A review of a limited number of cases of unresponsive patients with severe traumatic brain injuries raised questions about a custom of making a decision within 72 hours.When a patient with a severe traumatic brain injury is comatose, in intensive care, unresponsive and hooked up to a ventilator, but not brain-dead, when is the time to withdraw life support? A small study on the fates of people in such situations suggests that doctors and patients’ families may make better decisions if they wait even a few days longer than usual.Often, a doctor sits down with family members within 72 hours of the patient’s admission to intensive care to discuss the patient’s prognosis, and whether they want to keep their loved one alive, or to remove life support.Experts say that many doctors would describe the outlook as grim — most likely death or severe disability. Reported outcomes of patients who had severe traumatic brain injuries show that most times the decision is to remove life support. The patient dies.The researchers behind the new study say that their limited data suggests that doctors’ predictions so soon after the injury frequently are wrong.The study, published Monday in Journal of Neurotrauma, used a national database that included 1,392 traumatic brain injury patients.Sifting through the data, they ended up comparing 80 patients with severe injuries who died after life support was withdrawn, with 80 similar patients whose life support was not withdrawn.We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.

Published21 minutes agoShareclose panelShare pageCopy linkAbout sharingThis video can not be playedTo play this video you need to enable JavaScript in your browser.Health Secretary Victoria Atkins has compared talks with junior doctors in England to a “peace process away from the glare of the media”. She told the BBC she wanted to give people the time and space for discussions, away from social media. Formal negotiations over the doctors’ pay dispute collapsed in December.But on Thursday, the British Medical Association said it had agreed to fresh talks with the government and an unnamed independent mediator.A spokesperson for the association has said there was a need to restore trust and an independent mediator could help break the logjam.Junior doctors and government agree to talksJunior doctors vote to continue strike action’Horrendous birth experience left me in therapy’The row has run for more than a year and led to a number of strikes since March 2023. The BMA wants a 35% pay rise phased over a few years. Ministers awarded an average of just under 9% for the last financial year and have suggested anything higher would be unaffordable.Speaking to the Political Thinking with Nick Robinson podcast, Ms Atkins said she wanted to ensure people round the negotiating table did not feel beholden to deadlines or tweets.She agreed with the suggestion that the negotiations would be “effectively talks in secret… like a peace process where people are going away for some time. away from the glare of the media” to try to get a settlement. She added that in addition to pay, working conditions were also an issue and that she wanted to “help junior doctors with some of the working conditions that they are facing that make life really tough for them”.Asked by Nick Robinson whether the prime minister and chancellor were “a block to progress” she replied: “Very much not.”‘By men for men’During the interview, Ms Atkins was also asked if she stood by her comment to Stylist magazine,

Published30 minutes agoShareclose panelShare pageCopy linkAbout sharingImage source, BBC/Charlie RoseBy Charlie RoseBBC NewsThousands of children in England with complex needs are missing out on support as councils fail to meet care plan deadlines, BBC News has found.Councils have a legal time limit of 20 weeks, in most cases, to issue an education, health and care plan (EHCP), after a parent or school asks for one.BBC News has found eight councils met the deadline in fewer than 5% of cases, from April to December last year.Councils say growing demand and insufficient funding cause delays.An EHCP sets out the extra help a child needs to access education, on top of what is available through special education needs support. Examples of extra support might include one-to-one lesson time, or help to learn at home for those with such complex needs that school is unsuitable.’He’s been completely forgotten about’Sarah Kilgariff, who lives near Stoke-on-Trent, Staffordshire, applied for an EHCP for her son Freddie last July, after the five-year-old suffered a stroke because of a complication from chickenpox. Ms Kilgariff says Freddie now suffers from fatigue, struggles to regulate his emotions, and is back to wearing nappies.She says because of his needs, her son cannot attend school full-time. The family are still waiting for their EHCP – more than five months after the 20-week deadline. “It’s horrific because I can’t do anything because it’s out of my control, and that’s really frustrating,” she says. “He’s been neglected for a year. He’s been completely forgotten about by the system.”Staffordshire County Council apologised to the family for the delays. It said Freddie was assessed for a second time in April, after the first test in February failed to meet quality standards. It said a significant increase in requests for EHCP assessments had been made worse by a shortage of educational psychologists, and it had now recruited more. ‘My autistic daughter has not been in school for 10 months’Cash-strapped councils target arts and parks cutsWhy do councils go bust and what happens when they do?More than 1.5 million pupils in England have special educational needs or disabilities (Send).The latest figures,

The treatment is for patients with small cell lung cancer, which afflicts about 35,000 people in the U.S. a year.The Food and Drug Administration on Thursday approved an innovative new treatment for patients with a form of lung cancer. It is to be used only by patients who have exhausted all other options to treat small cell lung cancer, and have a life expectancy of four to five months.The drug tarlatamab, or Imdelltra, made by the company Amgen, tripled patients’ life expectancy, giving them a median survival of 14 months after they took the drug. Forty percent of those who got the drug responded.After decades with no real advances in treatments for small cell lung cancer, tarlatamab offers the first real hope, said Dr. Anish Thomas, a lung cancer specialist at the federal National Cancer Institute who was not involved in the trial.“I feel it’s a light after a long time,” he added.Dr. Timothy Burns, a lung cancer specialist at the University of Pittsburgh, said that the drug “will be practice-changing.”(Dr. Burns was not an investigator in the study but has served on an Amgen advisory committee for a different drug.)The drug, though, has a side effect that can be serious — cytokine release syndrome. It’s an overreaction of the immune system that can result in symptoms like a rash, a rapid heartbeat and low blood pressure.We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.

In the United States, about 30-40% of donor hearts aren’t considered for transplant due to inadequate function in the donor.
This creates a drop in the number of donated hearts that are available to be matched with someone who needs a heart transplant.
A team at University of Michigan Health led by Alvaro Rojas-Pena, M.D., a research investigator with the section of transplantation surgery at University of Michigan Health has spent the past eight years looking at better ways to transport organs for donation, specifically hearts, to improve the number of organs that can be used for transplants.
Rojas-Pena’s team found through using a modified normothermic perfusion system heart preservation is feasible for up to 24 hours.
The system uses a blood-derived solution to perfuse the organs and has a hemofilter to remove toxins.
This system allows for prolonged preservation of longer than 12 hours without creating edema or damage to the organs.
The current standard for heart preservation between donation and transplant is up to six hours in cold static storage.

While some hearts can still be transplanted after this six-hour mark, they have increased posttransplant morbimortality rates.
“We can maintain heart viability by perfusion at coronary flows and we are able to remove toxins and control edema to the tissue,” said Rojas-Pena.
“Most importantly, our system can be used to objectively assess function of the organ prior to transplant including the ability to perform echocardiograms, compared to assessment of function in the donor.”
This research and current data prove the concept that normothermic perfusion has the potential to increase the organ pool by considering previously discarded hearts, performing an objective assessment of heart function, increasing the donor/recipient distance and developing heart-specific perfusion therapies.
By extending the time of organ preservation, logistics will become less of an issue and organs with borderline or questionable function can objectively be assessed and potentially considered for transplant.
This opens the option for “organ” therapy and conditioning prior to transplant.
Additional authors include Brianna L. Spencer, Spencer K. Wilhelm, Christopher Stephan, Kristopher A. Urrea, Daniela Pelaez Palacio and Robert H. Bartlett from the Extracorporeal Live Support Laboratory, Department of Surgery, University of Michigan Medical School. Daniel H. Drake from the Extracorporeal Live Support Laboratory, Department of Surgery, University of Michigan Medical School and the Department of Cardiac Surgery, University of Michigan Medical School.
This work was funded by the Maxime and Stuart Frankel Foundation, Michigan Fast Forward, and current work by the NIH R01-HL161139-02

In what they believe is a solution to a 30-year biological mystery, neuroscientists at Johns Hopkins Medicine say they have used genetically engineered mice to address how one mutation in the gene for the light-sensing protein rhodopsin results in congenital stationary night blindness.
The condition, present from birth, causes poor vision in low-light settings.
The findings, published May 14 in Proceedings of the National Academy of Sciences, demonstrate that the rhodopsin gene mutation, called G90D, produces an unusual background electrical “noise” that desensitizes the eye’s rods, those cells in the retina at the back of the eye responsible for nighttime vision, thus causing night blindness.
The identification of the unusual electrical activity could “provide future targets for therapeutic interventions,” the study’s authors write.
These electrical events could help scientists better understand how the eye’s rods and cones function, says King-Wai Yau, Ph.D., professor in the department of neuroscience at the Johns Hopkins University School of Medicine.
The research was led by Yau and postdoctoral fellow Zuying Chai.
“The G90D mutation in rhodopsin is known to produce background electrical noise to desensitize rods, but the nature of the ‘noise’ and its precise molecular source have not been resolved for almost 30 years,” Yau says. “We were able to help solve the mechanism of this disease with a mouse model with a very low expression level of G90D rhodopsin.”
When comparing the low expression level of G90D found in genetically engineered mice versus the level of G90D found in human patients with this night blindness, the authors concluded that the unusual electrical activity with a low amplitude but extremely high frequency may be the greatest contributor to the disease in people.

Besides the unusual electrical noise, rhodopsin is known to produce another type of electrical activity called spontaneous thermal isomerization, in which the thermal energy inside the rhodopsin molecule triggers rhodopsin to activate at random. Contrasting the observed unusual electrical activity, the spontaneous isomerization of G90D rhodopsin demonstrated a high amplitude but low frequency. In their experiments, the researchers found that the spontaneous-isomerization rate of G90D rhodopsin is about two hundred-fold higher than normal rhodopsin, but their rod-adapting effect is not high enough to contribute significantly to night blindness in humans.
In most circumstances, rods are very sensitive to light, but in people with night blindness, the rods cannot accurately detect changes in light, and fail to function in the dark. People with this condition require brighter light to see in low-light settings, Yau said.
For decades, although researchers knew about the G90D mutation, they had difficulty determining how it caused night blindness because prior mouse models with this mutation would generate a high level of background noise, producing effects similar to background light, which the mouse’s rods quickly adapt to. That made it difficult for researchers to accurately measure the mutation’s signaling effects.
To circumvent this issue, the researchers at Johns Hopkins Medicine genetically modified mice to have a low expression of G90D, a level equal to .1% of normal rhodopsin found in the natural population of mice.
This enabled the researchers to distinguish between different types of activity produced in mice with the G90D mutation as if little or no equivalent background light were present.
The scientists used a high-resolution method to record the electrical activity in individual rods in the mouse retina, which they accessed with an ultra-tiny glass pipette — the width of about one-seventieth the size of a human hair — filled with saline solution capable of conducting electricity.

“You can actually see these events,” Yau says. “We used a very special technique called suction-pipette recording to record the activity at such a high resolution that if one rhodopsin molecule isomerizes, or activates, we can see it, because it causes a change in electrical current.”
G90D is one of four mutations of rhodopsin associated with night blindness. First author Chai says the next steps are to identify how other rhodopsin mutations, T94I, A292E and A295V, lead to this condition.
“The mechanism that causes G90D night blindness could be similar in the three other rhodopsin mutations that cause this condition,” Chai says.
Other scientists who contributed to the research include Yaqing Ye, Daniel Silverman and Randall Reed of Johns Hopkins, and Kasey Rose, Alana Madura and Jeannie Chen from the University of Southern California.Funding for the study was provided by the National Institutes of Health grant EY006837, the António Champalimaud Vision Award, Portugal, the Multiphoton Imaging Core at Johns Hopkins, the Daniel Nathans Scientific Innovator Award from the Johns Hopkins University School of Medicine, and the Beckman-Argyros Vision Award from the Arnold and Mabel Beckman Foundation.

Eye diseases are extremely prevalent worldwide, with recent estimates suggesting that one-third of the global population suffers from some type of vision impairment. Given the high complexity of the human eye, the precise origin and nature of many eye diseases remain unclear, leaving affected people with limited diagnostic and treatment options.
Now, in a study made available online on March 7, 2024 and published in Volume 142, Number 4 of JAMA Ophthalmology on April 1, 2024, a team of researchers from Tokyo Medical and Dental University (TMDU) in Japan have pioneered the use of a novel kind of optical coherence tomography (OCT), a technique otherwise widely used in clinical ophthalmology, to investigate the detailed structure of the sclera — the white outer layer of the eyeball.
The motivation underlying this work stems from the limited options currently available to ophthalmologists for investigating the finer details of the sclera in living patients and specimens. “The sclera, composed of collagen fibers, plays an important role in protecting the retina, optic nerve, and other nerve tissues in the eye. Therefore, abnormalities in the shape of the sclera can cause various complications leading to blindness,” explains lead author Dr. Kyoko Ohno-Matsui. “Until now, however, the sclera of live subjects has only been measured in terms of its thickness, with no way to obtain details such as the orientation of the collagen fibers over a wide area of the eye.”
To overcome this limitation, the researchers developed a setup to conduct polarization-sensitive OCT (PS-OCT), a technique where the polarization of light acts as a contrast mechanism. “The sclera has a property called birefringence, which is an optical property of materials in which the refractive index depends on polarization. Birefringence is typically observed in fibrous tissues that have periodically organized nanostructures, such as the sclera,” comments senior author Dr. Tae Igarashi-Yokoi. “Thus, in addition to the magnitude of birefringence, which gives us information about the density of fibers, PS-OCT can also show the axis of orientation of the birefringence, which is related to the orientation of the fiber bundles themselves.”
Using this technique, the team investigated the properties of the collagen fibers in the sclera of patients with highly myopic eyes. They also focused on the link between myopathy and a sometimes-pathological condition known as dome-shaped macula (DSM), in which a specialized area in the retina bulges outwards. Their analysis included 89 highly myopic eyes from a total of 72 patients, mostly adults over 50 years old.
After careful observation of the acquired PS-OCT images, the researchers found that the sclera is divided into inner and outer layers with different structural arrangement for each. In the inner layer, the fibers extend radially from the periphery of the optic nerve. In contrast, fibers in the outer layer run perpendicularly to those of the inner layer. Interestingly, in patients with DSM, the fibers of the inner layer were aggregated and thickened, whereas those of the outer layer were compressed and thinned.
The successful use of PS-OCT to visualize the organization of fibrous tissue in eye structures could have huge implications for clinical research, diagnostics, and therapeutics. “Given the common occurrence of scleral pathologies, such as DSM and staphylomas in eyes with myopia, recognizing fiber patterns could provide important insights that may be relevant to developing targeted therapies to address scleral abnormalities early and mitigate potential damage to the overlying neural tissue,” remarks senior author Dr. Masahiro Yamanari.
We certainly hope PS-OCT leads to impactful medical discoveries that will enable more people to protect their treasured sense of vision.

Important brain structures that are key for signaling in the brain are narrower and less dense in females, and more likely to be damaged by brain injuries, such as concussion. Long-term cognitive deficits occur when the signals between brain structures weaken due to the injury. The structural differences in male and female brains might explain why females are more prone to concussions and experience longer recovery from the injury than their male counterparts, according to a preclinical study led by the Perelman School of Medicine at the University of Pennsylvania, published this week in Acta Neuropathologica.
Each year, approximately 50 million individuals worldwide suffer a concussion, also referred to as mild traumatic brain injury (TBI). However, there is nothing “mild” about this condition for the more than 15 percent of individuals who suffer persisting cognitive dysfunction, which includes difficulty concentrating, learning and remembering new information, and making decisions.
Although males make up the majority of emergency department visits for concussion, this has been primarily attributed to their greater exposure to activities with a risk of head impacts compared to females. In contrast, it has recently been observed that female athletes have a higher rate of concussion and appear to have worse outcomes than their male counterparts participating in the same sport.
“Clinicians have observed for a long time that females suffer from concussion at higher rates than males in the same sports, and that they take longer to recover cognitive function, but couldn’t explain the underlying mechanisms of this phenomenon,” said senior author Douglas Smith, MD, a professor of Neurosurgery and director of Penn’s Center for Brain Injury and Repair. “The variances in brain structures of females and males not only illuminate why this disparity exists, but also exposes biomarkers, such as axon protein fragments, that can be measured in the blood to determine injury severity, monitor recovery, and eventually help identify and develop treatments that help patients repair these damaged structures and restore cognitive function.”
If neurons are telephones that send messages between brain cells, axons are the lines that connect them, allowing communication across the brain. These axons form bundles that make up white matter in the brain and play a large role in learning and communication between different brain regions. Axons are delicate structures and are vulnerable to damage from concussion.
Communication between axons in the brain is powered by sodium channels that serve as the brain’s electric grid. When axons are damaged, these sodium channels are also impaired, which causes loss of signaling in the brain. The loss of signaling causes the cognitive impairment experienced by individuals after concussion.
In this study, researchers used large animal models of concussion to identify differences in brains of males and females after a concussion. They found that females had a higher population of smaller axons, which researchers demonstrated are more vulnerable to injury. They also reported that in these models, females had greater loss of sodium channels after concussion.
“The differences in brain structure not only tell us a lot about how brain injury affects males and females differently but could offer insights in other brain conditions that impact axons, like Alzheimer’s and Parkinson’s disease,” said Smith. “If female brains are more vulnerable to damage from concussion, they might also be more vulnerable to neurodegeneration, and it’s worth further research to understand how sex influences the structure and functions of the brain.”
This research was funded by the National Institutes of Health (R01NS092398, R01NS038104, R01NS094003, U54NS115322, K08NS110929, K23NS123340), the Department of Defense (HT94252311039, W81XWH-21-1-0590, HT9425-23-1-0981), and the Alzheimer’s Association (AARFD-23-1144656).

B cells can control responses of myeloid cells through the release of particular cytokines (small proteins that control the growth and activity of cells in the immune system), challenging the prevailing view that T cells are the principle orchestrators of immune responses. In individuals with Multiple Sclerosis (MS), abnormally active respiration in B cells drives pro-inflammatory responses of myeloid cells and T cells, leading them to attack the protective sheath (myelin) that covers nerve fibers, and leading to nerve damage that causes symptoms of MS.
An emerging class of drugs, called Bruton’s tyrosine kinase (BTK) inhibitors may alter this abnormal B cell respiration and stop the signaling that leads to MS flare-ups. The research, led by the Perelman School of Medicine at the University of Pennsylvania, was published today in Science Immunology.
“Experts previously thought that T cells were the main orchestrators of responses by other immune cell types, and that MS was principally caused by overly activated T cells,” said Amit Bar-Or, MD, a professor of Neurology, and director of Penn’s Center for Neuroinflammation and Neurotherapeutics. “This research highlights that it is actually how multiple cell types interact that matters, and that B cells modulating myeloid cells play a much more active role in the immune system than we thought.”
A healthy immune system is always responding to stimuli by activating or suppressing immune responses, in part through release of different cytokines which tell other cell types how to respond. Normally, every immune response generates a counter response, and this constant “push-me-pull-you” helps maintain the proper balance between immune responses. This way, an individual’s immune system can, on one hand, respond to an infection but also ensure that the response does not become overactive and cause damage to the body, as might occur in an autoimmune disease like MS.
In this study, researchers used both human samples and mouse models of MS to show that not only does the cytokine signaling between B cells and T cells go awry in MS, but also that B cells of MS patients produce an abnormal cytokine profile that drives myeloid cells to generate an inflammatory response.
They found that these actions can all be traced back to metabolic dysregulation in a process within the B cells called oxidative phosphorylation, a type of mitochondrial respiration. Researchers found that normal B cells can break down oxygen and release chemical energy signals that illicit a further response in the B cells themselves, and subsequently also in myeloid cells, telling them to produce a pro- or anti-inflammatory response. However, when this B cell metabolism is over-active, as it is in MS, the signaling results in abnormal myeloid as well as T cell responses which have been implicated in MS symptom flare-ups.
“An exciting approach for new MS treatments, then, might be to partially mute respiration in B cells, which could then stop the cascade of interactions between immune cells that drives inflammation and MS activity,” said Bar-Or.
The authors further showed that an emerging class of drugs, called BTK inhibitors, does just that. These agents slow overactive B cell respiration and “calm down” B cells of MS patients, so that they don’t release the same abnormal cytokine profile that drives abnormal pro-inflammatory myeloid cell and T cell responses.
Existing MS therapies, like anti-CD20 treatments, deplete B cells. However, since B cells are eliminated, the individual’s immune system may be compromised, struggling to mount certain immune responses — for example antibody responses to infections or vaccinations. In contrast, BTK inhibitors do not deplete B cells, but correct the metabolic abnormality, making the B cells less prone to drive pro-inflammatory responses of other cells.
This research was funded primarily by the Melissa and Paul Anderson Gift Fund and the National Institutes of Health Autoimmunity Center of Excellence (ACE) with partial support also from the Children’s Hospital of Philadelphia (CHOP) Center for Mitochondrial and Epigenomic Medicine grant, a grant from the National Natural and Science Foundation of China (U23A20428, 32370962, 2271845) and a sponsored research agreement between The University of Pennsylvania and Biogen.

It has long been known that a hallmark of Alzheimer’s disease, and most other neurodegenerative diseases, is the clumping together of insoluble protein aggregates in the brain. During normal disease-free aging, there is also an accumulation of insoluble proteins.
To date, approaches to treatments for Alzheimer’s disease have not addressed the contribution of protein insolubility as a general phenomenon, instead focusing on one or two insoluble proteins. Buck researchers have recently completed a systematic study in worms that paints an intricate picture of the connections between insoluble proteins in neurodegenerative diseases and aging. Furthermore, the work demonstrated an intervention that could reverse the toxic effects of the aggregates by boosting mitochondrial health.
“Based on our discoveries, targeting insoluble proteins could provide a strategy for the prevention and treatment of a variety of age-related diseases,” said Edward Anderton, PhD, a postdoctoral fellow in Gordon Lithgow’s lab and co-first author of a study that appears in the May 16 issue of the journal GeroScience.
“Our study shows how maintaining healthy mitochondria can combat protein clumping linked to both aging and Alzheimer’s,” said Manish Chamoli, PhD, a research scientist in Gordon Lithgow’s and Julie Andersen’s lab, and co-first author of the study. “By boosting mitochondrial health, we can potentially slow down or reverse these harmful effects, offering new ways to treat both aging and age-related diseases.”
Results support the geroscience hypothesis
The strong link between insoluble proteins promoting normal aging and diseases also builds a case for the bigger picture of how aging and age-related diseases occur. “We would argue that this work really supports the geroscience hypothesis that there is a common pathway to Alzheimer’s disease and aging itself,” said Buck Professor Gordon Lithgow. PhD, Vice President of Academic Affairs and the senior author of the study. “Aging is driving the disease, but the factors that put you on the track toward the disease actually occur very early.”
The fact that the team found a core insoluble proteome enriched with numerous proteins that had not been considered before creates new targets for exploration, said Lithgow. “In some ways it raises the flag about whether we should be thinking about what Alzheimer’s looks like in very young people,” he said.

Beyond amyloid and tau
The focus of most research on Alzheimer’s disease to date has been targeting accumulations of two proteins: amyloid beta and tau. But there are actually thousands of other proteins in these insoluble aggregations, said Anderton, and their role in Alzheimer’s disease was unknown. Additionally, he added, their lab and others’ have observed that during the normal disease-free aging process there is also an accumulation of insoluble proteins. These insoluble proteins from aged animals, when mixed with amyloid beta in the test tube, accelerate the aggregation of the amyloid.
What was the connection between the accumulation aggregates Alzheimer’s and disease-free aging, the team wondered. Focusing on the amyloid beta protein, they used a strain of the microscopic worm Caenorhabditis elegans, long been used in aging studies, that has been engineered to produce human amyloid protein.
Anderton said the team suspected they might see that amyloid beta is driving some level of insolubility in other proteins. “What we found is that amyloid beta causes a massive amount of insolubility, even in a very young animal,” said Anderton. They found that there is a subset of proteins that seem to be very vulnerable to becoming insoluble, either by adding amyloid beta or during the normal aging process. They called that vulnerable subset the “core insoluble proteome.”
The team went on to demonstrate that the core insoluble proteome is full of proteins that have already been linked to different neurodegenerative diseases in addition to Alzheimer’s disease, including Parkinson’s disease, Huntington’s disease and prion disease.
“Our paper shows that amyloid could be acting as a driver of this normal aging aggregation,” said Anderton. “Now we’ve got clear evidence, I think for the first time, that both amyloid and aging are affecting the same proteins in a similar way. It’s quite possibly a vicious cycle where aging is driving insolubility and amyloid beta is also driving insolubility, and they’re just making each other worse.”
The amyloid protein is very toxic to the worms and the team wanted to find a way to reverse that toxicity. “Since hundreds of mitochondrial proteins become insoluble both during aging and after expressing amyloid beta, we thought if we can boost the mitochondrial protein quality using a compound, then maybe we can reverse some of the negative effects of amyloid beta,” said Anderton. That’s exactly what they found, using Urolithin A, a natural gut metabolite produced when we eat raspberries, walnuts, and pomegranates which is known to improve mitochondrial function: it significantly delayed the toxic effects of amyloid beta.
“Something that was glaringly obvious from our dataset is that the importance of mitochondria keeps coming up,” said Anderton. A takeaway, the authors say, is the reminder that the health of mitochondria is critical to overall health. “Mitochondria have a strong link with aging. They’ve got a strong link with amyloid beta,” he said. “I think ours is one of the few studies that shows that insolubility and aggregation of those proteins might be the link between the two.”
“Because the mitochondria are so central to all of this, one way to break the vicious cycle of decline is to replace damaged mitochondria with new mitochondria,” said Lithgow. “And how do you do that? You exercise and follow a healthy diet.”