Never Steady, Never Still borne out of filmmaker's connection to Parkinson's

By: Steve Gow - Mar 01 2018

Kathleen Hepburn's feature tells the tale of a small-town mother and son coping with independence after tragedy befalls the family.

Shirley Henderson as Judy in Never Steady, Never Still. “I wanted someone who felt fragile (with) more of an internal strength than external strength,” said director Kathleen Hepburn of Henderson (Trainspotting).

Kathleen Hepburn may adore making movies for many reasons but above all, the acclaimed filmmaker insists she loves learning about the world through character and storytelling.

“I feel like each project is about trying to learn more about the world,” said the Vancouver-born director recently. “And the people who exist outside of myself.”

While Hepburn may seek inspiration externally, she remained fairly close-to-home for her feature Never Steady, Never Still. Inspired by her own mother’s struggles with Parkinson’s disease, the movie tells the tale of a small-town mother and son coping with independence after tragedy befalls the family.

“It’s a huge part of the film but to me the film is about a lot more,” said Hepburn of the drama’s spotlight on Parkinson’s. “It seemed to be an important story that I needed to tell because it's such an important part of my life, (but) it’s about communication and strength; about the person struggling and dealing with things.”

Still, Hepburn discovered that by breathing life into Parkinson’s disease, she not only was able to provide insight to moviegoers, but she also uncovered an ability to provide hope through cinema — even as she avoided sugar-coating Parkinson’s debilitating effects on the central nervous system.

“I know people like to see stories about overcoming things, and I think in this film, that is there,” said Hepburn on the realist drama. “She is overcoming in that she’s carrying on, and carrying on is a really overlooked achievement in life; we’re faced with so many struggles in so many ways and to just not give up is a huge achievement.”

And Hepburn should know — her own persistence with the movie is an achievement. Adapted from her 2015 short film, Never Steady now boasts eight nominations at the upcoming Canadian Screen Awards and is being rewarded as one of the nation’s brightest movies of the year.

“It's nice to have someone say they watched the film and it resonates, (but the awards) are really great in that they get audiences to come see films, which is most important,” said Hepburn. “How (else) do you market a film in this day if it's not a blockbuster?”

https://youtu.be/3a6ca9bm6NA
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https://youtu.be/LP-Kfh6S4c4

http://www.metronews.ca/entertainment/2018/03/01/never-steady-never-still-borne-out-of-filmmaker-s-connection-to-parkinson-s.html

Wellfleet library hosts ‘Women in Science’ series

March 2, 2018

Wellfleet Public Library will celebrate Women’s History Month in March with its Third Annual Women in Science Series. The events are held on Sundays at 3 p.m.

The series, which is free and open to all ages, is made possible by the Friends of the Wellfleet Library. Here’s the line up:

March 18: Studying Neurodegenerative Diseases with Assistant Professor of Biology at Northeastern Illinois University, Cindy Voisine.

As the brain ages, it becomes susceptible to a variety of neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease and Amyotrophic lateral sclerosis (ALS).

A common feature of these age-related neurodegenerative disorders is that specific proteins associated with each disease tend to clump and form large aggregated masses in nerve cells leading to loss of neuron function and death.

Voisine’s research group examines the problems of disease protein aggregation, focusing on ALS, more commonly known as Lou Gehrig’s disease. ALS is a fatal neurodegenerative disease characterized by the progressive loss of motor neurons. Motor neurons are responsible for innervating muscle cells.

Recent studies suggest that these clumping proteins act like prions and infect neighboring cells, spreading neurotoxicity. Deciphering the mechanism of cell-to-cell transmissibility will reveal pathways underlying the spread of ALS within the brain and spinal cord, she says. Identifying these pathways is a necessary first step for development of therapeutics to treat ALS.

http://brewster.wickedlocal.com/news/20180302/wellfleet-library-hosts-women-in-science-series

Networks of Brain Activity Predict Vulnerability to Depression

NEUROSCIENCE NEWS   MARCH 2, 2018
Source: Duke University.

A new mouse study discovers different networks of brain activity in animals more susceptible to developing depression following a stressful event.

Mice that are more vulnerable to developing depression-like symptoms show different networks of electrical brain activity than mice that are more resilient. NeuroscienceNews.com image is credited to Jeff Macinnes and Kafui Dzirasa, Duke University.

Tapping into the electrical chatter between different regions of the brain may provide a new way to predict and prevent depression, according to new research by Duke University neuroscientists and electrical engineers.

The researchers found different networks of electrical brain activity in mice that were more susceptible to developing depression-like symptoms following stressful events than in more resilient mice.

If replicated in humans, these results could be the first step toward a test to predict a person’s vulnerabilty to developing mental illnesses like depression.

“What we are essentially creating is an electrical map of depression in the brain,” said Dr. Kafui Dzirasa, associate professor of psychiatry and behavioral sciences, neurobiology and biomedical engineering at the Duke University School of Medicine. “We hope this could be used as a predictive signature of depression, in the same way that blood pressure is a predictive signature of who will ultimately have a heart attack or stroke.”

The study appeared March 1 in the journal Cell.

Most people experience major life stressors from time to time. The death of a loved one, loss of a job or challenging medical diagnosis can cause difficult emotions such as grief, sadness, anxiety or anger. But while some are able to bounce back from these stressors relatively quickly, others go on to experience mental illnesses such as depression or anxiety.

For the past three decades, neuroscientists have used imaging and electrical monitoring to study how activity in individual brain regions may predispose an individual to developing mental illness.

In 2010, Dzirasa and his graduate mentor, Dr. Miguel Nicolelis, developed a technique that can monitor electrical activity in not just one region of the mouse brain, but in many regions simultaneously. The results reveal how different areas of the brain work together to create specific mental states.

“You can think of different brain regions as individual instruments in an orchestra,” Dzirasa said. “We are interested in not just what each instrument is doing, but how the instruments coordinate themselves to generate music.”

In the experiment, each test mouse was placed in a cage with a larger and more aggressive mouse. After residing with this pugnacious roommate for ten days, many mice developed symptoms that resemble depression in humans, including anxiety, social avoidance and difficulty sleeping.

Before and after experiencing this stress, Dzirasa and postdoctoral fellow Rainbo Hultman measured brain activity in seven different brain regions that have been linked to depression, including the prefrontal cortex, the amygdala and the hippocampus.

Using machine learning techniques developed by Duke colleagues Kyle Ulrich, David Carlson and Lawrence Carin, the team constructed the brain “music” for each mouse. They found the mice who developed depression-like symptoms exhibited different patterns of brain activity both before and after the stress test than those who were more resilient to the experience.

The results may be useful for treatment as well as prevention of depression, Dzirasa said.

“To date, the most effective treatment for depression remains electroconvulsive therapy, but it comes along with a lot of side-effects,” Dzirasa said. “It might be possible to target electricity to the right place in the right way to create a treatment that doesn’t have the same side-effects as putting electricity everywhere.”

Monitoring networks of electrical brain activity holds promise for understanding not only depression, but other forms of mental illness as well, said Conor Liston, an assistant professor of neuroscience and psychiatry at Weill Cornell Medicine who was not involved in the study.

“Many scientists believe that the behavioral and clinical symptoms that define most psychiatric conditions — not just depression — are driven by changes at the brain network level,” Liston said in an email. “This report defines a new approach combining machine learning and other state-of-the-art statistical methods with multi-circuit recordings in mice that will probably inspire investigators to apply similar methods to advance our understanding of the neurobiology underlying other forms of mental illness.”

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Funding: This work was supported by the National Institutes of Health (MH79201-03S1, MH099192-05S1, MH099192-05S2 and MH096890) the Lennon Family Foundation, the DARPA HIST program and the One Mind Institute Rising Star Award. Additional support was provided by Kerima L. Collier.

Source: Kara Manke – Duke University

Publisher: Organized by NeuroscienceNews.com.

Image Source: NeuroscienceNews.com image is credited to Jeff Macinnes and Kafui Dzirasa, Duke University.

Original Research: Abstract in Cell.

doi:10.1016/j.cell.2018.02.012

Abstract

Brain-wide Electrical Spatiotemporal Dynamics Encode Depression Vulnerability

Highlights

•Brain-wide electrical spatiotemporal dynamic map of stress states

•Hippocampally directed network signals stress vulnerability in stress-naive animals

•Early life stress increases activity in stress vulnerability network

•Stress vulnerability network is mechanistically distinct from pathology networks

Summary

Brain-wide fluctuations in local field potential oscillations reflect emergent network-level signals that mediate behavior. Cracking the code whereby these oscillations coordinate in time and space (spatiotemporal dynamics) to represent complex behaviors would provide fundamental insights into how the brain signals emotional pathology. Using machine learning, we discover a spatiotemporal dynamic network that predicts the emergence of major depressive disorder (MDD)-related behavioral dysfunction in mice subjected to chronic social defeat stress. Activity patterns in this network originate in prefrontal cortex and ventral striatum, relay through amygdala and ventral tegmental area, and converge in ventral hippocampus. This network is increased by acute threat, and it is also enhanced in three independent models of MDD vulnerability. Finally, we demonstrate that this vulnerability network is biologically distinct from the networks that encode dysfunction after stress. Thus, these findings reveal a convergent mechanism through which MDD vulnerability is mediated in the brain.

http://neurosciencenews.com/depression-brain-activity-8561/

A Better Way to Treat Depression

NEUROSCIENCE NEWS    MARCH 1, 2018
Source: Scripps Researcher Institute.

Researchers have identified a new target for the treatment of major depressive disorder.

The researchers say there is an urgent need for new drug targets in major depressive disorder. NeuroscienceNews.com image is in the public domain.

Scientists on the Florida campus of The Scripps Research Institute (TSRI) have discovered a new target for treating major depressive disorder, a disease that affects more than 16 million American adults. Their research shows that individuals with high levels of an enigmatic receptor called GPR158 may be more susceptible to depression following chronic stress.

“The next step in this process is to come up with a drug that can target this receptor,” says Kirill Martemyanov, PhD, co-chair of the TSRI Department of Neuroscience and senior author of the new study, published recently in the journal eLife.

The researchers say there is an urgent need for new drug targets in major depressive disorder. Current pharmacological treatments for depression can take a month to start working–and they don’t work in all patients.

“We need to know what is happening in the brain so that we can develop more efficient therapies,” says Cesare Orlandi, PhD, senior research associate at TSRI and co-first author of the study.

The researchers zeroed in on GPR158 as a player in depression after discovering that the protein is elevated in people with major depressive disorder. To better understand GPR158’s role, the scientists studied male and female mice with and without GPR158 receptors.

Behavioral tests revealed that both male and female mice with elevated GPR158 show signs of depression following chronic stress. On the flip side, suppression of GPR158 protects mice from developing depressive-like behaviors and make them resilient to stress.

Next, the researchers examined why GPR158 has these effects on depression. The team demonstrated that GPR158 affects key signaling pathways involved in mood regulation in the region of the brain called prefrontal cortex, though the researchers emphasized that the exact mechanisms remain to be established.

Martemyanov explains that GPR158 is a so-called “orphan receptor” (which gets its name because its binding partner/partners are unknown) with a poorly understood biology and mechanism of action. GPR158 appears to work downstream from other important brain systems, such as the GABA, a major player in the brain’s inhibitory control and adrenergic system involved in stress effects.

“This is really new biology and we still need to learn a lot,” says Martemyanov.

The study also offers a potential clue to why some people are more susceptible to mental illness. Because mice without GPR158 don’t alter their behavior after chronic stress, the researchers concluded these mice were naturally more resilient against depression. Their genetics, or gene expression, offer a layer of protection.

Laurie Sutton, PhD, a research associate at TSRI and co-first author of the study, says this finding matches what doctors have noticed in people who have experienced chronic stress. “There’s always a small population that is resilient–they don’t show the depressive phenotype,” says Sutton.

As the search goes on for additional targets for depression, Martemyanov says scientists areincreasingly using new tools in genome analysis to identify orphan receptors like GPR158. “Those are the untapped biology of our genomes, with significant potential for development of innovative therapeutics,” he says.

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Additional authors of the study, “Orphan receptor GPR158 controls stress-induced depression,” were Chenghui Song, Brian S. Muntean, Keqiang Xie, Xiangyang Xie and Baoji Xu of The Scripps Research Institute; Won Chan Oh and Rachel Satterfield of the Max Planck Florida Institute for Neuroscience; Alice Filippini of the University of Brescia; Jazmine D. W. Yaeger and Kenneth J. Renner of the University of South Dakota; Samuel M. Young of the Max Planck Florida Institute for Neuroscience and the University of Iowa; and Hyungbae Kwon of the Max Planck Florida Institute for Neuroscience and the Max Planck Institute of Neurobiology.

Funding: The research was supported by the National Institutes of Health (grants MH105482, HL105550, DA01992, MH107460, 762 DC014093, the University of Iowa, the Max Planck Society and by the Canadian Institutes of Health Research Fellowship.

Source: Stacey Singer DeLoye – Scripps Researcher Institute

Publisher: Organized by NeuroscienceNews.com.

Image Source: NeuroscienceNews.com image is in the public domain.

Original Research: Open access research in eLife.

doi:10.7554/eLife.33273

Abstract

Orphan receptor GPR158 controls stress-induced depression

Stress can be a motivational force for decisive action and adapting to novel environment; whereas, exposure to chronic stress contributes to the development of depression and anxiety. However, the molecular mechanisms underlying stress-responsive behaviors are not fully understood. Here, we identified the orphan receptor GPR158 as a novel regulator operating in the prefrontal cortex (PFC) that links chronic stress to depression. GPR158 is highly upregulated in the PFC of human subjects with major depressive disorder. Exposure of mice to chronic stress also increased GPR158 protein levels in the PFC in a glucocorticoid-dependent manner. Viral overexpression of GPR158 in the PFC induced depressive-like behaviors. In contrast GPR158 ablation, led to a prominent antidepressant-like phenotype and stress resiliency. We found that GPR158 exerts its effects via modulating synaptic strength altering AMPA receptor activity. Taken together, our findings identify a new player in mood regulation and introduce a pharmacological target for managing depression.

http://neurosciencenews.com/depression-treatment-8589/

77-Year-Old Coloradan With Parkinson’s Does An About Face On Marijuana

March 2, 2018  By Mark Ackerman

https://youtu.be/SgX4zwiYvDM

CASTLE ROCK, Colo. (CBS4) – For more than seven decades, Gary Griffin never tried marijuana. The Castle Rock businessman and former Airman considered it “The Devil’s Weed.”

Gary Griffin (credit: CBS)

But at 74, everything changed for Griffin when he was diagnosed with Parkinson’s disease. He started looking for anything that might calm the constant shaking of his hands and the sleepless nights associated with the disease. He read anecdotal accounts from other patients about the benefitsof CBD oil, derived from a non-psychoactive part of the cannabis plant.

Reluctantly, he tried it.

“My first drop,” Griffin remembered thinking. “I may not survive. I may go wild kicking off the balcony.”

“My doctor said,’Don’t go confusing your Googling with my medical degree.'”

Soon Griffin enrolled in Colorado’s first study measuring the effects of CBD oil on patients with Parkinson’s disease. He and a dozen other Parkinson’s patients took pharmaceutical grade CBD oil they got from their neurologist Dr. Maureen Leehey at the University of Colorado Hospital.

“We legalized medical marijuana before we knew it was effective for medical disorders,” said Dr. Leehey who has researched Parkinson’s disease for more than 30 years. “I heard anecdotal accounts from my patients about marijuana use and was concerned it might be dangerous.”

Dr. Maureen Leehey (credit: CBS)

In the first phase of her study, Dr. Leehey’s patients tolerated a low dose of CBD oil well. Many of her patients reported positive effects.

“They had a reduction in our assessment of their motor symptoms and improvement in their night time sleep,” she said. 

But, she cautioned an upcoming “placebo controlled” phase of the study will be necessary to produce meaningful scientific results. Everyone in the first phase knew they were receiving CBD oil which can influence results.

As for Griffin, he only saw a small improvement with the shaking in his hands.

“I hoped for a miracle but it didn’t happen,” he said.

But, he saw a dramatic improvement in his sleep.

“Once I started taking CBD oil, I never had a sleepless night because I couldn’t relax my muscle groups,” he said.

It was so much of an improvement, the man who called marijuana “The Devil’s Weed” has started growing it and processing his own CBD oil at home. 

“I’m not a stoner, but I am a proponent,” he said.

In addition to Parkinson’s Disease, Colorado researchers are currently working to determine if marijuana helps with sleep, pain and epilepsy.

http://denver.cbslocal.com/2018/03/02/pot-shows-promise-parkinsons/

Measuring Levels of Critical Protein May Aid Earlier Diagnosis of Parkinson’s

 MARCH 2, 2018  BY JOSE MARQUES LOPES, PHD 

A new way to measure levels of a critical protein in Parkinson’s disease could lead to improved diagnosis and treatments.

Using a positron emission tomography (PET) imaging camera, Swedish researchers were able to measure  levels of a protein called dopamine transporter (DAT) as a way to investigate the dopamine system in the brains of patients who have Parkinson’s disease.

The research, “Nigrostriatal dopamine transporter availability in early Parkinson’s disease,” was published in the journal Movement Disorders.

Parkinson’s is characterized by selective loss of cells that produce dopamine in a brain area called substantia nigra, which controls the body’s balance and movement. Dopamine is a substance responsible for controlling our movements; as such, loss of dopaminergic cells leads to motor symptoms, such as shaking, slowed movement and difficulty walking.

DAT is responsible for collecting dopamine from the outside of cells and putting it back into neurons,  thereby regulating its effects in the communication between nerve cells (synapse).

DAT functions as a biomarker for dopamine neurons and can be found on their surface, in cell bodies, and in axons (long nerve fibers). So, analyzing DAT’s location enables researchers to map dopamine cells in the brain, a useful tool not only for diagnosis, but also for classifying patients and monitoring their treatment.

The team studied 20 patients (15 men/five women, mean age 62) suffering from mild Parkinsonism, and an equal number of healthy “control” participants. The analysis focused on a specific brain region called the nigrostriatal pathway, which arises from the substantia nigra and also is affected in Parkinson’s disease.

Results showed significantly lower amounts of DAT in nerve endings (36-70 percent) in Parkinson’s patients when compared to healthy controls. However, the amount of DAT remained relatively intact in cell bodies and nerve fibers.

“The results suggest that at early stages of symptomatic Parkinson’s a greater loss is observed at the level of the axonal terminals when compared with cell bodies and axons of dopaminergic neurons,” the researchers wrote.

“These results suggest that in the early stages of the disease dopamine cells are still viable and that, given the correct treatment, it should be possible to restore their function,” Andrea Varrone, MD, PhD, the study’s senior author, said in a press release.

“The method we have developed is likely to be able to assist in the diagnosis of Parkinson’s disease at an earlier stage and predict the development of the disease. DAT can also be used as a biomarker in clinical trials of new medicines and treatment strategies,” Varrone added.

Researchers now plan to examine patients in more advanced stages of the disease to better understand the correlation between DAT and clinical variables in Parkinson’s.

https://parkinsonsnewstoday.com/2018/03/02/measuring-protein-may-enable-earlier-parkinsons-diagnosis/

MRI-Focused Ultrasound Undergoing Phase 3 Clinical Trial for Parkinson’s Treatment

MARCH 2, 2018  BY PATRICIA INACIO, PHD

New technology that uses MRI-guided focused ultrasound to target areas of the brain affected by Parkinson’s disease and improve motor symptoms will be further tested in a pivotal Phase 3 clinical trial.

Led by the University of Maryland Medical Center (UMMC) and the University of Maryland School of Medicine (UMSOM), the randomized trial will assess the safety and effectiveness of the novel procedure. It is the final step before the U.S. Food and Drug Administration (FDA) will consider approving it as a nonsurgical treatment for  Parkinson’s.

“The goal of the focused ultrasound treatment is to both lessen the main symptoms of Parkinson’s disease, which include tremors, rigidity and slow movement, as well as treat the dyskinesia that is a medication side effect, so that less medication is needed,” Howard M. Eisenberg, MD, the trial’s lead investigator, said in a press release.  Eisenberg is a professor and the chair of neurosurgery at both UMSOM and UMMC.

Participants are currently being recruited for the new trial (NCT03319485), which follows a previous study where MRI-guided focused ultrasound led to a 62% improvement in upper-limb tremors, compared with 22% in the control group, in patients with tremor-dominant Parkinson disease who did not respond to other forms of therapy.

Findings were published in the study, “Safety and Efficacy of Focused Ultrasound Thalamotomy for Patients With Medication-Refractory, Tremor-Dominant Parkinson Disease: A Randomized Clinical Trial,” in the journal JAMA Neurology.

“The results of the pilot trial, so far, are very encouraging,” said Eisenberg about the first trial conducted in 2015 with 20 patients, the majority of whom were treated at UMMC.

With the new technology, clinicians direct ultrasound waves to a brain structure called the globus pallidus, which helps regulate voluntary movement, to destroy damaged tissue, decreasing the uncontrolled movements that characterize Parkinson’s disease.

Doctors use magnetic resonance imaging (MRI) to create a temperature map of the brain, giving them a real-time picture of the region they want to hit with the sound waves. They then raise the energy, directly targeting that area of the brain to destroy the tissue.

Patients are awake and alert the entire time in the MRI scanner, enabling them to give clinicians constant feedback. They are fitted with a helmet through which the energy is converted into sound waves, which are then targeted to the globus pallidus. The approach is noninvasive, meaning there is no surgery or radiation treatment involved.

Current therapies to lessen movement and coordination problems in Parkinson’s patients include levodopa (sold under the brand name Dopar, among others), which is the most common. Patients with advanced Parkinson’s may undergo surgery, known as deep brain stimulation, to implant micro-electrodes in the brain that help control tremors, rigidity and dyskinesia (abnormal, uncontrolled, involuntary movement).

“For people with Parkinson’s disease and other movement disorders such as essential tremor, focused ultrasound is an appealing alternative to deep brain stimulation because it does not involve more invasive surgery,” said Paul S. Fishman, MD, PhD, professor of neurology at UMSOM and a neurologist at UMMC.

Enrollment in the study is approximately 80 to 100 participants, and the inclusion criteria were designed to include a wider population of Parkinson’s patients. Sponsored by InSightec, the trial is recruiting participants in the U.S. at the University of Maryland Medical System, Maryland; Weill Cornell Medicine, New York; and The Ohio State Wexner Medical Center, Ohio.

“University of Maryland Medicine is a world leader in pioneering MRI-guided focused ultrasound to become a new standard of care for treating many devastating brain diseases including Parkinson’s, essential tremor and glioblastoma, an often deadly type of brain cancer,” said E. Albert Reece, MD, PhD, MBA, vice president of medical affairs at the University of Maryland and dean of UMSOM.

https://parkinsonsnewstoday.com/2018/03/02/focused-ultrasound-clinical-trial-treatment-motor-symptoms-parkinsons-disease/

Footage shows the incredible moment surgeons 'burned' part of a Parkinson's sufferer's brain, instantly curing her debilitating tremors

2 March 2018  - By ALEXANDRA THOMPSON HEALTH REPORTER 

Footage shows the incredible moment surgeons 'burned' a part of a Parkinson's sufferer's brain, instantly stopping the debilitating tremors that she had endured for seven years

Before the procedure, Jyoti's left arm can be seen convulsing uncontrollably 

Grandmother-of-four Jyoti, 67, whose family thought her violent shakes were caused by an invading evil spirit, suffered from severe convulsions in her arms and legs for seven years.

Her symptoms were so extreme she was barely able to sleep.

On February 13, brain surgeons at Jain Hospital, in Bengaluru, India, cut into Jyoti's brain while she was fully awake, destroying a pathway that caused the involuntary movements.

Image shows a scan of the patient Jyoti's brain. While she was awake, surgeons cut into her vital organ , destroying a pathway that caused the involuntary movement

Brain surgeons at Jain Hospital, in Bengaluru, India performed the life-changing operation

Nearly four weeks on, Jyoti's neurosurgeon Dr Sharan Srinivasan says she is still symptom free. 

Video:

http://www.dailymail.co.uk/health/article-5455121/Surgeons-burned-Parkinsons-sufferers-brain.html#v-5262866897184600211

http://www.dailymail.co.uk/health/article-5455121/Surgeons-burned-Parkinsons-sufferers-brain.html

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Researchers develop model to determine quantity of bisphenol A that reaches the fetus through the mother

March 2, 2018, Universitat Rovira i Virgili

This finding has carried out by researchers from the Universitat Rovira i Virgili. Credit: URV

Various studies have shown that when pregnant women come into contact with bisphenol, it can go pass through the placenta and reach the fetus. Exposure to bisphenol can have negative effects on fertility, the development of the brain, and behavioural changes in adulthood. So far, however, no method has been available for quantifying the amount of the compound that can reach the fetus through the mother. Now, researchers from the Centre for Environmental, Food and Toxicological Technology (Tecnatox) have created a mathematical model that can calculate the amount of bisphenol and tested it with a sample of 100 pregnant women to determine the consequences it can have on the future health of their children.

The researchers, headed by Marta Schuhmacher, developed a pharmacokinetic model known as P-PBPK, which is customized for each subject in the study. It immediately detects bisphenol A ingestion, inhalation or skin absorption. The model then monitors it and analyses that effects it has on the body until it is flushed out.

Exactly how bisphenol A reacts inside the body depends on a large number of variables including body mass, age, respiration, medications and others. The model makes it possible to personalize all this information in real time, and detects the period of highest foetal exposure to bisphenol, in this case, after six months of pregnancy. It also provides more accurately determines the effects that exposure can have on an individual's health.

The researchers monitored the women in the study after the first term of pregnancy, after birth, and then during breastfeeding. The study has determined how much bisphenol A reaches the fetus through the mother, and the researchers are now studying the effects it has in each particular case. This means that personalised recommendations can be made about changes in habits and diet to reduce the impact of this chemical.

The challenge now is to determine what probabilities patients have of developing metabolic disorders, reproductive problems, immunological conditions or neurodegenerative diseases such as Parkinson's or Alzheimer's, since the concentration of this compound in the body can affect the actions of certain biomarkers that predispose to these diseases.

More information: Raju Prasad Sharma et al, The development of a pregnancy PBPK Model for Bisphenol A and its evaluation with the available biomonitoring data, Science of The Total Environment (2017).  DOI: 10.1016/j.scitotenv.2017.12.023 

Journal reference: Science of the Total Environment

Provided by: Universitat Rovira i Virgili

https://medicalxpress.com/news/2018-03-quantity-bisphenol-fetus-mother.html