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Published9 minutes agoSharecloseShare pageCopy linkAbout sharingImage source, Getty Images US president Joe Biden has said that women travelling for abortions will be protected by the federal government.Millions of women in the US lost the constitutional right to abortion in June, after the Supreme Court overturned its 50-year-old Roe v Wade decision.The judgement has paved the way for individual states to ban the procedure.They have become local battlegrounds in the fight to overturn or uphold abortion services. Women in states where abortion is banned or restricted may be forced to cross state lines to parts of the country where the procedure remains legal.Speaking at a virtual meeting with Democratic state governors, Mr Biden said he believed some US states would attempt to arrest women who crossed state lines for abortion access. “I don’t think people believe that’s going to happen. But it’s going to happen,” he said. What is the Roe v Wade ruling on abortion? The woman who helped to end Roe v WadeWho is on the US Supreme Court?The president added that the government would ensure access to pills that caused abortion in states where it was prohibited.The overturning of Roe v Wade has sent shockwaves throughout the US.It was the Supreme Court ruling that ensured that pregnant women were entitled to an abortion during the first three months of their pregnancy, while allowing for legal restrictions and bans in the second and third trimester.Thirteen states have already severely curtailed or blocked abortion access since the court’s decision.This video can not be playedTo play this video you need to enable JavaScript in your browser.More on this storyOklahoma bans most abortions after conception20 MayWho is on the US Supreme Court?6 days agoThe women in the running for the US Supreme Court27 January

A self-described “simple country doctor,” he won national attention in 2020 when the White House embraced his hydroxychloroquine regimen.Vladimir Zelenko, a self-described “simple country doctor” from upstate New York who rocketed to prominence in the early days of the Covid-19 pandemic when his controversial treatment for the coronavirus gained White House support, died on Thursday in Dallas. He was 48.His wife, Rinat Zelenko, said he died of lung cancer at a hospital where he was receiving treatment.Until early 2020, Dr. Zelenko, who was also known by his Hebrew name, Zev, spent his days caring for patients in and around Kiryas Joel, a village of about 35,000 Hasidic Jews roughly an hour northwest of New York City.Like many health care providers, he scrambled when the coronavirus began to appear in his community. Within weeks he had landed on what he insisted was an effective cure: a three-drug cocktail of the antimalarial drug hydroxychloroquine, the antibiotic azithromycin and zinc sulfate.He was not the first physician to promote hydroxychloroquine. But he began to draw national attention on March 21 — two days after President Donald J. Trump first mentioned the drug in a press briefing — when Dr. Zelenko posted a video to YouTube and Facebook in which he claimed a 100 percent success rate with the treatment. He implored Mr. Trump to adopt it.A day later, Mark Meadows, Mr. Trump’s chief of staff, reached out to Dr. Zelenko for more information. So did talk-show bookers. Over the next week Dr. Zelenko made the rounds on conservative media, speaking on podcasts hosted by Steve Bannon and Rudolph W. Giuliani. Sean Hannity of Fox News touted his research during an interview with Vice President Mike Pence.“At the time, it was a brand-new finding, and I viewed it like a commander in the battlefield,” Dr. Zelenko told The New York Times. “I realized I needed to speak to the five-star general.”On March 28, the Food and Drug Administration granted emergency authorization to doctors to prescribe hydroxychloroquine and another antimalarial drug, chloroquine, to treat Covid. Mr. Trump called the treatment “very effective” and possibly “the biggest game changer in the history of medicine.”But, as fellow medical professionals began to point out, Dr. Zelenko had only his own anecdotal evidence to support his case, and what little research had been done painted a mixed picture.Still, he became something of a folk hero on the right, someone who offered not just hope amid the pandemic but also an alternative to the medical establishment and Dr. Anthony Fauci, the director of the National Institute of Allergy and Infectious Diseases, who insisted that months of research would be needed to find an effective treatment.Dr. Zelenko continued to text and speak with Mr. Meadows, Mr. Giuliani and several members of Congress. But he clashed with leaders in Kiryas Joel, who said that his talk of treating hundreds of Covid patients gave the impression that the community was overwhelmed by Covid, potentially stoking antisemitism.Over the next few months, researchers cast further doubt on the efficacy of hydroxychloroquine. A study published in The New England Journal of Medicine found no benefit from the treatment, and other studies highlighted a risk of dangerous heart arrhythmias in some patients.Those results and others led the F.D.A. to revoke its emergency authorization on June 15, 2020.A quiet, unassuming man, Dr. Zelenko seemed unprepared for the attention he received, which included harassing phone calls and even death threats. In May 2020, a federal prosecutor opened an investigation into whether he had falsely claimed F.D.A. approval for his research.That same month, Dr. Zelenko announced in a video that he was closing his practice and leaving the Kiryas Joel community. He accused several of its leaders of instigating a campaign against him.After the F.D.A. rescinded its approval of hydroxychloroquine as a Covid treatment, he founded a company, Zelenko Labs, to promote other nonconventional treatments for the disease, including vitamins and quercetin, an anti-inflammatory drug.And while he claimed to be apolitical, he embraced the image of a victim of the establishment. He founded a nonprofit, the Zelenko Freedom Foundation, to press his case. In December 2020, Twitter suspended his account, stating that it had violated standards prohibiting “platform manipulation and spam.”Dr. Zelenko was born on Nov. 27, 1973, in Kyiv, Ukraine, and immigrated to the United States with his family when he was 3, settling in the Sheepshead Bay section of Brooklyn.His father, Alex, drove a taxi, and his mother, Larisa (Portnoy) Zelenko, worked in a fur factory and later, after studying computer programming, for Morgan Stanley.In a memoir, “Metamorphosis” (2018), Dr. Zelenko wrote that he grew up nonreligious and entered Hofstra University as an avowed atheist.“I enjoyed debating with people and proving to them that G-d did not exist,” he wrote. “I studied philosophy and was drawn to nihilistic thinkers such as Sartre and Nietzsche.”But after a trip to Israel, he began to change his mind. He gravitated toward Orthodox Judaism, and in particular the Chabad-Lubavitch movement.He graduated from Hofstra in 1995 with a degree in chemistry, and he received his medical degree from the State University of New York at Buffalo in 2000. After returning to Brooklyn for his residency, he moved to Monroe, a town that neighbors Kiryas Joel, in 2004.Dr. Zelenko spent three years working for Ezras Choilim, a medical center in Monroe, and advising the local Hatzolah ambulance service. He opened his own practice in 2007, with offices in Monroe and Monsey, another upstate town with a large Orthodox Jewish population.In 2018, doctors found a rare form of cancer in his chest and, in hopes of treating it, removed his right lung.Dr. Zelenko’s first marriage ended in divorce. Along with his second wife, he is survived by their two children, Shira and Liba; six children from his first marriage, Levi Yitzchok, Esther Tova, Eta Devorah, Nochum Dovid, Shmuel Nosson Yaakov and Menachem Mendel; his parents; and a brother, Ephraim.

A factory making Jynneos, the safest vaccine, has been closed since August, threatening global supplies as the virus spreads.As the United States begins a vaccination campaign against monkeypox, concerns are mounting among some experts that the demand may soon far exceed the available supply.Jynneos, the only vaccine developed for monkeypox, is made by a small Danish company, Bavarian Nordic. The company is expected to send about two million doses to the United States by the end of the year, but can produce less than five million more for the rest of the world.The manufacturing facility that could make more has been shut for a planned expansion since last August. The facility is not expected to reopen until late this summer at the earliest, and additional vaccine manufactured there may not become available for at least six months after that.Because testing has been patchy, the scope of the monkeypox outbreak, and therefore the need for vaccines, is uncertain, said Angela Rasmussen, a research scientist at the Vaccine and Infectious Disease Organization at the University of Saskatchewan in Canada.But the current supply “is certainly not enough to vaccinate everybody who’s going to be at risk,” she said.Roughly 60 countries are grappling with monkeypox cases, and all except the United States will need to share available doses — enough for fewer than 2.5 million people — until early 2023.Bavarian Nordic has “a very small inventory of finished products” already distributed, said Paul Chaplin, the chief executive. The company has been able to fulfill all of the orders it has so far received, he said.But, already, several countries are vaccinating close contacts of patients and anyone else at high risk — an approach that may rapidly ratchet up the number of doses required worldwide.“We still have a window of opportunity to contain the virus,” said Zain Rizvi, who studies access to medicines at the advocacy group Public Citizen. “But that means that everyone who needs access to the vaccine needs it now.”If the number of cases continues to rise unchecked, he warned, monkeypox may become permanently entrenched in several countries, leading to outbreaks for years to come.The global count has risen to about 5,500 cases, and at least another 5,000 are under investigation. Cases in Europe have tripled in the last two weeks, according to the World Health Organization. The United States has identified 400 monkeypox cases, but the real number is believed to be much higher — and the number of at-risk people orders of magnitude larger than that.The outbreak has largely been concentrated among men who have sex with men. An estimated six million men who have sex with men live in the United States alone.The U.S. stockpile holds about 56,000 doses that will be distributed immediately, and federal officials expect to receive another 300,000 doses in the next few weeks.An additional 1.1 million doses have been manufactured for the United States, but the Food and Drug Administration must inspect them and sign off before they can be released — a process that typically takes three months or longer, according to Mr. Chaplin.The agency is expediting its review, but a spokeswoman declined to say how long it might take.In addition, the United States previously had purchased “bulk” vaccine that could be “finished” to produce up to 15 million doses, which would require five months, according to Mr. Chaplin.The administration has ordered 2.5 million doses from that stock, the first 500,000 of which are expected to be delivered by the end of the year.Bavarian Nordic is talking to other manufacturers that could produce more doses, but that, too, generally takes at least four to six months, Mr. Chaplin said.A Bavarian Nordic laboratory near Munich. A main manufacturing facility has been closed for months. Lukas Barth/ReutersThe situation will potentially leave the United States with about two million doses by the end of the year, but may hamper the response in other countries, particularly African countries where the virus has been endemic for decades, experts noted.The United States helped Bavarian Nordic develop Jynneos, a safer alternative to older smallpox vaccines, primarily to prevent smallpox in the event of a bioterrorist attack. Instead, Jynneos has become a crucial tool in the race to contain monkeypox.There is an alternative: ACAM2000, a version of the vaccine used to eradicate smallpox decades ago, which is also likely to be effective against monkeypox. But that vaccine has harsh side effects, including heart problems, and can be fatal in people with certain conditions.What to Know About the Monkeypox VirusCard 1 of 4What is monkeypox?

One way cells can control the activities of their genes is by adding small chemical modifications to the DNA that determine which genes are turned on or off. Methyl groups are one of these chemical modifications or tags. Researchers have found that in bacteria DNA methylation plays a role in regulating virulence, reproduction and gene expression. In other organisms, including humans, DNA methylation is essential in regulating tissue-specific gene expression, which defines the nature of a cell, for instance, whether it would be a skin cell or a brain cell.
“The study of DNA methylation is part of the field of epigenetics. It is important because it helps us understand why one particular type of bacteria causes a more severe disease than another or how a normal cell can change and give rise to diseases, such as cancer,” said corresponding author Dr. Tao Wu, assistant professor of molecular and human genetics at Baylor College of Medicine. The Wu Lab is a cancer epigenetics lab. Its long-term goal is to overcome cancer therapeutic resistance by better understanding the role of epigenetics in this disease.
In bacteria, there are three different forms of DNA methylation. The most common is one that tags the DNA base or building block adenine (N6-methyladenine or 6mA). The other two tag the DNA base cytosine (N4-methylcytosine or 4mC and 5-methylcytosine or 5mC). Although there are many methods to study DNA methylation, a few can efficiently map the three types simultaneously, Wu explained.
“It was thought that organisms other than bacteria, including mammals, mostly only used methyl-cytosine tags — the 5mC — to regulate gene activity. But in 2016, when I was at Yale University, we reported in Nature the discovery that DNA 6mA also is present in mammals,” Wu said. “This finding opened a whole new set of possibilities in the study of cancer epigenetics.”
The traditional methods to study the 5mC do not capture the adenine methylation in mammalian tissues. “This motivated us to develop a novel method to profile not only 6mA, but also 4mC and 5mC,” Wu said.
In the current study, published in the journal Genome Biology, Wu and his colleagues report the development of a chemical-based sequencing method to quantify different epigenetic markers simultaneously. Their method, called NT-seq, short for nitrite treatment followed by next-generation sequencing, is a sequencing method for detecting multiple types of DNA methylation genome-wide. The method also can amplify limited clinical samples, something other methods cannot do.
“We show that NT-seq can detect 6mA, 4mC and 5mC both in bacterial and non-bacterial cells, including mammalian cells,” Wu said. “Compared to other methods, NT-seq is efficient, cost-effective, quicker and has high resolution. Some of its limitations are specific to the particular composition of some genomes. We have suggestions in the paper on how to compensate for this limitation.”
“We are excited about NT-seq,” Wu said. “It can uncover new DNA methylation patterns or motifs, validate results obtained with other methods, generate datasets for developing machine-learning tools for methylation analysis and paves the way to further the epigenetic study of genomic DNA 6mA in non-bacterial organisms, including studies on the epigenetics of cancer.”
Other contributors to this work include leading first author Xuwen Li, Shiyuan Guo, Yan Cui, Zijian Zhang, Xinlong Luo, Margarita T. Angelova, Laura F. Landweber and Yinsheng Wang. The authors are affiliated with one or more of the following institutions: Baylor College of Medicine, University of California Riverside, Columbia University, Baylor’s Huffington Center on Aging and Dan L Duncan Comprehensive Cancer Center.
This work is supported by grants from CPRIT (RR180072), NIH (R35 ES031707) and a Rivkin Center Scientific Scholar Award.
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Materials provided by Baylor College of Medicine. Original written by Ana María Rodríguez, Ph.D.. Note: Content may be edited for style and length.

Curing debilitating genetic diseases is one of the great challenges of modern medicine. During the past decade, development of CRISPR technologies and advancements in genetics research brought new hope for patients and their families, although the safety of these new methods is still of significant concern.
Publishing July 1 in the journal Science Advances, a team of biologists at the University of California San Diego that includes postdoctoral scholar Sitara Roy, specialist Annabel Guichard and Professor Ethan Bier describes a new, safer approach that may correct genetic defects in the future. Their strategy, which makes use of natural DNA repair machinery, provides a foundation for novel gene therapy strategies with the potential to cure a large spectrum of genetic diseases.
In many cases, those suffering from genetic disorders carry distinct mutations in the two copies of genes inherited from their parents. This means that often, a mutation on one chromosome will have a functional sequence counterpart on the other chromosome. The researchers employed CRISPR genetic editing tools to exploit this fact.
“The healthy variant can be used by the cell’s repair machinery to correct the defective mutation after cutting the mutant DNA,” said Guichard, the senior author of the study, “Remarkably, this can be achieved even more efficiently by a simple harmless nick.”
Working in fruit flies, the researchers designed mutants permitting visualization of such “homologous chromosome-templated repair,” or HTR, by the production of pigments in their eyes. Such mutants initially featured entirely white eyes. But when the same flies expressed CRISPR components (a guide RNA plus Cas9), they displayed large red patches across their eyes, a sign that the cell’s DNA repair machinery had succeeded in reversing the mutation using the functional DNA from the other chromosome.
They then tested their new system with Cas9 variants known as “nickases” that targeted just one strand of DNA instead of both. Surprisingly, the authors found that such nicks also gave rise to high-level restoration of red eye color nearly on par with normal (non-mutated) healthy flies. They found a 50-70% repair success rate with the nickase compared with just 20-30% in dual-strand cutting Cas9, which also generates frequent mutations and targets other sites throughout the genome (so-called off-target mutations). “I could not believe how well the nickase worked — it was completely unanticipated,” said Roy, the lead author of the study. The versatility of the new system could serve as a model for fixing genetic mutations in mammals, the researchers noted.

University at Buffalo scientists have discovered a convergent mechanism that may be responsible for how two top-ranked genetic risk factors for autism spectrum disorder/intellectual disability (ASD/ID) lead to these neurodevelopmental disorders.
While ASD is distinct from ID, a significant proportion — approximately 31% — of people with ASD also exhibit ID. Neither condition is well-understood at the molecular level.
“Given the vast number of genes known to be involved in ASD/ID and the many potential mechanisms contributing to the disorders, it is exciting to find a shared process between two different genes at the molecular level that could be underlying the behavioral changes,” said Megan Conrow-Graham, PhD, first author and an MD/PhD candidate in the Jacobs School of Medicine and Biomedical Sciences at UB.
Published today in the journal Brain, the paper focuses on ADNP and POGZ, the two top-ranked risk factor genes for ASD/ID. The research demonstrates that mutations in these genes result in abnormal activation and overexpression of immune response genes and genes for a type of immune cell in the brain called microglia.
“Our finding opens the possibility of targeting microglia and immune genes for treating ASD/ID, but much remains to be studied, given the heterogeneity and complexity of these brain disorders,” said Zhen Yan, PhD, senior author and SUNY Distinguished Professor in the Department of Physiology and Biophysics in the Jacobs School.
The UB scientists found that mutations in the two genes studied activate microglia and cause immune genes in the brain to be overexpressed. The hypothesized result is the abnormal function of synapses in the brain, a characteristic of ASD/ID.

Published2 days agocommentsCommentsSharecloseShare pageCopy linkAbout sharingImage source, Getty ImagesCovid infections are rising again across the UK, the latest figures from the Office for National Statistics (ONS) show.An estimated 2.3 million people or one in 30 has the virus – a rise of 32% on the week before.The rise is being driven by two new fast-spreading sub-variants of Omicron – called BA.4 and BA.5. People can be infected even if they’ve had Covid before, but jabs are helping to protect against serious illness.Health officials are urging anyone over 75 who has not had a vaccine or booster in the past six months, to get one.How worried should we be about new variants?How long will my vaccine last?What is the guidance across the UK now?Coronavirus hotspots in the UKIn the week ending 24 June, the ONS estimates Covid rates were:One in 30 in England – up from one in 40 the week beforeOne in 30 in Wales – up from one in 45 One in 25 in Northern Ireland – up from one in 30One in 18 in Scotland – up from one in 20Sarah Crofts, from the ONS, said: “Across the UK we’ve seen a continued increase of over half a million infections, likely caused by the growth of BA.4 and BA.5 variants.”In its analysis of England, it found infections were going up in all regions and in all age groups.In Scotland, which has had the highest Covid rates in the UK since the end of May, the rise in infections may be slowing slightly. What’s happening in hospitals?In England, almost 9,000 hospital beds were taken up with Covid patients on 30 June – and that number has doubled since the start of the month.Data from the other UK nations is not as up-to-date but suggests a similar rise over the last month.The number of Covid patients in hospital is currently still way below the record high of more than 34,000 in January 2021, during the wave of the Alpha variant of coronavirus.Not all hospital patients testing positive for Covid are being treated for it – some are there for another reason, but it can make their care more difficult.This applies to about two-thirds of patients in hospital at the moment.The number of Covid patients in intensive care has reached 211 in England, which is an increase from 111 at the start of June.Back in January 2021, more than 3,700 people needed this type of care at a time where intensive care units were in danger of being overwhelmed.Health officials are advising anyone aged over 75 who hasn’t had a vaccine in the past six months, to get a booster jab to help protect against becoming seriously ill with Covid and ending up in hospital.About 16% of that age group haven’t yet taken up the offer, says Dr Mary Ramsay, director of clinical programmes, from the UK Health Security Agency (UKHSA).She also urged people to think about reducing spread when mixing with others.”It is sensible to wear a face covering in crowded, enclosed spaces. “If you have any symptoms of a respiratory infection, and a high temperature or feel unwell, try to stay at home or away from others – especially elderly or vulnerable people,” Dr Ramsay said.Dr Susan Hopkins, chief medical adviser for Covid at UKHSA, told the BBC: “I think it’s far from a bad cold.”People are experiencing illness for seven to 10 days, she said, and while they had symptoms “they should avoid other people”.”Avoid going to those festivals, avoid going to events and avoid indoor places, because that increases the risk of transmission in all of those places,” she added.Virologist Dr Julian Tang, from the University of Leicester, said the sub-variants now spreading were likely to cause more problems.”We may see more cases with more hospitalisations during the summer – especially in the unvaccinated, and in those whose vaccine and natural immunity is waning.”More on this storyBA.4 and BA.5 Omicron: How worried should we be?2 days agoWhat’s the guidance for Covid in the UK now?2 days agoCovid-19 in the UK2 days ago

The World Health Organization (WHO) recently listed a new sibling diagnosis for post-traumatic stress disorder (PTSD), termed complex post-traumatic stress disorder (CPTSD). An international team with the involvement of the University of Zurich has now summarized the symptoms of the long-awaited new diagnosis and issued guidelines for clinical assessment and treatment.
One of the most widely known responses to trauma is post-traumatic stress disorder, or PTSD. People affected by this mental disorder typically suffer intrusive memories or flashbacks that may overwhelm them. But international experts have been aware for decades that some trauma victims or survivors exhibit a broader pattern of psychological changes, most commonly after prolonged or repetitive events — such as exposure to war, sexual abuse, domestic violence or torture — now termed CPTSD.
Expanded criteria
Many experts have thus been calling for the diagnostic requirements for PTSD to be adapted. Earlier this year, the WHO issued a new version of its International Classification of Diseases (ICD-11). The updated ICD now includes a new diagnosis for complex post-traumatic stress disorder (complex PTSD). New symptoms — such as self-organization disturbances — were added to the previous symptoms of PTSD, which include flashbacks, nightmares, avoidance, social withdrawal and hypervigilance. Key features of self-organization disturbances include excessive or heightened emotional responses, feelings of worthlessness and persistent difficulties in sustaining relationships and in feeling close to others.
An international team with the involvement of UZH has now published a study in The Lancet describing in detail how to diagnose complex PTSD based on a patient’s symptoms. The study describes the difficulties that may occur, the distinct features of the disease in children and adolescents, and the diagnostic differences that need to be made to closely related mental health disorders such as severe depression, bipolar disorders, psychoses or personality disorders.
Precise description of diagnosis and therapy
“We elaborate how the CPTSD diagnosis can be made in routine situations in emergency medical facilities and in regions with underdeveloped health care systems, for example,” says first author Andreas Maercker, professor of psychopathology and clinical intervention at the University of Zurich. The study covers the latest findings on biopsychosocial correlations based on systematic selection criteria. The researchers also analyzed the evidence base for all available therapeutic studies and developed guidelines for treating CPTSD.
“This is particularly important, since not all countries use the WHO’s disease classification. Some have adopted the DSM-5 classification published by the American Psychiatric Association, which currently doesn’t list a diagnosis for complex PTSD,” explains Maercker, emphasizing the significance of their study.
New classification developed globally
The University of Zurich was also involved in updating the WHO’s new International Classification of Diseases. Based on their own research and clinical experience, Andreas Maercker from the UZH Department of Psychology and Marylene Cloitre from Stanford University came out in favor of a new diagnosis for complex post-traumatic stress disorder. In addition, global surveys among psychiatrists and psychologists also showed that there was a need for a more detailed assessment of this mental disorder. A systematic review of previous research as well as new findings then led to the creation of the new diagnosis for complex post-traumatic stress disorder.
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Materials provided by University of Zurich. Note: Content may be edited for style and length.

Neurodegenerative diseases like Alzheimer’s and Parkinson’s are defined by pathogenic accumulation of toxic proteins in the brain. Now, however, scientists from the National Institutes for Quantum Science and Technology have established that the p62 protein, which is involved in cellular protein degradation, can prevent the accumulation of toxic oligomeric tau species in mouse brains, proving — for the first time — the “neuroprotective” function of p62 in a living model.
In order to maintain cellular homeostasis (i.e., a state of equilibrium), cells undergo selective autophagy or self-degradation of unwanted proteins. Autophagy receptors control this process, by mediating the selection of a target protein that is then “cleared.”
Tau proteins — which otherwise play an important role in stabilizing and maintaining the internal organization of neurons in the brain — abnormally accumulate inside neurons in conditions like dementia and Alzheimer’s disease. This build-up of hyper-phosphorylated tau proteins (or tau oligomers) causes the formation of neurofibrillary tangles (NFTs) and eventual cell death of neurons in the brains of people with dementia, contributing to the disease’s progressive neurodegenerative symptoms. Now, while tau proteins can be degraded by selective autophagy, the exact mechanism of how this occurs remains a mystery.
In a recent breakthrough, however, a study done by scientists at the National Institutes for Quantum Science and Technology in Japan proved the critical role played by a certain gene — the p62 gene — in the selective autophagy of tau oligomers. The team included researcher Maiko Ono, and group leader Naruhiko Sahara — both from the Department of Functional Brain Imaging at the National Institutes for Quantum Science and Technology in Japan. Their paper, published in Aging Cell, was made available online on 5 June 2022.
Previous studies have reported that the abnormal accumulation of the tau proteins may be selectively suppressed by autophagy pathways, through the p62 receptor protein (which is a selective autophagy receptor protein). Says Maiko Ono, “This protein’s ubiquitin-binding ability helps in the identification of toxic protein aggregates (like tau oligomers), which can then be degraded by cellular processes and organelles.”
This study’s novelty, however, lay in the demonstration of p62’s “neuroprotective” role in a living model, which had never been done before. So, how did the researchers achieve this? They used mouse models of dementia. The p62 gene had been deleted (or knocked out) in one group of these mice, so they did not express p62 receptor proteins.
On studying the brains of these mice using immunostaining and comparative biochemical analyses, an interesting picture was revealed. Neurotoxic tau protein aggregates were found in the hippocampus — the area of the brain associated with memory — and brainstem — the center that coordinates the body’s breathing, heartbeat, blood pressure, and other voluntary processes — of p62 knockout (KO) mice. When we consider this along with the symptoms of dementia, which include memory loss, confusion, and mood changes, these findings make a lot of sense.
MRI scans revealed that the hippocampus of p62 KO mice was degenerated (atrophied) and inflamed. A postmortem assessment of their brains revealed a greater loss of neurons in their hippocampus. Further immunofluorescent studies showed that the abnormal tau species aggregates can cause cytotoxicity leading to inflammation and cell death of neurons in p62 KO mice. Oligomeric tau, specifically, accumulated more in the brains of p62 KO mice.
Overall, the findings of this study prove that by eliminating and, hence, preventing the aggregation of oligomeric tau species in the brain, p62 played a neuroprotective role in models of dementia.
At a time when researchers across the word are trying to develop drugs for dementia and other related neurodegenerative disorders, the findings of this study will be of great importance in providing evidence for the accurate targeting of tau oligomers. The global population of ageing humans is increasing each year; hence, the need to develop methods to slow down the onset and progression of various neurodegenerative diseases is also expanding. This study provides a positive step towards addressing that need.

Adolescents are over three times more vulnerable to developing a cannabis addiction than adults, but may not be at increased risk of other mental health problems related to the drug, finds a new study led by UCL and King’s College London researchers.
The study, published today in the Journal of Psychopharmacology, found that adolescents who used cannabis were no more likely to have higher levels of subclinical depression or anxiety than adults who use cannabis, nor were they more vulnerable than adult users to the associations with psychotic-like symptoms.
These findings build on a separate study by the same team, published recently in Psychopharmacology that found adolescents were not more vulnerable to associations between chronic cannabis use and cognitive impairment.
Lead author Dr Will Lawn (UCL Clinical Psychopharmacology Unit and Institute of Psychiatry, Psychology and Neuroscience at King’s College London) said: “There is a lot of concern about how the developing teenage brain might be more vulnerable to the long-term effects of cannabis, but we did not find evidence to support this general claim.
“Cannabis addiction is a real issue that teenagers should be aware of, as they appear to be much more vulnerable to it than adults.
“On the other hand, the impact that cannabis use has during adolescence on cognitive performance or on depression and anxiety may be weaker than hypothesised.