Month: September 2024

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fMRI Discovers Where Love Resides in the Brain

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The image represents a statistical average of how different types of love light up different regions of the brain. Photo: Pärttyli Rinne et al 2024, Aalto University.

We use the word ‘love’ in a bewildering range of contexts, from sexual adoration to parental love or the love of nature. Now, more comprehensive imaging of the brain may shed light on why we use the same word for such a diverse collection of human experiences.

“You see your newborn child for the first time. The baby is soft, healthy and hearty – your life’s greatest wonder. You feel love for the little one.”

The above statement was one of many simple scenarios presented to 55 parents, self-described as being in a loving relationship. Researchers from Aalto University utilised functional magnetic resonance imaging (fMRI) to measure brain activity while subjects mulled brief stories related to six different types of love.

“We now provide a more comprehensive picture of the brain activity associated with different types of love than previous research,” says Pärttyli Rinne, the philosopher and researcher who coordinated the study. “The activation pattern of love is generated in social situations in the basal ganglia, the midline of the forehead, the precuneus and the temporoparietal junction at the sides of the back of the head.”

Love for one’s children generated the most intense brain activity, closely followed by romantic love.

“In parental love, there was activation deep in the brain’s reward system in the striatum area while imagining love, and this was not seen for any other kind of love,” says Rinne. Love for romantic partners, friends, strangers, pets and nature were also part of the study, which was published in the journal Cerebral Cortex.

According to the research, brain activity is influenced not only by the closeness of the object of love, but also by whether it is a human being, another species or nature.

Unsurprisingly, compassionate love for strangers was less rewarding and caused less brain activation than love in close relationships. Meanwhile, love of nature activated the reward system and visual areas of the brain, but not the social brain areas.

Pet-owners identifiable by brain activity

The biggest surprise for the researchers was that the brain areas associated with love between people ended up being very similar, with differences lying primarily in the intensity of activation. All types of interpersonal love activated areas of the brain associated with social cognition, in contrast to love for pets or nature – with one exception.

Subjects’ brain responses to a statement like the following, on average, revealed whether or not they shared their life with a furry friend:

“You are home lolling on the couch and your pet cat pads over to you. The cat curls up next to you and purrs sleepily. You love your pet.”

“When looking at love for pets and the brain activity associated with it, brain areas associated with sociality statistically reveal whether or not the person is a pet owner. When it comes to the pet owners, these areas are more activated than with non-pet owners,” says Rinne.

Love activations were controlled for in the study with neutral stories in which very little happened. For example, looking out the bus window or absent-mindedly brushing your teeth. After hearing a professional actor’s rendition of each ‘love story’, participants were asked to imagine each emotion for 10 seconds.

This is not the first effort at finding love for Rinne and his team, which includes researchers Juha Lahnakoski, Heini Saarimäki, Mikke Tavast, Mikko Sams and Linda Henriksson. They have undertaken several studies seeking to deepen our scientific knowledge of human emotions. The group released research mapping subjects’ bodily experiences of love a year ago, with the earlier study also linking the strongest physical experiences of love with close interpersonal relationships.

Not only can understanding the neural mechanisms of love help guide philosophical discussions about the nature of love, consciousness, and human connection, but also, the researchers hope that their work will enhance mental health interventions in conditions like attachment disorders, depression or relationship issues.

Source: Aalto University

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Brain Ages at Different Paces According to Social and Physical Environments

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An international study employing advanced measurements of brain ageing on a wide range of participants found that people from more disadvantaged countries and backgrounds had older biological ages for their brains compared to chronological ages. The results are published in Nature Medicine.

The pace at which the brain ages can vary significantly among individuals.  This difference between biological and chronological ages may be affected by environmental factors like pollution and social factors like income or health inequalities, especially in older people and those with dementia. Until now, it was unclear how these combined factors could either accelerate or delay brain ageing across diverse geographical populations. 

The study used advanced brain clocks based on deep learning of brain networks, involved a diverse dataset of 5306 participants from 15 countries. By analysing data from functional magnetic resonance imaging (fMRI) and electroencephalography (EEG), the researchers quantified brain age gaps in healthy individuals and those with neurodegenerative conditions such as mild cognitive impairment (MCI), Alzheimer’s disease, and frontotemporal lobe degeneration (FTLD). 

Participants with a diagnosis of dementia, particularly Alzheimer’s disease, exhibited the most critical brain age gaps. The research also highlighted sex differences in brain ageing, with women in Latin American and Caribbean countries showing greater brain age gaps, particularly in those with Alzheimer’s disease. These differences were linked to biological sex and gender disparities in health and social conditions. Variations in signal quality, demographics, or acquisition methods did not explain the results. These findings underscore the role of environmental and social factors in brain health disparities. 

The findings of this study have profound implications for neuroscience and brain health, particularly in understanding the interaction between macro factors (exposome) and the mechanisms that underlie brain ageing across diverse populations in healthy ageing and dementia. The study’s approach, which integrates multiple dimensions of diversity into brain health research, offers a new framework for personalised medicine. This framework could be crucial for identifying individuals at risk of neurodegenerative diseases and developing targeted interventions to mitigate these risks. Moreover, the study’s results highlight the importance of considering the biological embedding of environmental and social factors in public health policies. Policymakers can reduce brain age gaps and promote healthier ageing across populations by addressing issues such as socioeconomic inequality and environmental pollution. 

Source: University of Surrey

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Competition Law has again Worked to Fight a Bad Drug Patent, but We Need Other Solutions

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By Fatima Hassan and Leena Menghaney

A Competition Commission probe recently resulted in a patent on an important tuberculosis medicine being dropped in South Africa. Twenty years ago, a similar Competition Commission case resulted in a settlement that helped drive down the prices of several antiretrovirals, thereby helping to set the stage for the country’s HIV treatment programme. Fatima Hassan and Leena Menghaney connect the dots between the two landmark cases and map out what has and has not changed over the last two decades.

In the late 1990s and early 2000s, South Africa faced a major uncontrolled AIDS epidemic, worsened by state sponsored AIDS denialism. South Africa was at the epicentre of a global epidemic, with hundreds of thousands of people getting sick and dying, needlessly, because lifesaving antiretroviral medicines were out of reach.

This was in the main because of the Mbeki government’s deadly science denialism denying public sector patients antiretrovirals and the high cost of some of these medicines, which at the turn of the century was available in the private sector but only for the very rich or medically insured. The private sector price for the combination of three antiretrovirals needed by most people living with HIV was exorbitant.

This was because of patent monopolies held at the time by multinational pharmaceutical companies, particularly GlaxoSmithKline (GSK) and Boehringer Ingelheim (BI). In essence, people in South Africa living with HIV had to beg to live – by seeking donations and charity or pressuring their respective medical schemes to provide coverage. Meanwhile, lifesaving antiretrovirals were generally available in the Global North and in some parts of the Global South where governments like those in Thailand and Brazil had taken action to reduce prices.

Hundreds of thousands of people in South Africa died prematurely because they did not get access to these medicines in time.

The landmark Hazel Tau case

Looking for a way to challenge the high prices of key antiretrovirals, activists turned to South Africa’s newly revamped post-apartheid competition law. In September 2002, the Treatment Action Campaign, Hazel Tau, a woman living with HIV and several others lodged a complaint with the country’s Competition Commission. They alleged that the price that GSK and BI were charging for important antiretrovirals was excessive and anti-competitive, undermining not just Competition Law but also the right to health as enshrined in the country’s still fairly new Constitution.

The Competition Commission agreed to investigate. Several months later, they announced that there was a prima facie case of excessive pricing and that they would be referring the matter to the Competition Tribunal (the next phase of a complaint to the Competition authorities). Almost immediately after that announcement, TAC was approached by GSK and BI to “settle” the matter. This meant there would be no public hearings, and the companies would not have to defend their pricing decisions in the dock.

The terms of the settlement, negotiated by the TAC’s legal team, mirrored what TAC had publicly demanded at the beginning of the case. Most importantly, GSK and BI agreed to grant voluntary licenses to several generic manufacturers that would allow them to make and sell the antiretrovirals in question. It was this generic competition that would drive down the prices of antiretrovirals in the years that followed.

Even though the Competition Commission only has jurisdiction in South Africa, the licenses included many other African countries, which meant those countries could also benefit from the generic competition and lower prices. The settlement (including the terms of the voluntary licenses) was agreed to by the Competition Commission, made an order and publicly announced, leading to the conclusion of the complaint.

The case, which came to be known as the Hazel Tau case, would in the years to come be recognised as one of the foundations that made large HIV treatment programmes possible in South Africa and other African countries. Despite this victory, the ongoing effects of AIDS denialism meant that it would in reality be several years before the more affordable generic antiretrovirals would be made widely available in South Africa.

20 years later, the spotlight is on TB drugs

HIV has not been the only health crisis to affect SA. According to the World Health Organization (WHO), Tuberculosis (TB) is one of the leading infectious causes of death globally, and drug-resistant TB (DR-TB) remains a public health crisis. The WHO estimates that around 304 000 people fall ill with TB in South Africa per year, and it claims over 50 000 lives, which means it remains one of the country’s top killers. While TB rates are slowly declining, there is concern that rates of drug-resistant forms of TB (DR-TB) are increasing. DR-TB requires newer, more expensive treatments.

Republished from Spotlight under a Creative Commons licence.

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Scientists Develop a Way to Turbocharge Genetic Therapy

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Source: Pixabay CC0

Gene therapy, the idea of fixing faulty genes with healthy ones, has held immense promise. But a major hurdle has been finding a safe and efficient way to deliver those genes.

Now, researchers at the University of Hawaiʻi’s John A. Burns School of Medicine (JABSOM) have made a significant breakthrough in gene editing technology that could revolutionise how we treat genetic diseases. Their new method offers a faster, safer, and more efficient way to deliver healthy genes into the body, potentially leading to treatments for hundreds of conditions.

Current methods can fix errors in genes, but they can also cause unintended damage by creating breaks in the DNA. Additionally, they struggle to insert large chunks of genetic material such as whole genes.

The new technique, developed by Dr Jesse Owens along with his team Dr Brian Hew, Dr Ryuei Sato and Sabranth Gupta, from JABSOM’s Institute for Biogenesis Research and Cell and Molecular Biology Department, addresses these limitations. They used laboratory evolution to generate a new super-active integrase capable of inserting therapeutic genes into the genome at record-breaking efficiencies.

“It’s like having a “paste” function for the human genome,” said Dr Owens. “It uses specially engineered ‘integrases’ to carefully insert healthy genes into the exact location needed, without causing breaks in the DNA. This method is much more efficient, with success rates of up to 96% in some cases.”

“This could lead to faster and more affordable treatments for a wide range of diseases, potentially impacting hundreds of conditions with a single faulty gene,” said Dr. Owens.

Faster treatment development and a broader application

The implications of this research extend beyond gene therapy. The ability to efficiently insert large pieces of DNA has applications in other areas of medicine.

When making cell lines to produce therapeutic proteins, the gene encoding the protein is usually randomly inserted into the genome, and it rarely lands in a location in the genome that is good for production. This is like searching for a needle in a haystack. Additionally, finding a cell with the gene inserted correctly and producing the desired protein can take many months.

Instead of searching for a needle in a haystack, Dr Owens’ technique makes a stack of needles. It delivers the gene directly to the desired location, significantly speeding up the development process.

“JABSOM takes pride in nurturing talented researchers like Jesse Owens, whose work has the power to create a global impact,” said Sam Shomaker, dean of the University of Hawaiʻi John A. Burns School of Medicine. “This research, conducted in our lab in the middle of the Pacific, has the potential to significantly improve the way we treat genetic diseases.”  

Dr Owens’ team is exploring how this technique could accelerate the development and manufacture of biologics and advanced therapies such as antibodies. Currently, finding the right cell line for efficient production can be a time-consuming process. However, Dr Owens’ new genome engineering tool can reduce the cell line development timeline and accelerate the manufacture of life-saving therapeutics. 

Source: University of Hawaii at Manoa

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Treatment with Dopamine Alleviates Symptoms in Alzheimer’s Disease

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Neurons in the brain of an Alzheimer’s patient, with plaques caused by tau proteins. Credit: NIH

A new way to combat Alzheimer’s disease has been discovered by Takaomi Saido and his team at the RIKEN Center for Brain Science (CBS) in Japan. Using mouse models, the researchers found that treatment with dopamine could alleviate physical symptoms in the brain as well as improve memory. Published in Science Signaling, the study examines dopamine’s role in promoting the production of neprilysin, an enzyme that can break down the harmful plaques in the brain that are the hallmark of Alzheimer’s disease. If demonstrated in human clinical trials, it could lead to a fundamentally new way to treat the disease.

The formation of hardened plaques around neurons is one of the earliest signs of Alzheimer’s disease, often beginning decades before behavioural symptoms such as memory loss are detected. These plaques are formed from pieces of the peptide beta-amyloid that accumulate over time. In the new study, Saido’s team at RIKEN CBS focuses on the enzyme neprilysin because previous experiments showed that genetic manipulation that produces excess neprilysin in the brain (a process called upregulation) resulted in fewer beta-amyloid plaques and improved memory in mice.

Neprilysin by itself cannot be a medication as it cannot enter the brain from the blood stream, so the researchers screened molecules to determine which ones can naturally upregulate neprilysin in the correct parts of the brain. The team’s previous research led them to narrow down the search to hormones produced by the hypothalamus, and they discovered that applying dopamine to brain cells cultured in a dish yielded increased levels of neprilysin and reduced levels of free-floating beta-amyloid.

Now the serious experiments began. Using a DREADD system, they inserted tiny designer receptors into the dopamine producing neurons of the mouse ventral tegmental area. By adding a matching designer drug to the mice’s food, the researchers were able to continuously activate those neurons, and only those neurons, in the mouse brains. As in the dish, activation led to increased neprilysin and decreased levels of free-floating beta-amyloid, but only in the front part of the mouse brain. But could the treatment remove plaques? Yes. The researchers repeated the experiment using a special mouse model of Alzheimer’s disease in which the mice develop beta-amyloid plaques. Eight weeks of chronic treatment resulted in significantly fewer plaques in the prefrontal cortex of these mice.

The DREADD system is an incredible system for precise manipulation of specific neurons. But it is not very useful for human clinical settings. The final experiments tested the effects of L-DOPA treatment. L-DOPA is a dopamine precursor molecule often used to treat Parkinson’s disease because it can enter the brain from the blood, where it is then converted into dopamine. Treating the model mice with L-DOPA led to increased neprilysin and decreased beta-amyloid plaques in both frontal and posterior parts of the brain. Model mice treated with L-DOPA for three months also performed better on memory tests than untreated model mice.

Tests showed that neprilysin levels naturally decreased with age in normal mice, particularly in the frontal part of the brain, perhaps making it a good biomarker for preclinical or at-risk Alzheimer’s disease diagnoses. How dopamine causes neprilysin levels to increase remains unknown, and is the next research topic for Saido’s group.

“We have shown that L-DOPA treatment can help reduce harmful beta-amyloid plaques and improve memory function in a mouse model of Alzheimer’s disease,” explains Watamura Naoto, first author of the study. “But L-DOPA treatment is known to have serious side effects in patients with Parkinson’s disease. Therefore, our next step is to investigate how dopamine regulates neprilysin in the brain, which should yield a new preventive approach that can be initiated at the preclinical stage of Alzheimer’s disease.”

Source: RIKEN

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Oestrogen’s Protection against Fatty Liver Points to New Drug Treatment

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Photo by The Creative Exchange on Unsplash

New research from Karolinska Institutet shows how oestrogen protects against MASLD, a fatty liver disease on the increase in the obesity epidemic. The study, published in Molecular Systems Biology, shows how a new drug under development could become a future treatment for fatty liver disease and liver cancer.

The global obesity epidemic has resulted in a dramatic increase in fatty liver, a disease in which fat that does not fit into fat cells is stored in liver cells instead.

Since last year, fatty liver due to obesity (and not excessive alcohol consumption) is known as MASLD (metabolic dysfunction-associated steatotic liver disease). According to previous research, as many as one in three adults are affected by some degree of MASLD, which in the worst cases can develop into cirrhosis and liver cancer.

Protection until menopause

However, the disease is very unevenly distributed between the sexes, with a large majority of affected individuals being men.

“Women have a natural protection until menopause due to the female sex hormone oestrogen,” explains study leader Claudia Kutter, senior researcher at the Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet.

Although women’s protection has been known for some time, the mechanism behind the protective effect has been less clear. Now Claudia Kutter’s research team may have found the answer.

Through genetic analyses of mice of both sexes fed a high-fat diet, with some of the male mice also receiving oestrogen, the researchers were able to identify a key protein in the development of fatty liver. 

The protein, called TEAD1, was found to play an overall role in regulating how liver cells absorb fat. Blocking TEAD1 protected liver cells from the harmful accumulation of fat. Mice receiving oestrogen treatment had lower TEAD1 activity and less fat accumulation in the liver.

New drug under development

In the next step, the researchers tested blocking TEAD1 in human liver cells with the same result. The fact that this was possible at all, however, was a bit of luck.

“It turned out that a pharmaceutical company is developing an anti-cancer drug that blocks TEAD1, which allowed us to test our hypothesis,” says Claudia Kutter.

The fact that TEAD1 is also involved in cancer does not worry her, quite the contrary.

“Since the activity of TEAD proteins is elevated in cancer, blocking TEAD at an early stage can also be positive from a cancer point of view,” she says. “Patients suffering from liver cancer are currently diagnosed very late. If the patient is given this drug early in the process to protect against fatty liver, it can hopefully also prevent the development of liver cancer.”

The pharmaceutical company will now start clinical trials of the drug as a protection against fatty liver disease, while Claudia Kutter’s research team will continue researching further ways to tackle the disease.

“We want to focus on how to find the disease earlier and identifying new treatment targets,” she says. “Different approaches may be needed for different patients depending on their gender and hormonal status.”

Source: Karolinska Institutet

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Weekend Sleep Catchup may Lower Heart Disease Risk by up to 20%

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Photo by Mert Kahveci on Unsplash

The demands of the working week, often influenced by school or work schedules, can lead to sleep disruption and deprivation. Fortunately, new research presented at ESC Congress 2024 shows that people that ‘catch up’ on their sleep by sleeping in at weekends may see their risk of heart disease fall by one-fifth.  

“Sufficient compensatory sleep is linked to a lower risk of heart disease,” said study co-author Mr Yanjun Song of the State Key Laboratory of Infectious Disease, Fuwai Hospital, National Centre for Cardiovascular Disease, Beijing, China. “The association becomes even more pronounced among individuals who regularly experience inadequate sleep on weekdays.” 

It is well known that people who suffer sleep deprivation ‘sleep in’ on days off to mitigate the effects of sleep deprivation. However, there is a lack of research on whether this compensatory sleep helps heart health.  

The authors used data from 90 903 subjects involved in the UK Biobank project, and to evaluate the relationship between compensated weekend sleep and heart disease, sleep data was recorded using accelerometers and grouped by quartiles (divided into four approximately equal groups from most compensated sleep to least). Q1 (n = 22 475 was the least compensated, having -16.05 hours to -0.26 hours (ie, having even less sleep); Q2 (n = 22 901) had -0.26 to +0.45 hours; Q3 (n=22 692) had +0.45 to +1.28 hours, and Q4 (n=22 695) had the most compensatory sleep (1.28 to 16.06 hours). 

Sleep deprivation was self-reported, with those self-reporting less than 7 hours sleep per night defined as having sleep deprivation.  A total of 19 816 (21.8%) of participants were defined as sleep deprived. The rest of the cohort may have experienced occasional inadequate sleep, but on average, their daily hours of sleep did not meet the criteria for sleep deprivation – the authors recognise this a limitation to their data. 

Hospitalisation records and cause of death registry information were used to diagnose various cardiac diseases including ischaemic heart disease (IHD), heart failure (HF), atrial fibrillation (AF), and stroke. 

With a median follow-up of almost 14 years, participants in the group with the most compensatory sleep (quartile 4) were 19% less likely to develop heart disease than those with the least (quartile 1). In the subgroup of patients with daily sleep deprivation those with the most compensatory sleep had a 20% lower risk of developing heart disease than those with the least. The analysis did not show any differences between men and women. 

Co-author Mr Zechen Liu, also of State Key Laboratory of Infectious Disease, Fuwai Hospital, National Centre for Cardiovascular Disease, Beijing, China, added: “Our results show that for the significant proportion of the population in modern society that suffers from sleep deprivation, those who have the most ‘catch-up’ sleep at weekends have significantly lower rates of heart disease than those with the least.”  

Source: European Society of Cardiology

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When is the Best time of Day for Chemotherapy?

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Photo by Malvestida on Unsplash

Researchers from Charité are developing new methods to use the internal clock inside tumour cells to optimise cancer therapies

One of the factors determining the effectiveness of certain medications depends on various factors, including the time of day when they are administered. This is due to circadian rhythms, which vary across individuals and makes it difficult to tailor medication schedules. Researchers at Charité – Universitätsmedizin Berlin have now developed a method for determining the optimum time of cancer treatment based on certain breast cancer cell lines. They describe their approach in the journal Nature Communications.

As well as bodily functions and metabolic processes, such as sleep and digestion, individual cells also follow a circadian rhythm. This is hugely important to chemotherapy. Previous studies have shown that chemotherapy is most effective when the tumour cells are dividing. But this finding has been hardly used at all in clinical treatment to date.

An interdisciplinary team at Charité headed by Dr. Adrián Enrique Granada from the Charité Comprehensive Cancer Center (CCCC) set out to close this gap. The team began looking for the optimum time to administer medication, based on the individual circadian rhythms of the tumors.

Triple-negative breast cancer as an example

“We cultured cells from patients with triple-negative breast cancer to observe how they respond at different times of day to the medications administered,” explains Carolin Ector, a research associate in Granada’s working group. Triple-negative breast cancer is a highly aggressive form of breast cancer, with few effective treatments available. “We used live imaging, a method of continuously monitoring living cells, and complex data analysis techniques to monitor and evaluate the circadian rhythms, growth cycles, and medication responses of these cancer cells in detail.”

In this way, the researchers identified certain times of the day at which cancer cells are most responsive to medication-based treatments. For example, the chemotherapeutic drug 5-fluorouracil (5-FU) turned out to have peak efficacy against a certain cancer cell line between eight and ten a.m. As the study also shows, the crucial aspects here are certain cellular and genetic factors. The scientists were even able to identify which genes are key to the circadian effects of certain medications. “We call them ‘core clock genes’. They have a significant impact on how responsive cancer cells are to treatments administered at different times of day,” Granada explains.

Profiles show how cancer cell types respond to medications

This approach can be used to create detailed profiles showing how different types of cancer cells respond to different medications at various times. “This can help to identify the most effective combinations of drugs,” Granada says. “Overall, our findings indicate that personalized treatment plans based on individual circadian rhythms could substantially improve the efficacy of cancer treatment”, he concludes. Moreover, undesirable side effects could also be reduced.

For these findings to contribute to clinical practice soon, the results should be validated in studies involving larger groups of patients. “We’re also planning to study the molecular mechanisms behind the circadian influences on medication sensitivity to further optimize treatment times and identify new therapeutic targets,” Granada says.

Source: Charité – Universitätsmedizin Berlin

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Hospital Association Tables Proposal for Enhanced Healthcare through a Viable Proven Solution

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Netcare Christiaan Barnard Memorial Hospital

Monday, 2 September – Johannesburg, South Africa

Mandatory health cover of formally employed is tried and tested and if put to use in South Africa could reduce the public health burden, increase public per capita spend on health, and free up resources that could help address the country’s most pressing health crises.

With widespread concern that the National Health Insurance Fund is unaffordable and will take too long to implement while most South Africans already struggle to access quality healthcare services, Netcare Chief Executive Office Dr Richard Friedland has raised the possibility of near-term solutions including an under-explored alternative.

Speaking at the Hospital Association of South Africa Conference in Sandton, he stated that private hospitals wish to work with government to find solutions to our country’s healthcare problems. He pointed to mandatory medical cover for the formally employed as a potential solution that has been well-researched over two decades and is a “workable solution that if implemented will be quick to roll out and in a very short time provide enhanced healthcare to all South Africans.”

Friedland pointed out that the African National Congress’ 1994 Health Plan recommended mandatory cover for the formally employed and the National Department of Health Social Health Insurance Working Group in 1997 recommended that mandatory cover for formal sector employees should be confined to those above the income tax threshold, due to affordability concerns.

What this all offers, explained Friedland, is a middle ground option. If the government mandates those South Africans who are formally employed together with their families to be covered by some form of health insurance or medical aid, “This will enable public health sector resources to be dedicated to the informally employed, unemployed and indigent.”

“With a formally employed population of 11.5 million, together with the estimated number of dependants, based on a 2.4 beneficiary ratio, this could result in up to 27.5 million of our population that could potentially over time become covered, leaving the remaining 35.5 (56% of the population) people dependent on public health resources,” Friedland said.

Government public health per capita spend, he said, could increase over time by 52% without any additional funding of the public sector budget.

“In simple terms, if one considered the entire population in South Africa, government’s responsibility would reduce from the current 85% of the population covered by public health to 56%,” he said.

The latest per capita public expenditure based on a consolidated health budget of R271 billion works out to R5054, when considering the population and excluding medical scheme users. With formal employment coverage, that per capita public expenditure on public health users would increase 52% to R7 659, research shows.

Friedland also told the audience that getting the scheme off the ground could be done in three phases.

Phase one would involve including the formally employed and their dependants who are above the tax threshold. This would grow the medical scheme coverage from 9,2 to 15,4 million. The completion of Phase 1 would also expand public per capita spend by 12,9% at present day levels.

Phase 2 would include those formally employed and dependents who are below the tax threshold. This would push medical scheme coverage to 27,5 million and expand public per capita spend to 52%.

Phase 3, Friedland explained, will allow for the expansion of the economy through recovery and an increase in employment.

This will have further benefits to South Africa’s health care system with research showing that for every one million formal jobs created, the public health system would benefit with a reduction of approximately 2.4 million people, it will no longer have to serve. Additionally, this will add a 7% increase from Phase 2 on per capita public health spend.

“The health system stands to benefit in more immediate and visceral ways. The reduced load on the public sector will result in a reduced burdens on doctors, nurses and other healthcare workers, will reduce overcrowding, shorten queues and free up funding to fix infrastructure, fund unfunded medical posts, and grow our medical skills training capacity – remember, we have a shortage of 27 000 nurses in South Africa, and this is expected to grow to 70 000 by 2030.

Not only is the idea not new, says Friedland, but similar approaches are adopted elsewhere. In Africa 61% of countries have contributory mandatory programmes for civil servants and 50% of them programmes for sector employees.

The private hospital sector, says Friedland, stands ready to explore this idea and others that result in lessening the load on the shoulders of all South Africans who need accessible quality healthcare today.

“We stand ready to collaborate on further system strengthening, to more private public partnerships, to addressing public sector elective surgery waiting lists, to joint efforts on human resource training collaboration,” he says.

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Pulling Back the Curtain on the Brain Circuit for Memory Recall

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Photo by Anna Shvets

Deep within either hemisphere of the brain is the “claustrum complex”, which contributes to consciousness and awareness. Many diseases known to be related to higher cognitive function, such as Alzheimer’s, schizophrenia, and ADD/ADHD, are also closely linked to abnormal function of this particular part of the brain. But how the different parts of the claustrum complex work or how its circuits and communication system are organised is not fully understood.

Researchers at Aarhus University have now uncovered this, and their results identify, down to the cellular level, which part of the claustrum complex controls our ability to discriminate familiar and novel things.

“Our study focuses on an area of the claustrum called the ‘endopiriform,’ which is a relatively unknown brain structure despite its unique brain network and cellular properties,” explains Asami Tanimura, an associate professor and the lead researcher of the study appearing as a preprint in eLife.

“For the first time, we have dissected the circuit of endopiriform to the hippocampus, and demonstrated how this pathway is crucial for recognition memory.”

In mouse models, researchers were able to observe how the mice’s behaviour changed when they respectively ‘turned on’ and ‘turned off’ the activity in this specific cell group.

Asami explains: “We observed that the cells in the endopiriform were active when the mice interacted with new conspecifics or objects, and when we inhibited this cell group, it reduced the mice’s ability to distinguish novel mouse or object from familiar ones.”

Based on this, the researchers concluded that this specific cell group in the claustrum seems to play a key role in sending memory-guided attention signal to the hippocampus.

“This is entirely new knowledge about this small but important part of the brain, and it gives us a unique understanding of the special circuit involved in recognition memory,” explains Asami.

What this knowledge might mean, and whether it could lead to the development of new treatment methods targeted at disorders in this part of the brain, remains to be seen. However, Asami and her colleagues are optimistic:

“To develop effective treatment methods, a very detailed understanding of the cells’ circuits is required. With our study, we have at least opened a door that has previously been closed in terms of specific role of the endopiriform-hippocampal circuit on higher cognitive function.”

Source: Aarhus University