemical Engineering at U-M and co-lead author of the study. “In this case, we wanted to expand our understanding of NK exosomes and try to harness their cancer-killing potential.” Compared to NK cells, NK exosomes are more stable and easier to modify for therapeutic purposes, Dr. Kang says. The system also has potential to help diagnose and monitor cancer, the study notes. Harnessing the power of NK cells has long presented a tantalizing possibility for researchers.

LSD May Offer Viable Treatment for Certain Mental Disorders; New Work in Mouse Model Increases Understanding of the Mechanism of Psychedelic’s Impact on Brain and Potential for Therapeutic Use

Researchers from McGill University (Montreal, Canada) have discovered, for the first time, one of the possible mechanisms that contributes to the ability of lysergic acid diethylamide (LSD) to increase social interaction. The findings, which could help unlock potential therapeutic applications in treating certain psychiatric diseases, including anxiety and alcohol use disorders, we published online on January 25, 2021 in PNAS. The open-access article is titled “Lysergic Acid Diethylamide (LSD) Promotes Social Behavior Through mTORC1 in the Excitatory Neurotransmission.” Psychedelic drugs, including LSD, were popular in the 1970s (see image of early LSD advocate Dr. Timothy Leary) and have been gaining popularity over the past decade, with reports of young professionals claiming to regularly take small non-hallucinogenic micro-doses of LSD to boost their productivity and creativity and to increase their empathy. The mechanism of action of LSD on the brain, however, has remained a mystery. To conduct their study, the researchers administered a low dose of LSD to mice over a period of seven days, resulting in an observable increase in the sociability of the mice. "This increased sociability occurs because the LSD activates the serotonin 5-HT2A receptors and the AMPA receptors, which is a glutamate receptor--the main brain excitatory neurotransmitters--in the prefrontal cortex, and also activates a cellular protein called mTORC 1," explains Danilo De Gregorio, PharmD, PhD, who is a postdoctoral fellow in the Neurobiological Psychiatry Unit at McGill, and the study's first author. "These three factors, taken together, promote social interaction in mice, which is the equivalent of empathy and social behavior in humans." [Editor’s Note: 5-HT2A is the abbreviation for 5-hydroxytryptamine receptor 2A.

January 27th

Scientists Discover New Transmission Mechanism (Exosome-Mediated) of Sorafenib Resistance Among Hepatocellular Carcinoma Cells; A Circular RNA (circRNA-SORE) Increases Sorafenib Resistance & Silencing of circRNA-SORE Overcomes This Resistance in Models

Hepatocellular carcinoma (HCC) is the most common primary liver tumor with an increasing global incidence. In 2018, HCC was the sixth most frequently diagnosed cancer and the fourth-leading cause of cancer-related death worldwide. Sorafenib is the first FDA-approved targeted therapy for advanced HCC. A previous study showed that sorafenib prolonged the median overall survival (OS) by 2.3−3 months in advanced HCC patients that did not qualify for liver transplantation or resection. However, sorafenib resistance in HCC is usually observed within 6 months of treatment, thereby making the follow-up therapy rather formidable. Recently, a research team led by Professor Xiujun Cai (photo) (, PhD, from Sir Run-Run Shaw Hospital affiliated with the Zhejiang University School of Medicine has made breakthroughs in sorafenib resistance. Dr. Cai is the President of Sir Run Run Shaw Hospital of Zhejiang University and the Director of both the Institute of Minimally Invasive Surgery of Zhejiang University and the Key Lab of Surgery of Zhejiang Province. The new findings were published online on December 26, 2020 in Signal Transduction and Targeted Therapy. The open-access article is titled “CircRNA-SORE Mediates Sorafenib Resistance in Hepatocellular Carcinoma by Stabilizing YBX1” ( The experiment results elucidate the crucial role of circRNA-SORE (a circular RNA upregulated in sorafenib-resistant HCC cells) in sorafenib resistance and its functioning mechanism.