A neurosurgeon alleged during his employment tribunal that a “gang culture” exists within the neurosurgery department of an NHS hospital already beset by claims of a toxic culture and investigations into negligence.
As reported by the BBC, Dr Mansoor Foroughi was dismissed from University Hospitals Sussex in 2022 for misconduct. At a separate employment tribunal, Krish Singh, the former clinical director for general surgery, claimed that rota changes reduced the number of “safe” consultants, putting patients at risk.
Four whistleblowers had also told the BBC of a “Mafia-like” culture, where patients had died unnecessarily and others “maimed”. These new allegations came to light as the BBC and The Times fought a nine-month court battle to have the employment tribunal documents unsealed.
Dr Foroughi alleges that one colleague was signed off to do complex spinal procedures despite lacking training, another performed procedures with a “disproportionate” mortality rate, and yet another took on private work while on call to the NHS – a serious breach of conduct.
University Hospital Sussex encompasses several hospitals, which includes Royal Sussex Country Hospital, which has been the source of many complaints, and a history of poor service delivery, which was put into special measures between 2016 and 2019.
At least 105 cases of alleged medical negligence from failings at the hospital’s neurosurgery and general surgery departments are being investigated by police. According to court documents, there was “serious dysfunctionality in the neurosurgery department” with “stark divisions between colleagues”.
An investigation by the Royal College of Surgeons found that “a culture of fear” existed in the hospital’s surgery department, and that senior staff were “dismissive and disrespectful”. Two staff were allegedly assaulted.
In a statement, the trust said: “The trust will vigorously contest these claims at the Employment Tribunals, which we are keen take place at the earliest opportunity so they can be examined properly and fairly.
“Dismissing anyone, or removing someone from a leadership role, is an absolute last resort and we would always seek to avoid this outcome if possible.
“In both of these cases, due process was followed, and we are confident we did the right things, in the right way, for the benefit of our patients, their care and safety.”
Neurons in the brain of an Alzheimer’s patient, with plaques caused by tau proteins. Credit: NIH
In findings published in Cell Reports, researchers discovered that the biological instructions within vesicles that communicate between cells differed significantly in postmortem brain samples donated from patients suffering from Alzheimer’s disease.
Small extracellular vesicles (sEVs) are tiny containers are produced by most cells in the body to ferry a wide variety of proteins, lipids and byproducts of cellular metabolism, as well as RNA nucleic acid codes used by recipient cells to construct new proteins.
Because this biologically active cargo can easily elicit changes in other cells, scientists are interested in brain sEVs as a medium for passing along normal as well as bungled instructions for misfolded proteins that accumulate in the brain as neurodegenerative diseases such as Alzheimer’s disease progress.
To be a potential contributor to the buildup of unwanted proteins, sEVs would have to carry blueprints with sufficient information to enable other cells to produce the problematic proteins. Most previous research had indicated that the messenger RNA (mRNA) carrying plans for proteins were chopped into too many shorter fragments to allow recipient cells to change their construction patterns.
“We found quite the opposite to be true in our study,” says senior author Jerold Chun, MD, PhD, professor in the Center for Genetic Disorders and Aging Research at Sanford Burnham Prebys. “We identified more than 10 000 full-length mRNAs through the use of a relatively newer DNA sequencing technique called PacBio long-read sequencing.”
The team isolated sEVs from the prefrontal cortex of 12 postmortem brain samples donated from patients diagnosed with Alzheimer’s disease and 12 from donors without Alzheimer’s disease (or any other known neurological disease). Nearly 80% of identified mRNAs were full-length, allowing them to be transcribed by recipient cells into viable proteins.
“To corroborate the results of long-read sequencing in the human samples, we also looked at vesicles isolated from mouse cells,” says first author Linnea Ransom, PhD, postdoctoral fellow. “We found similar averages of between 78% and 86% full-length transcripts in three brain cell types: astrocytes, microglia and neurons.”
The researchers also compared the sequence of genes reflected in the sEV mRNA transcriptome. In Alzheimer’s disease samples, 700 genes showed increased expression whereas nearly 1500 were found to have reduced activity.
The scientists determined that the 700 upregulated genes are associated with inflammation and immune system activation, which fits within known patterns of brain inflammation present in neurodegenerative diseases such as Alzheimer’s disease. The researchers also found many genes associated with Alzheimer’s disease in prior genome-wide association studies also were present in Alzheimer’s disease sEVs.
“The changes in gene expression contained in these vesicles reveal an inflammatory signature that may serve as a window into disease processes occurring in the brain as Alzheimer’s disease progresses,” says Chun.
Following this study, Chun and team will dig deeper into how cells package sEVs and how the enclosed mRNA codes lead to functional changes in other brain cells affected in Alzheimer’s disease. Better understanding of sEVs and their mRNA contents may enable the discovery of biomarkers that could be used to improve early detection of Alzheimer’s disease and potentially other neurological conditions, while identifying new disease mechanisms to provide new therapeutic targets.
“Additionally, sEVs naturally occur as a vehicle for transporting biologically active cargo between cells, so it also may be possible to leverage them as a targeted delivery system for future brain therapies” says Chun.
Brain organoids (BOs), though often referred to as “mini brains,” are not truly human brains. But the concerns over these lab-grown brain tissues, especially when they are developed from human foetal tissues, can be very human indeed.
In a paper published in EMBO Reports, researchers from Hiroshima University offer valuable insights into the complexities inherent in brain organoid research, highlighting often-overlooked ethical dilemmas for better decision-making, especially for foetal brain organoids (FeBOs).
Brain organoids are three-dimensional human brain tissues derived from stem cells. They replicate the complexity of the human brain in vitro, allowing researchers to study brain development and diseases.
Traditionally, brain organoids (BOs) are grown from pluripotent stem cells, an especially potent sub-type that is typical of early embryonic development, but new technologies now make it possible to generate these organoids from human foetal brain cells.
The research comes amid increasingly heated debates over human BOs. Central concerns are that lab-grown BOs might achieve consciousness and the ethical implications of transplanting them into animal models. The discourse includes matters of consent, commercialisation, integration with computational technologies, and legal ramifications. In addition, the public perception of BOs, often shaped by inaccurate media depictions.
Issues of consciousness arising and transplantation into animal models are particularly morally sensitive for tissue donors, and so rigorous informed consent is needed. With FeBOs, these become even more important. FeBOs, for example, can grow past the developmental stage of the initial foetal donor tissue.
“Our research seeks to illuminate previously often-overlooked ethical dilemmas and legal complexities that arise at the intersection of advanced organoid research and the use of foetal tissue, which is predominantly obtained through elective abortions,” said Tsutomu Sawai, an associate professor at Hiroshima University and lead author of the study.
The study highlights the urgent need for a sophisticated and globally harmonised regulatory framework tailored to navigate the complex ethical and legal landscape of FeBO research. One example is the 14-day rule used in embryo research, as neurogenesis does not occur in embryos prior to 14 days post-fertilisation. Using FeBOs derived from 12-15 week old foetuses therefore raises significant ethical questions, especially as there is a proposed 20-week ethical boundary.
The paper emphasises the importance of informed consent protocols, ethical considerations surrounding organoid consciousness, transplantation of organoids into animals, integration with computational systems, and broader debates related to embryo research and the ethics of abortion.
“Our plan is to vigorously advocate for the development of thorough ethical and regulatory frameworks for brain organoid research, including FeBO research, at both national and international levels,” said Masanori Kataoka, a fellow researcher at Hiroshima University.
“Rather than being limited to issues of consciousness, it’s imperative, now more than ever, to systematically advance the ethical and regulatory discussion in order to responsibly and ethically advance scientific and medical progress,” Sawai said.
Moving forward, the research duo plans to continue supporting the advancement of ethical and regulatory discussions surrounding brain organoid research. By promoting responsible and ethical progress in science and medicine, they aim to ensure that all research involving brain organoids, including FeBOs, is conducted within a framework that prioritises human dignity and ethical integrity.
People with aphantasia – who cannot visualise an image in their mind’s eye – are less likely to remember the details of important past personal events or to recognise faces, according to a review of nearly ten years of research. People who cannot bring to mind visual imagery are also less likely to experience imagery of other kinds, like imagining music, according to new research by the academic who first discovered the phenomenon.
Professor Adam Zeman, of the University of Exeter, first coined the term aphantasia in 2015, to describe those who can’t visualise. Since then, tens of thousands of people worldwide have identified with the description. Many say they knew they processed information differently to others but were unable to describe how. Some of them expressed shock on discovering that other people can conjure up an image in their mind’s eye.
Now, Professor Zeman has conducted a review of around 50 recent studies, published in Trends in Cognitive Sciences, to summarise findings in a field that has emerged since his first publication. Research indicates that aphantasia is not a single entity but has subtypes. For example, not everyone with aphantasia has a poor autobiographical memory or difficulty in recognising faces, and in a minority of people, aphantasia appeared to be linked to autism. People who cannot visualise are more likely to have scientific occupations. Unexpectedly, although people with aphantasia can’t visualise at will, they often dream visually.
Professor Zeman’s review provides evidence that whether people have aphantasia or hyperphantasia – a particularly vivid visual imagination – is linked to variations in their physiology and neural connectivity in the brain, as well as in behaviour. For example, listening to scary stories alters skin conductance in those with imagery, meaning people sweat – but this does not occur in people with aphantasia.
Aphantasia is thought to affect around 1% of the population, while 3% are hyperphantasic. These figures rise to 5–10% with more generous criteria for inclusion. Both aphantasia and hyperphantasia often run in families, hinting at the possibility of a genetic basis.
Professor Zeman, who now holds honorary contracts at the universities of Exeter and Edinburgh, said: “Coining the term ‘aphantasia’ has unexpectedly opened a window on a neglected aspect of human experience. It is very gratifying that people who lack imagery have found the term helpful, while a substantial surge of research is shedding light on the implications of aphantasia.
“Despite the profound contrast in subjective experience between aphantasia and hyperphantasia, effects on everyday functioning are subtle – lack of imagery does not imply lack of imagination. Indeed, the consensus among researchers is that neither aphantasia nor hyperphantasia is a disorder. These are variations in human experience with roughly balanced advantages and disadvantages. Further work should help to spell these out in greater detail.”
“I struggle to fully immerse myself in role-play with my children”
Solicitor Mary Wathen’s frustration that she struggled to engage in role playing games with her two young children, when she found all other engagement with her children so fulfilling, was her sign that she had aphantasia, meaning she cannot visualise imagery.
The 43-year-old, from Newent near Cheltenham, said: “One of my friends said that he uses the images in his head to enhance role play. When I asked him to explain this in more detail it became clear that he – and everyone else in the room – could easily create an image in their head and use that as the backdrop for the role play. This was totally mind-blowing to me. I just cannot understand what they really mean – where is this image and what does it look like? To me, unless you can see something with your eyes, it’s not there.”
Mary’s shock intensified when she realised her husband, has such vivid visual imagery that he is probably hyperphantasic. “He thinks in moving pictures, like movies – sometimes to the point that he can mistake those thoughts for memories. To me, that’s unfathomable.”
Mary has come to realise that her lack of visual imagery may well account for her difficulties with memory. She said: “I can comprehend and retain concepts and principles really well but I’m unable to recall facts and figures. I can’t recreate something in my head or ‘re see’ something that is not actually there in that moment.
“I’ve found it quite saddening to learn that other people can call to mind an image of their children when they’re not there. I’d love to be able to do that, but I just can’t – but I’ve learned to compensate by taking plenty of photos, so that I can relive those memories through those images.
“Whilst I’m sure there are wonderful advantages to being able to think in pictures, I think it’s important to remind myself that there are advantages to having aphantasia too. I’m a really good written and verbal communicator – I think that’s because I’m not caught up with any pictures, so I just focus on the power of the word. I’m also a deeply emotional person and perhaps that’s my brain’s way of overcompensating; I feel things as a way of experiencing them, rather than seeing them.
“I think it’s really important to raise awareness that some people just don’t have this ability – particularly as using visual imagination is a key way that young children are taught to learn and engage. Primary teachers need to know that some children just won’t be able to visualise and that could be why they’re not engaging in those kinds of activities. We need to ensure we cater for everyone and encourage other ways of learning and engaging.”
Disturbed gut flora during the first years of life is associated with diagnoses such as autism and ADHD later in life. One explanation for this disturbance could be from antibiotic treatment. This is according to a study led by researchers at the University of Florida and Linköping University and published in the journal Cell.
The study is the first prospective study to examine gut flora composition and a large variety of other factors in infants, in relation to the development of the children’s nervous system. The researchers have found many biological markers that seem to be associated with future neurological development disorders, such as autism spectrum disorder, ADHD, communication disorder and intellectual disability.
“The remarkable aspect of the work is that these biomarkers are found at birth in cord blood or in the child’s stool at one year of age over a decade prior to the diagnosis,” says Eric W Triplett, professor at the Department of Microbiology and Cell Science at the University of Florida, USA, one of the study leaders.
Antibiotic treatment could be involved
The study is part of the ABIS (All Babies in Southeast Sweden) study led by Johnny Ludvigsson at Linköping University. More than 16 000 children born in 1997–1999, representing the general population, have been followed from birth into their twenties. Of these, 1197 children (7.3%), have been diagnosed with autism spectrum disorder, ADHD, communication disorder or intellectual disability. Many lifestyle and environmental factors have been identified through surveys conducted on several occasions during the children’s upbringing. For some of the children, the researchers have analysed substances in umbilical cord blood and bacteria in their stool at the age of one.
“We can see in the study that there are clear differences in the intestinal flora already during the first year of life between those who develop autism or ADHD and those who don’t. We’ve found associations with some factors that affect gut bacteria, such as antibiotic treatment during the child’s first year, which is linked to an increased risk of these diseases,” says Johnny Ludvigsson, senior professor at the Department of Biomedical and Clinical Sciences at Linköping University, who led the study together with Eric W. Triplett.
Children who had repeated ear infections before one year of age had a higher risk of a developmental neurological disorder diagnosis later in life. It is probably not the infection itself that is the culprit, but the researchers suspect a link to antibiotic treatment. They found that the presence of Citrobacter bacteria or the absence of Coprococcus bacteria increased the risk of future diagnosis. One possible explanation may be that antibiotic treatment has disturbed the composition of the gut flora in a way that contributes to neurodevelopmental disorders. The risk of antibiotic treatment damaging the gut flora and increasing the risk of diseases linked to the immune system, such as type 1 diabetes and childhood rheumatism, has been shown in previous studies.
“Coprococcus and Akkermansia muciniphila have potential protective effects. These bacteria were correlated with important substances in the stool, such as vitamin B and precursors to neurotransmitters which play vital roles orchestrating signalling in the brain. Overall, we saw deficits in these bacteria in children who later received a developmental neurological diagnosis,” says study first author Angelica Ahrens, Assistant Scientist in Eric Triplett’s research group at the University of Florida.
The present study also confirms that the risk of developmental neurological diagnosis in the child increases if the parents smoke. Conversely, breastfeeding has a protective effect, according to the study.
Differences at birth
In cord blood taken at the birth of children, the researchers measured substances such as fatty acids and amino acids, as well as exogenous ones such as nicotine and environmental toxins. They compared substances in the umbilical cord blood of 27 children diagnosed with autism with the same number of children without a diagnosis.
It turned out that children who were later diagnosed had low levels of several important fats in the umbilical cord blood. One of these was linolenic acid, which is needed for the formation of omega 3 fatty acids with anti-inflammatory properties and other effects in the brain. The same group also had higher levels than the control group of a PFAS substance, used as flame retardants and shown to negatively affect the immune system in several different ways. PFAS substances can enter the body via drinking water, food and the air we breathe.
Opens up new possibilities
As the relationships found in the Swedish children may not be generalisable to other populations, studies in other populations are needed. Another question is whether gut flora imbalance is a triggering factor or whether it has occurred as a result of underlying factors, such as diet or antibiotics. Yet even accounting for risk factors that might affect the gut flora, they found that the link between future diagnosis remained for many of the bacteria.
The research is at an early stage and more studies are needed, but the discovery that many biomarkers for future developmental neurological disorders can be observed at an early age opens up the possibility of developing screening protocols and preventive measures in the long term.
A global collaborative research group has identified brain energy metabolism dysfunction leading to altered pH and lactate levels as common hallmarks in numerous animal models of neuropsychiatric and neurodegenerative disorders. These include models of intellectual disability, autism spectrum disorders, schizophrenia, bipolar disorder, depressive disorders, and Alzheimer’s disease. The findings were published in eLife.
The research group, comprising 131 researchers from 105 laboratories across seven countries, sheds light on altered energy metabolism as a key factor in various neuropsychiatric and neurodegenerative disorders. While considered controversial, an elevated lactate level and the resulting decrease in pH is now also proposed as a potential primary component of these diseases. Unlike previous assumptions associating these changes with external factors like medicationa, the research group’s previous findings suggest that they may be intrinsic to the disorders. This conclusion was drawn from five animal models of schizophrenia/developmental disorders, bipolar disorder, and autism, which are exempt from such confounding factorsb. However, research on brain pH and lactate levels in animal models of other neuropsychiatric and neurological disorders has been limited. Until now, it was unclear whether such changes in the brain were a common phenomenon. Additionally, the relationship between alterations in brain pH and lactate levels and specific behavioural abnormalities had not been clearly established.
This study, encompassing 109 strains/conditions of mice, rats, and chicks, including animal models related to neuropsychiatric conditions, reveals that changes in brain pH and lactate levels are a common feature in a diverse range of animal models of conditions, including schizophrenia/developmental disorders, bipolar disorder, autism, as well as models of depression, epilepsy, and Alzheimer’s disease. This study’s significant insights include:
I. Common Phenomenon Across Disorders: About 30% of the 109 types of animal models exhibited significant changes in brain pH and lactate levels, emphasising the widespread occurrence of energy metabolism changes in the brain across various neuropsychiatric conditions.
II. Environmental Factors as a Cause: Models simulating depression through psychological stress, and those induced to develop diabetes or colitis, which have a high comorbidity risk for depression, showed decreased brain pH and increased lactate levels. Various acquired environmental factors could contribute to these changes.
III. Cognitive Impairment Link: A comprehensive analysis integrating behavioural test data revealed a predominant association between increased brain lactate levels and impaired working memory, illuminating an aspect of cognitive dysfunction.
IV. Confirmation in Independent Cohort: These associations, particularly between higher brain lactate levels and poor working memory performance, were validated in an independent cohort of animal models, reinforcing the initial findings.
V. Autism Spectrum Complexity: Variable responses were noted in autism models, with some showing increased pH and decreased lactate levels, suggesting subpopulations within the autism spectrum with diverse metabolic patterns.
“This is the first and largest systematic study evaluating brain pH and lactate levels across a range of animal models for neuropsychiatric and neurodegenerative disorders. Our findings may lay the groundwork for new approaches to develop the transdiagnostic characterisation of different disorders involving cognitive impairment,” states Dr Hideo Hagihara, the study’s lead author.
Professor Tsuyoshi Miyakawa, the corresponding author, explains, “This research could be a stepping stone towards identifying shared therapeutic targets in various neuropsychiatric disorders. Future studies will centre on uncovering treatment strategies that are effective across diverse animal models with brain pH changes. This could significantly contribute to developing tailored treatments for patient subgroups characterized by specific alterations in brain energy metabolism.”
The exact mechanism behind the reduction in pH and the increase in lactate levels remains elusive. But the authors suggest that, since lactate production increases in response to neural hyperactivity to meet the energy demand, this might be the underlying reason.
Just as you can’t make an omelette without breaking eggs, scientists at Albert Einstein College of Medicine have found that you can’t make long-term memories without DNA damage and inflammation in the brain. Their surprising findings were published online today in the journal Nature.
“Inflammation of brain neurons is usually considered to be a bad thing, since it can lead to neurological problems such as Alzheimer’s and Parkinson’s disease,” said study leader Jelena Radulovic, MD, PhD, professor of psychiatry and behavioural sciences at Einstein. “But our findings suggest that inflammation in certain neurons in the brain’s hippocampal region is essential for making long-lasting memories.”
The hippocampus has long been known as the brain’s memory centre. Dr Radulovic and her colleagues found that a stimulus sets off a cycle of DNA damage and repair within certain hippocampal neurons that leads to stable memory assemblies, ie clusters of brain cells representing past experiences.
From shocks to stable memories
The researchers discovered this memory-forming mechanism by giving mice brief, mild shocks sufficient to form an episodic memory of the shock event. Then, they analysed neurons in the hippocampal region and found that genes participating in an important inflammatory signalling pathway had been activated.
“We observed strong activation of genes involved in the Toll-Like Receptor 9 (TLR9) pathway,” said Dr Radulovic, who is also director of the Psychiatry Research Institute at Montefiore Einstein (PRIME). “This inflammatory pathway is best known for triggering immune responses by detecting small fragments of pathogen DNA. So at first we assumed the TLR9 pathway was activated because the mice had an infection. But looking more closely, we found, to our surprise, that TLR9 was activated only in clusters of hippocampal cells that showed DNA damage.”
Brain activity routinely induces small breaks in DNA that are repaired within minutes. But in this population of hippocampal neurons, the DNA damage appeared to be more substantial and sustained.
Triggering inflammation to make memories
Further analysis showed that DNA fragments, along with other molecules resulting from the DNA damage, were released from the nucleus, after which the neurons’ TLR9 inflammatory pathway was activated; this pathway in turn stimulated DNA repair complexes to form at an unusual location: the centrosomes. These organelles are present in the cytoplasm of most animal cells and are essential for coordinating cell division. But in neurons – which don’t divide – the stimulated centrosomes participated in cycles of DNA repair that appeared to organise individual neurons into memory assemblies.
“Cell division and the immune response have been highly conserved in animal life over millions of years, enabling life to continue while providing protection from foreign pathogens,” Dr. Radulovic said. “It seems likely that over the course of evolution, hippocampal neurons have adopted this immune-based memory mechanism by combining the immune response’s DNA-sensing TLR9 pathway with a DNA repair centrosome function to form memories without progressing to cell division.”
Resisting inputs of extraneous information
During the week required to complete the inflammatory process, the mouse memory-encoding neurons were found to have changed in various ways, including becoming more resistant to new or similar environmental stimuli. “This is noteworthy,” said Dr Radulovic, “because we’re constantly flooded by information, and the neurons that encode memories need to preserve the information they’ve already acquired and not be ‘distracted’ by new inputs.”
“This is noteworthy,” said Dr Radulovic, “because we’re constantly flooded by information, and the neurons that encode memories need to preserve the information they’ve already acquired and not be ‘distracted’ by new inputs.”
Importantly, the researchers found that blocking the TLR9 inflammatory pathway in hippocampal neurons not only prevented mice from forming long-term memories but also caused profound genomic instability, ie, a high frequency of DNA damage in these neurons.
“Genomic instability is considered a hallmark of accelerated aging as well as cancer and psychiatric and neurodegenerative disorders such as Alzheimer’s,” Dr Radulovic said.
“Drugs that inhibit the TLR9 pathway have been proposed for relieving the symptoms of long COVID. But caution needs to be shown because fully inhibiting the TLR9 pathway may pose significant health risks.”
PhD Student Elizabeth Wood and Ana Cicvaric, a postdoc in the Radulovic lab, were the study’s first authors at Einstein.
Forming social bonds facilitates effective communication and neural synchronisation across individuals of different social status within a group
When small hierarchical groups bond, neural activity between leaders and followers aligns, promoting quicker and more frequent communication, according to a study published on March 19th in the open-access journal PLOS Biology by Jun Ni from Beijing Normal University, China, and colleagues.
Social groups are often organised hierarchically, where status differences and bonds between members shape the group’s dynamic. To better understand how bonding influences communication within hierarchical groups and which brain regions are involved in these processes, the researchers recorded 176 three-person groups of human participants (who had never met before) while they communicated with each other, sitting face-to-face in a triangle. Participants wore caps with fNIRS (functional near-infrared spectroscopy) electrodes to non-invasively measure brain activity while they communicated with their group members. Each group democratically selected a leader, so each group of three ultimately included one leader and two followers. After strategising together, groups played two economic games designed to test their willingness to make sacrifices to benefit their group (or harm other groups).
Experimenters assigned some triads to go through a bonding session, where they were grouped according to colour preferences, given uniforms, and led through an introductory chat session to build familiarity. Bonded groups spoke more freely and bounced between speakers more frequently and rapidly, relative to groups that didn’t experience this bonding session. This bonding effect was stronger between leaders and followers than between two followers. Neural activity in two brain regions linked to social interaction, the right dorsolateral prefrontal cortex (rDLPFC) and the right temporoparietal junction (rTPJ), aligned between leaders and followers if they had bonded. The authors state that this neural synchronisation suggests that leaders may be anticipating followers’ mental states during group decision-making, though they acknowledge that their findings are restricted to East Asian Chinese individuals communicating via text (without non-verbal cues), whose culture emphasises group cohesion and commitment towards group leaders.
The authors add, “Social bonding increases information exchange and prefrontal neural synchronisation selectively among individuals with different social statuses, providing a potential neurocognitive explanation for how social bonding facilitates the hierarchical structure of human groups.”
A new study by researchers at UC Davis Health found human brains are getting larger. Study participants born in the 1970s had 6.6% larger brain volumes and almost 15% larger brain surface area than those born in the 1930s. The researchers hypothesise that the increased brain size may lead to an increased brain reserve, potentially reducing the overall risk of age-related dementias.
“The decade someone is born appears to impact brain size and potentially long-term brain health,” said first author Charles DeCarli, a distinguished professor of neurology and director of the UC Davis Alzheimer’s Disease Research Center.
“Genetics plays a major role in determining brain size, but our findings indicate external influences – such as health, social, cultural and educational factors – may also play a role.”
75-year study reveals brain changes between generations
The researchers used brain magnetic resonance imaging (MRIs) from participants in the Framingham Heart Study (FHS). The community-based study was launched in 1948 in Framingham, Massachusetts, to analyse patterns of cardiovascular and other diseases.
The original cohort consisted of 5209 men and women between the ages of 30 and 62. The research has continued for 75 years and now includes second and third generations of participants.
The MRIs were conducted between 1999 and 2019 with FHS participants born during the 1930s through the 1970s.
The brain study consisted of 3226 participants (53% female, 47% male) with an average age of about 57 at the time of the MRI.
The research led by UC Davis compared the MRIs of people born in the 1930s to those born in the 1970s.
It found gradual but consistent increases in several brain structures.
For example, a measure that looked at brain volume (intracranial volume) showed steady increases decade by decade.
For participants born in the 1930s, the average volume was 1234mL, but for those born in the 1970s, the volume was 1321 mL, or about 6.6% greater volume.
Cortical surface area showed an even greater increase over the decades.
Participants born in the 1970s had an average surface area of 2104cm2 compared to 2056cm2 for participants born in the 1930s — almost a 15% increase in volume.
The researchers found brain structures such as white matter, gray matter and hippocampus (a brain region involved in learning and memory) also increased in size when comparing participants born in the 1930s to those born in the 1970s.
Larger brains may mean lower incidence of dementia
Although the numbers are rising with America’s aging population, the incidence of Alzheimer’s – the percentage of the population affected by the disease – is decreasing.
A previous study found a 20% reduction in the incidence of dementia per decade since the 1970s.
Improved brain health and size may be one reason why.
“Larger brain structures like those observed in our study may reflect improved brain development and improved brain health,” DeCarli said.
“A larger brain structure represents a larger brain reserve and may buffer the late-life effects of age-related brain diseases like Alzheimer’s and related dementias.”
One of the study’s strengths is the design of the FHS study, which allows the researchers to examine brain imaging of three generations of participants with birthdates spanning almost 80 years.
A limitation is that non-Hispanic white participants make up the majority of the FHS cohort, which is not representative of the U.S. population.
Anorexia nervosa, a mental health disorder in which people dangerously restrict their eating or purge their stomachs soon after a meal, is one of the deadliest psychological diseases. Yet, the neural mechanisms behind this have remained unclear, and therapies are limited.
Scientists have been tailing a lead for years, though. They’ve known that the disorder is often associated with anxiety and depression, hinting that the biological basis for anorexia could be regulated by neurons somewhere in the brain region that controls emotion – the amygdala.
That’s exactly where Haijiang Cai, a University of Arizona associate professor in the Department of Neuroscience and BIO5 Institute member, and his team found it: Anorexia is caused by a combination of two subregions in the amygdala, according to new research published in Cell Reports.
One knot of neurons in the central nucleus of the amygdala curbs appetite when a person gets full, feels nauseous or tastes something bitter. The other is in the oval region of the bed nucleus of the stria terminalis, which also halts eating due to inflammation and sickness.
Cai and his research team found that when they destroyed a certain type of brain cell, called PKC-delta neurons, in both of these regions, they could prevent anorexia development.
They also found that PKC-delta neurons become more active in response to eating during the anorexia development. What’s more, when they artificially activated these neurons, they caused a suppression in eating habits and increased exercise.
“This study suggests two important insights to treat anorexia,” Cai said. “One is that we need to target multiple brain regions to develop therapies. We also need to treat multiple conditions. For example, maybe one drug will target nausea and another drug target will target inflammation, and you have to combine them, like a cocktail therapy, to have better therapeutic effects.”
The team relied on mice models for their research.
“There’s no animal model that can mimic human disease completely, but this is as close as we can get,” Cai said. “For example, there are multiple common features, including a warped body image, a very low body weight, limited food intake and excessive exercise. We can’t know if an animal has a warped body image, but we can measure the other three features.”
One future step – since researchers cannot destroy neurons for human treatment – is to develop a method to silence the neurons temporarily, using drugs or some other method to test if that can prevent anorexia development or speed up recovery for people who have already developed the disorder.
