Category Archives: Neuroscience

Neuroscience

Hereditary Alzheimer’s Transmitted Via Bone Marrow Transplants – Neuroscience News

Summary: Alzheimers disease, traditionally seen as a brain-centric condition, may have systemic origins and can be accelerated through bone marrow transplants from donors with familial Alzheimers to healthy mice.

A new study underscores the diseases potential transmission via cellular therapies and suggests screening donors for Alzheimers markers to prevent inadvertent disease transfer.

By demonstrating that amyloid proteins from peripheral sources can induce Alzheimers in the central nervous system, this research shifts the understanding of Alzheimers towards a more systemic perspective, highlighting the need for cautious screening in transplants and blood transfusions.

Key Facts:

Source: Cell Press

Familial Alzheimers disease can be transferred via bone marrow transplant, researchers show March 28 in the journalStem Cell Reports. When the team transplanted bone marrow stem cells from mice carrying a hereditary version of Alzheimers disease into normal lab mice, the recipients developed Alzheimers diseaseand at an accelerated rate.

The study highlights the role of amyloid that originates outside of the brain in the development of Alzheimers disease, which changes the paradigm of Alzheimers from being a disease that is exclusively produced in the brain to a more systemic disease.

Based on their findings, the researchers say that donors of blood, tissue, organ, and stem cells should be screened for Alzheimers disease to prevent its inadvertent transfer during blood product transfusions and cellular therapies.

This supports the idea that Alzheimers is a systemic disease where amyloids that are expressed outside of the brain contribute to central nervous system pathology, says senior author and immunologist Wilfred Jefferies, of the University of British Columbia.

As we continue to explore this mechanism, Alzheimers disease may be the tip of the iceberg and we need to have far better controls and screening of the donors used in blood, organ and tissue transplants as well as in the transfers of human derived stem cells or blood products.

To test whether a peripheral source of amyloid could contribute to the development of Alzheimers in the brain, the researchers transplanted bone marrow containing stem cells from mice carrying a familial version of the diseasea variant of the human amyloid precursor protein (APP) gene, which, when cleaved, misfolded and aggregated, forms the amyloid plaques that are a hallmark of Alzheimers disease.

They performed transplants into two different strains of recipient mice: APP-knockout mice that lacked an APP gene altogether, and mice that carried a normal APP gene.

In this model of heritable Alzheimers disease, mice usually begin developing plaques at 9 to 10 months of age, and behavioral signs of cognitive decline begin to appear at 11 to 12 months of age. Surprisingly, the transplant recipients began showing symptoms of cognitive decline much earlierat 6 months post-transplant for the APP-knockout mice and at 9 months for the normal mice.

The fact that we could see significant behavioral differences and cognitive decline in the APP-knockouts at 6 months was surprising but also intriguing because it just showed the appearance of the disease that was being accelerated after being transferred, says first author Chaahat Singh of the University of British Columbia.

In mice, signs of cognitive decline present as an absence of normal fear and a loss of short and long-term memory. Both groups of recipient mice also showed clear molecular and cellular hallmarks of Alzheimers disease, including leaky blood-brain barriers and buildup of amyloid in the brain.

Observing the transfer of disease in APP-knockout mice that lacked an APP gene altogether, the team concluded that the mutated gene in the donor cells can cause the disease and observing that recipient animals that carried a normal APP gene are susceptible to the disease suggests that the disease can be transferred to health individuals.

Because the transplanted stem cells were hematopoietic cells, meaning that they could develop into blood and immune cells but not neurons, the researchers demonstration of amyloid in the brains of APP knockout mice shows definitively that Alzheimers disease can result from amyloid that is produced outside of the central nervous system.

Finally the source of the disease in mice is a human APP gene demonstrating the mutated human gene can transfer the disease in a different species.

In future studies, the researchers plan to test whether transplanting tissues from normal mice to mice with familial Alzheimers could mitigate the disease and to test whether the disease is also transferable via other types of transplants or transfusions and to expand the investigation of the transfer of disease between species.

In this study, we examined bone marrow and stem cells transplantation. However, next it will be important to examine if inadvertent transmission of disease takes place during the application of other forms of cellular therapies, as well as to directly examine the transfer of disease from contaminated sources, independent from cellular mechanisms, says Jefferies.

Funding:

This research was supported by the Canadian Institutes of Health Research, the W. Garfield Weston Foundation/Weston Brain Institute, the Centre for Blood Research, the University of British Columbia, the Austrian Academy of Science, and the Sullivan Urology Foundation at Vancouver General Hospital.

Author: Kristopher Benke Source: Cell Reports Contact: Kristopher Benke Cell Reports Image: The image is credited to Neuroscience News

Original Research: The findings will appear in Stem Cell Reports

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Hereditary Alzheimer's Transmitted Via Bone Marrow Transplants - Neuroscience News

Neuroscience

Household Chemicals Linked to Brain Health Risks – Neuroscience News

Summary: Certain household chemicals, including those found in personal-care products and furniture, pose a risk to brain health, potentially contributing to multiple sclerosis and autism. The study reveals that these chemicals damage oligodendrocytes, essential cells for nerve cell protection.

Key findings include the identification of harmful organophosphate flame retardants and quaternary ammonium compounds, with the latter increasing in use since the COVID-19 pandemic. This groundbreaking research suggests a need for further investigation into the impact of these chemicals on neurological diseases and calls for more rigorous scrutiny and regulation to protect public health.

Key Facts:

Source: Case Western Reserve

A team of researchers from theCase Western Reserve University School of Medicinehas provided fresh insight into the dangers some common household chemicals pose to brain health.

They suggest that chemicals found in a wide range of items, from furniture to hair products, may be linked to multiple sclerosis and autism spectrum disorders.

Neurological problems impact millions of people, but only a fraction of cases can be attributed to genetics alone, indicating that unknown environmental factors are important contributors to neurological disease.

The new study published today in the journalNature Neuroscience, discovered that some common home chemicals specifically affect the brains oligodendrocytes, a specialized cell type that generates the protective insulation around nerve cells.

Loss of oligodendrocytes underlies multiple sclerosis and other neurological diseases,said the studys principal investigator,Paul Tesar,the Dr. Donald and Ruth Weber Goodman Professor of Innovative Therapeutics and director of the Institute for Glial Sciences at the School of Medicine.

We now show that specific chemicals in consumer products can directly harm oligodendrocytes, representing a previously unrecognized risk factor for neurological disease.

On the premise that not enough thorough research has been done on the impact of chemicals on brain health, the researchers analyzed over 1,800 chemicals that may be exposed to humans.

They identified chemicals that selectively damaged oligodendrocytes belong to two classes: organophosphate flame retardants and quaternary ammonium compounds.

Since quaternary ammonium compounds are present in many personal-care products and disinfectants, which are being used more frequently since the COVID-19 pandemic began, humans are regularly exposed to these chemicals. And many electronics and furniture include organophosphate flame retardants.

The researchers used cellular and organoid systems in the laboratory to show that quaternary ammonium compounds cause oligodendrocytes to die, while organophosphate flame retardants prevented the maturation of oligodendrocytes.

They demonstrated how the same chemicals damage oligodendrocytes in the developing brains of mice. The researchers also linked exposure to one of the chemicals to poor neurological outcomes in children nationally.

We found that oligodendrocytesbut not other brain cellsare surprisingly vulnerable to quaternary ammonium compounds and organophosphate flame retardants, saidErin Cohn, lead author and graduate student in the School of MedicinesMedical Scientist Training Program.

Understanding human exposure to these chemicals may help explain a missing link in how some neurological diseases arise.

The association between human exposure to these chemicals and effects on brain health requires further investigation, the experts warned. Future research must track the chemical levels in the brains of adults and children to determine the amount and length of exposure needed to cause or worsen disease.

Our findings suggest that more comprehensive scrutiny of the impacts of these common household chemicals on brain health is necessary, Tesar said.

We hope our work will contribute to informed decisions regarding regulatory measures or behavioral interventions to minimize chemical exposure and protect human health.

Additional contributing researchers from Case Western Reserve School of Medicine and from theU.S. Environmental Protection Agencyincluded Benjamin Clayton, Mayur Madhavan, Kristin Lee, Sara Yacoub, Yuriy Fedorov, Marissa Scavuzzo, Katie Paul Friedman and Timothy Shafer.

The research was supported by grants from theNational Institutes of Health,National Multiple Sclerosis Society,Howard Hughes Medical InstituteandNew York Stem Cell Foundation, and philanthropic support by sTF5 Care and the Long, Walter, Peterson, Goodman and Geller families.

Author: William Lubinger Source: Case Western Reserve Contact: William Lubinger Case Western Reserve Image: The image is credited to Neuroscience News

Original Research: The findings will appear in Nature Neuroscience

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Household Chemicals Linked to Brain Health Risks - Neuroscience News

Neuroscience

Aging Brain Cells Have Prolonged Death Process – Neuroscience News

Summary: Mature oligodendrocytes, crucial for brain function and myelin production, have an unusually prolonged death process after damage, surviving up to 45 days post-trauma, a stark contrast to the rapid demise of their younger counterparts within 24 hours.

This study illuminates a previously unknown pathway of cell longevity, suggesting a potential shift in strategies for treating aging-related damage and neurodegenerative diseases like multiple sclerosis. By utilizing innovative techniques, including a living-tissue model and a cellular death ray, the team has highlighted the need for tailored approaches in preserving myelin and supporting brain health, challenging the one-size-fits-all treatment paradigm.

Key Facts:

Source: Dartmouth College

For oligodendrocytesthe central nervous system cells critical for brain functionage may not bring wisdom, but it does come with the power to cling to life for much, much longer than scientists knew.

Thatsaccording to a new studyfeatured on the March 27 cover of theJournal of Neuroscience.

Mature oligodendrocytes took a shocking 45 days to die following a fatal trauma that killed younger cells within the expected 24 hours, Dartmouth researchers report. The findings suggest theres a new pathway for efforts to reverse or prevent the damage that aging and diseases such as multiple sclerosis cause to these important cells.

In the brain, oligodendrocytes wrap around the long, skinny connections between nerve cells known as axons, where they produce a lipid membrane called a myelin sheath that coats the axon. Axons transmit the electrical signals that nerve cells use to communicate; myelin sheathslike the plastic coating on a copper wirehelp these signals travel more efficiently.

Old age and neurodegenerative diseases like MS damage oligodendrocytes. When the cells die, their myelin production perishes with them, causing myelin sheaths to break down with nothing to replenish them. This can lead to the loss of motor function, feeling, and memory as neurons lose the ability to communicate.

Scientists have assumed that damaged oligodendrocyteslike all injured cellsinitiate a cellular self-destruct called apoptosis in which the cells kill themselves. But Dartmouth researchers discovered that mature oligodendrocytes can experience an extended life before their death that has never been seen before.

The findings pose the critical question of what in these cells changes as they mature that allows them to persist.

We found that mature cells undertake a pathway that is still controlled, but not the classical programmed cell-death pathway, saidRobert Hill, an assistant professor ofbiological sciencesand corresponding author of the paper.

We think this is showing us what happens in brains as we age and revealing a lot about how these cells die in older people, Hill said.

That unique mechanism is important for us to investigate further. We need to understand why these cells are following this pathway so we can potentially encourage or prevent it, depending on the disease context.

First author Timothy Chapman, who led the project as a PhD candidate in Hills research group, said that efforts to develop treatments for preserving myelin have focused on cultivating young oligodendrocytes and protecting mature ones. But this study suggests the cells may change significantly as they age and that a one-size-fits-all treatment might not work.

In response to the same thing, young cells go one way and old cells go another, said Chapman, who is now a postdoctoral researcher at Stanford University. If you wanted to protect the old cells, you may have to do something completely different than if you wanted to help the young cells mature. Youll likely need a dual approach.

The paper builds on a living-tissue modelthe teamreportedin the journal Nature Neurosciencein March 2023 that allows them to initiate the death of a single oligodendrocyte to observe how the cells around it react.

They reported that when an oligodendrocyte in a young brain died, the cells around it immediately replenished the lost myelin. In a brain equivalent to that of a 60-year-old, however, the surrounding cells did nothing and the myelin was lost.

That model gets us as close as we can get to the cell-death process that happens in the brain, Hill said.

Were able to model the effects of aging really well. Our ability to select a single oligodendrocyte, watch it die, and watch it regenerate or fail to regenerate allows us to understand what drives this process at the cellular level and how it can be controlled.

For the latest study, the researchers used their model to fatally damage oligodendrocyte DNA using what amounts to a cellular death raya photon-based device called 2Phatal that Hill developed. They also used the standard method for removing myelin that uses the copper-based toxin cuprizone as a comparison.

As previous studies have reported, the immature cells died quickly. But the older cells lived on, which the Dartmouth team at first interpreted as a resistance to DNA damage.

The study came into focus when the researchers examined the mature cells 45 days later using a long-term, high-resolution imaging technique developed inthe Hill lab.

Thats when we saw that it wasnt that the cells were resistant to damagethey were experiencing this extended cell death instead, Hill said.

No ones ever checked for cell death that long after DNA damage. Its the only example we can find in the literature where a cell experiences such a traumatic event and sticks around longer than a week, he said.

Because humans have oligodendrocytes for life, the cells are known to accumulate DNA damage and be more resilient than other cells, Chapman said.

Thats why we think this effect is applicable to aging. One reason these cells may persist for such a long time is because theyre used to experiencing this kind of damage naturally in aging, he said.

The study opens the first door of a vast labyrinth of more questions, Hill and Chapman say, such as whether the extended death is a good thing. It may be the equivalent of dysfunctional myelin, which is worse just sitting on an axon than if there was no myelin at all, Hill said. It isolates the cell from the surrounding tissue and essentially starves it of nutrients.

Its almost like there is garbage sitting on the axon for 45 days. Do we want to save that garbage or speed up its removal? We didnt even know that was a question until we saw this, Hill said.

If we understand the cell-death mechanism, maybe we can speed it up and get rid of that dysfunctional myelin, he said. Were always trying to save the cells and save the tissue, but you have to know if theyre worth saving.

The version of record of Oligodendrocyte Maturation Alters the Cell Death Mechanisms That Cause Demyelination was published March 27, 2024, in the Journal of Neuroscience.

Funding: This work was supported by the National Institutes of Health (R01NS122800), the Esther A. and Joseph Klingenstein Fund, the Simons Foundation, and the Department of Biological Sciences at Dartmouth.

Author: Morgan Kelly Source: Dartmouth College Contact: Morgan Kelly Dartmouth College Image: The image is credited to Neuroscience News

Original Research: Closed access. Oligodendrocyte Maturation Alters the Cell Death Mechanisms That Cause Demyelination by Robert Hill et al. Journal of Neuroscience

Abstract

Oligodendrocyte Maturation Alters the Cell Death Mechanisms That Cause Demyelination

Myelinating oligodendrocytes die in human disease and early in aging. Despite this, the mechanisms that underly oligodendrocyte death are not resolved and it is also not clear whether these mechanisms change as oligodendrocyte lineage cells are undergoing differentiation and maturation.

Here, we used a combination of intravital imaging, single-cell ablation, and cuprizone-mediated demyelination, in both female and male mice, to discover that oligodendrocyte maturation dictates the dynamics and mechanisms of cell death.

After single-cell phototoxic damage, oligodendrocyte precursor cells underwent programmed cell death within hours, differentiating oligodendrocytes died over several days, while mature oligodendrocytes took weeks to die. Importantly cells at each maturation stage all eventually died but did so with drastically different temporal dynamics and morphological features.

Consistent with this, cuprizone treatment initiated a caspase-3dependent form of rapid cell death in differentiating oligodendrocytes, while mature oligodendrocytes never activated this executioner caspase.

Instead, mature oligodendrocytes exhibited delayed cell death which was marked by DNA damage and disruption in poly-ADP-ribose subcellular localization. Thus, oligodendrocyte maturation plays a key role in determining the mechanism of death a cell undergoes in response to the same insult.

This means that oligodendrocyte maturation is important to consider when designing strategies for preventing cell death and preserving myelin while also enhancing the survival of new oligodendrocytes in demyelinating conditions.

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Neuroscience

Anxiety Drives Wishful Thinking to Risky Levels – Neuroscience News

Summary: Individuals tend to become overly optimistic in situations marked by insecurity and anxiety, potentially to their detriment. The research, involving more than 1,700 participants, demonstrated that people are less accurate in recognizing patterns linked to negative outcomes, like electrical shocks or monetary loss, indicating a clear bias towards wishful thinking. Interventions to reduce this bias included simplifying tasks to reduce uncertainty and offering rewards for accuracy, which showed mixed results. The findings suggest that while wishful thinking can help cope with stress, it may also hinder necessary actions in critical situations like health or environmental crises.

Key Facts:

Source: University of Amsterdam

Everyone indulges in wishful thinking now and again. But when is that most likely to happen and when could it actually be harmful?

A new study, led by the University of Amsterdam (UvA), demonstrates unequivocally that the greater the insecurity and anxiety of a situation, the more likely people are to become overly optimistic even to the point where it can prevent us from taking essential action.

The studys results have now been published in the journalAmerican Economic Review.

People arent purely truth-seekers many beliefs are influenced by emotions and driven by what is pleasant or comforting. Like belief in an afterlife or optimism about health outcomes, says Jol van der Weele, professor of Economic Psychology at the UvA. Working alongside professor of Neuroeconomics Jan Engelmann and an international team, Van der Weele set out to answer whether people become overly optimistic when facing potential hardships.

So far studies havent provided clear evidence for wishful thinking, with many not backing up the idea, explains Engelmann. But these mainly focused on positive outcomes, like winning a lottery. We examined how both positive and negative outcomes influence biased beliefs.

Choosing the most pleasant outcome

Understanding self-deception and its causes is difficult in real-world situations. The study involved a set of experiments with over 1,700 participants, conducted in a lab and online.

Participants were briefly shown various patterns, such as sets of differently oriented stripes or coloured dots, and were asked what kind of pattern they saw. Some of these patterns were linked to a negative outcome to induce anxiety, either a mild and non-dangerous electrical shock (in the lab) or a loss of money (online).

We wanted to see if people make more mistakes in recognising patterns associated with a negative outcome, thinking it was actually a harmless pattern. That would indicate wishful thinking, explains Van der Weele.

The study consistently found that participants were less likely to correctly identify patterns associated with a shock or loss.

The participants tended to see a pattern that aligned with what was more desirable, Engelmann says.

Previous research looked at wishful thinking related to positive outcomes and found mixed results, with many studies not finding an effect. Our study demonstrates very clearly thatthe negative emotionof anxiety about an outcome leads to wishful thinking.

Making people more realistic

The researchers also tested interventions designed to make people more realistic. The first involved making the patterns easier to recognise.

Reducing uncertainty did indeed turn out to reduce wishful thinking, says Van der Weele.

The second intervention was to offer higher potential earnings for correct pattern recognition. This intervention had little effect, except when participants could gather more evidence about the exact pattern they were shown.

When people had more time to collect evidence and were better rewarded for a correct answer, they became more realistic, explains Engelmann.

Finally, in the experiments where negative outcomes were replaced by positive outcomes, participants showed no wishful thinking. According to the authors this shows that reducing negative emotions can lessen overoptimism.

Wishful thinking in the real world

The authors recognise that wishful thinking can be useful because it helps us deal with bad feelings and manage uncertainty.

Engelmann: Wishful thinking is important for humans in coping with anxiety about possible future events.

For Van der Weele and Engelmann, the concern is situations in which too much optimism stops people from getting the information they need or from acting in a way that would benefit them.

People can get too hopeful when things are uncertain. We observe this happening with climate change, when financial markets fluctuate, and even in personal health situations when people avoid medical help because they think everything will be fine. We need to know more about when wishful thinking helps and when it hurts.

Author: Laura Erdtsieck Source: University of Amsterdam Contact: Laura Erdtsieck University of Amsterdam Image: The image is credited to Neuroscience News

Original Research: Open access. Anticipatory Anxiety and Wishful Thinking by Jol van der Weele et al. American Economic Review

Abstract

Anticipatory Anxiety and Wishful Thinking

Across five experiments (N = 1,714), we test whether people engage in wishful thinking to alleviate anxiety about adverse future outcomes.

Participants perform pattern recognition tasks in which some patterns may result in an electric shock or a monetary loss.

Diagnostic of wishful thinking, participants are less likely to correctly identify patterns that are associated with a shock or loss.

Wishful thinking is more pronounced under more ambiguous signals and only reduced by higher accuracy incentives when participants cognitive effort reduces ambiguity.

Wishful thinking disappears in the domain of monetary gains, indicating that negative emotions are important drivers of the phenomenon.

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Neuroscience

Prolonged Progestogen Use Linked to Brain Tumor Risk – Neuroscience News

Summary: A new study highlights a significant link between prolonged use of certain progestogen hormone drugs and an increased risk of developing intracranial meningioma, a type of brain tumor. Researchers analyzed data from 18,061 women who underwent surgery for intracranial meningioma, comparing their progestogen use to 90,305 controls.

The study found that prolonged use of specific progestogens, including medrogestone, medroxyprogesterone acetate, and promegestone, is associated with an elevated risk of requiring surgery for meningioma. This research underscores the urgent need for further studies to understand this risk fully, especially given the widespread use of these hormones in treating conditions like endometriosis and as part of contraceptive methods.

Key Facts:

Source: BMJ

Prolonged use of certain progestogen hormone drugs is associated with an increased risk of developing a type of brain tumour known as an intracranial meningioma, finds a study from France published byThe BMJtoday.

The researchers say this study is the first to assess the risk associated with progestogens used by millions of women worldwide, and further studies are urgently needed to gain a better understanding of this risk.

Progestogens are similar to the natural hormone progesterone, which are widely used for gynaecological conditions such as endometriosis and polycystic ovary syndrome, and in menopausal hormone therapy and contraceptives.

Meningiomas are mostly non-cancerous tumours in the layers of tissue (meninges) that cover the brain and spinal cord. Factors such as older age, female sex, and exposure to three high-dose progestogens (nomegestrol, chlormadinone, and cyproterone acetate) are already known to increase the risk of meningioma.

But there are many other progestogens for which the risk of meningioma associated with their use has not been estimated individually.

To address this knowledge gap, researchers set out to evaluate the real life risk of intracranial meningioma requiring surgery in women associated with use of several progestogens with different routes of administration.

They used data from the French national health data system (SNDS) for 18,061 women (average age 58) who underwent intracranial meningioma surgery from 2009-18.

Each case was matched to five control women without intracranial meningioma (total 90,305) by year of birth and area of residence.

The progestogens examined were progesterone, hydroxyprogesterone, dydrogesterone, medrogestone, medroxyprogesterone acetate, promegestone, dienogest, and levonorgestrel intrauterine systems.

For each progestogen, use was defined as at least one prescription in the year before hospital admission or within 3-5 years for levonorgestrel intrauterine systems.

Use of at least one of the three high-dose progestogens known to increase the risk of meningioma in the 3 years before hospital admission was also recorded to minimise bias.

After taking account of other potentially influential factors, prolonged use (a year or more) of medrogestone was associated with a 4.1-fold increased risk of intracranial meningioma requiring surgery.

Prolonged use of medroxyprogesterone acetate injection was associated with a 5.6-fold increased risk, and prolonged use of promegestone was linked to a 2.7-fold increased risk.

There appeared to be no such risk for less than one year of use of these progestogens.

As expected, there was also an excess risk of meningioma for women exposed to chlormadinone acetate, nomegestrol acetate, and cyproterone acetate, all of which are known to increase the risk of meningioma.

However, results showed no excess risk of meningioma for progesterone, dydrogesterone, or the widely used hormonal intrauterine systems, regardless of the dose of levonorgestrel they contained.

No conclusions could be drawn about dienogest or hydroxyprogesterone as the number of exposed individuals was too small.

This is an observational study so cant establish cause and effect, and the authors acknowledge that the SNDS database lacked information on all the clinical details and medical indications for which progestogens are prescribed. Nor were they able to account for genetic predisposition and exposure to high dose radiation.

However, they say, given that medroxyprogesterone acetate is estimated to be used for birth control by 74 million women worldwide, the number of attributable meningiomas may be potentially high.

Further studies using other sources of data are urgently needed to gain a better understanding of this risk, they conclude.

Author: BMJ Media Relations Source: BMJ Contact: BMJ Media Relations BMJ Image: The image is credited to Neuroscience News

Original Research: The findings will appear in The BMJ

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Neuroscience

Cheers to Longevity: Couples Who Drink Together, Live Longer – Neuroscience News

Summary: Couples with similar drinking habits, specifically those who both consume alcohol, tend to live longer than those who dont share the same drinking patterns. This finding draws on the drinking partnership theory, suggesting that shared alcohol consumption correlates with improved marital outcomes and possibly, greater longevity.

While the study stops short of endorsing increased alcohol consumption among couples, it highlights the significance of shared lifestyle habits on health and relationship satisfaction. The research, part of the Health and Retirement study, followed 4,656 couples over two decades, providing a comprehensive look at the long-term implications of mutual drinking habits on life span.

Key Facts:

Source: University of Michigan

In a recentstudypublished inThe Gerontologist,Kira Birditt, research professor at the U-M Institute for Social Resarchs Survey Research Center, found that couples who are concordant in their drinking behavior (that is, both members drink alcohol) tend to live longer.

She says a theory in alcohol literature called the drinking partnership, where couples who have similar patterns of alcohol use tend to have better marital outcomes (such as less conflict and longer marriages), was the inspiration behind the study.

Although a great deal of research has examined the implications of couples drinking patterns for marital outcomes, the implications for health are less clear. Behaviors that are good for marriage are not necessarily good for health, Birditt says.

The purpose of this study was to look at alcohol use in couples in the Health and Retirement Study and the implications for mortality, she said.

And we found, interestingly, that couples in which both indicated drinking alcohol in the last three months lived longer than the other couples that either both indicated not drinking or had discordant drinking patterns in which one drank and the other did not.

And while it may sound like thats a recommendation to drink more with your spouse, Birditt cautions against that reading.

The study specifically looked at drinking patterns and defined drinking very broadly, examining whether or not a participant had had a drink within the last three months. However, it may suggest the importance of remembering how spouses can impact each others health.

Drinking concordance among couples may be a reflection of compatibility among partners in their lifestyles, intimacy and relationship satisfaction.

Weve also found in other studies that couples who drink together tend to have better relationship quality, and it might be because it increases intimacy, Birditt said.

That impact might merit further study. Birditt would like to explore further questions related to couples alcohol consumption and how it affects their relationship.

We dont know why both partners drinking is associated with better survival. I think using the other techniques that we use in our studies in terms of the daily experiences and ecological momentary assessment questionnaires could really get at that to understand, for example, focusing on concordant drinking couples, she said.

What are their daily lives like? Are they drinking together? What are they doing when they are drinking?

There is also little information about the daily interpersonal processes that account for these links. Future research should assess the implications of couple drinking patterns for daily marital quality, and daily physical health outcomes.

The Health and Retirement study is a nationally representative study of adults aged 50 and older in the United States. It includes couples who are interviewed every two years. Participants included 4,656 married/cohabiting different-sex couples (9,312 individuals) who completed at least three waves of the HRS from 1996 to 2016.

Author: Morgan Sherburne Source: University of Michigan Contact: Morgan Sherburne University of Michigan Image: The image is credited to Neuroscience News

Original Research: Closed access. Alcohol Use and Mortality Among Older Couples in the United States: Evidence of Individual and Partner Effects by Kira Birditt, et al. The Gerontologist

Abstract

Alcohol Use and Mortality Among Older Couples in the United States: Evidence of Individual and Partner Effects

Background and Objectives

Spouses with concordant (i.e., similar) drinking behaviors often report better quality marriages and are married longer compared with those who report discordant drinking behaviors. Less is known regarding whether concordant or discordant patterns have implications for health, as couples grow older. The present study examined whether drinking patterns among older couples are associated with mortality over time.

Research Design and Methods

The Health and Retirement Study (HRS) is a nationally representative sample of individuals and their partners (married/cohabiting) over age 50 in the United States, in which participants completed surveys every 2 years. Participants included 4,656 married/cohabiting different-sex couples (9,312 individuals) who completed at least 3 waves of the HRS from 1996 to 2016. Participants reported whether they drank alcohol at all in the last 3 months, and if so, the average amount they drank per week. Mortality data were from 2016.

Results

Analyses revealed concordant drinking spouses (both indicated they drank in the last 3 months) survived longer than discordant drinking spouses (1 partner drinks and the other does not) and concordant nondrinking spouses. Analysis of average drinks per week showed a quadratic association with mortality such that light drinking predicted better survival rates among individuals and their partners compared with abstaining and heavy drinking. Further, similar levels of drinking in terms of the amount of drinking were associated with greater survival, particularly among wives.

Discussion and Implications

This study moves the field forward by showing that survival varies as a function of ones own and ones partners drinking.

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Sleeplessness Makes You Feel Up To Ten Years Older – Neuroscience News

Summary: Researchers unveiled a link between sleep quality and subjective age, demonstrating that insufficient sleep can make individuals feel significantly older. Through two studies involving over 600 participants, they found that each night of inadequate sleep contributed to feeling 0.23 years older, with sleep restriction causing participants to feel on average 4.4 years older.

This research highlights the profound impact of sleep on subjective age, suggesting that feeling alert can make one feel four years younger, whereas feeling extremely sleepy can age ones perceived age by six years. The findings underscore the importance of quality sleep for maintaining a youthful sense of self and promoting health and activity.

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Source: Stockholm University

Do you ever find yourself longing for the energy and vitality of your younger years? Feeling young is not just a matter of perception it is actually related to objective health outcomes.

Previous studies have shown that feeling younger than ones actual age is associated with longer, healthier lives. There is even support for subjective age to predict actual brain age, with those feeling younger having younger brains.

Given that sleep is essential for brain function and overall well-being, we decided to test whether sleep holds any secrets to preserving a youthful sense of age, says Leonie Balter, researcher at the Department of Psychology, Stockholm University.

In the first study, 429 individuals aged 18 to 70 were asked how old they felt, how many days in the past month they had not gotten enough sleep, and how sleepy they were. It turned out that for each night with insufficient sleep in the past month, participants felt on average 0.23 years older.

In a second study, the researchers tested whether it was indeed the lack of sleep causing participants to feel older. Therefore, they conducted an experimental sleep restriction study involving 186 participants aged 18 to 46. Participants restricted their sleep for two nights only four hours in bed each night and another time slept sufficiently for two nights, with nine hours in bed each night.

After sleep restriction, participants felt on average 4.4 years older compared to when having enjoyed sufficient sleep. The effects of sleep on subjective age appeared to be related to how sleepy they felt. Feeling extremely alert was related to feeling 4 years younger than ones actual age, while extreme sleepiness was related to feeling 6 years older than ones actual age.

This means that going from feeling alert to sleepy added a striking 10 years to how old one felt, says Leonie Balter, and states that the implications for our daily lives are clear:

Safeguarding our sleep is crucial for maintaining a youthful feeling. This, in turn, may promote a more active lifestyle and encourage behaviours that promote health, as both feeling young and alert are important for our motivation to be active.

Author: Gunilla Nordin Source: Stockholm University Contact: Gunilla Nordin Stockholm University Image: The image is credited to Neuroscience News

Original Research: Open access. Sleep and subjective age: Protect your sleep if you want to feel young by Leonie Balter et al. Proceedings of the Royal Society B Biological Sciences

Abstract

Sleep and subjective age: Protect your sleep if you want to feel young

The current studies examined the impact of insufficient sleep and sleepiness on the subjective experience of age.

Study 1, a cross-sectional study of 429 participants (282 females (66%), 144 males, 3 other gender; age range 1870), showed that for each additional day of insufficient sleep in the last 30 days, subjective age increased by 0.23 years.

Study 2, an experimental crossover sleep restriction study (n= 186; 102 females (55%), 84 males; age range 1846), showed that two nights of sleep restriction (4 h in bed per night) made people feel 4.44 years older compared to sleep saturation (9 h in bed per night).

Additionally, moving from feeling extremely alert (Karolinska Sleepiness Scale (KSS) score of 1) to feeling extremely sleepy (KSS score of 9) was associated with feeling 10 years older in both studies.

These findings provide compelling support for insufficient sleep and sleepiness to exert a substantial influence on how old we feel, and that safeguarding sleep is probably a key factor in feeling young.

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Sleeplessness Makes You Feel Up To Ten Years Older - Neuroscience News

Neuroscience

The Genetic Secrets of Neuron Formation – Neuroscience News

Summary: Researchers illuminated the pivotal role of the protein MEIS2 in brain development, particularly in the differentiation of inhibitory projection neurons, crucial for motion control and decision-making. This protein, in conjunction with DLX5, activates specific genes that guide the development of these neurons.

A mutation in MEIS2, linked to intellectual disabilities in patients, hampers this process, underscoring the proteins significance in neurodevelopment. The study enriches our understanding of the genetic orchestration behind neuron diversity and highlights the intricate relationship between gene activation and neuronal fate, offering new insights into the genetic underpinnings of neurodevelopmental disorders.

Key Facts:

Source: Max Planck Institute

Brain development is a highly orchestrated process involving numerous parallel and sequential steps. Many of these steps depend on the activation of specific genes.

A team led by Christian Mayer at the Max Planck Institute for Biological Intelligence discovered that a protein called MEIS2 plays a crucial role in this process: it activates genes necessary for the formation of inhibitory projection neurons.

These neurons are vital for motion control and decision-making. A MEIS2 mutation, known from patients with severe intellectual disability, was found to disrupt these processes.

The study provides valuable insights into brain development and consequences of genetic mutations.

Nerve cells are a prime example for interwoven family relations. The specialized cells that form the brain come in hundreds of different types, all of which develop from a limited set of generalized progenitor cells their immature parents. During development, only a specific set of genes is activated in a single progenitor cell.

The precise timing and combination of activated genes decide which developmental path the cell will take. In some cases, apparently identical precursor cells develop into strikingly different neurons. In others, different precursors give rise to the same nerve cell type.

The complexity is mind-blowing and not easy to disentangle in the lab. Christian Mayer and his team set out to do so nevertheless (Diversity research in the brain). Together with colleagues in Munich and Madrid, they now added another puzzle piece to our understanding of neuron development.

The scientists studied the formation of inhibitory neurons that produce the neurotransmitter GABA cells, which are known to display a broad range of diversity. In the adult brain, inhibitory neurons can act locally, or they can extend long-range axons to remote brain areas.

Locally connected interneurons are an integral part of the cortical circuit, reciprocally linking cortical neurons. Long-range projection neurons, on the other hand, primarily populate subcortical regions. They contribute to motivated behavior, reward learning and decision-making.

Both types, interneurons and projection neurons, originate in the same area of the developing brain. From here, the newborn neurons migrate to their final locations in the brain.

Using abarcoding approach, Christian Mayer and his team followed the family relationships between precursor cells and young inhibitory neurons. They discovered that a protein called MEIS2 plays an important role when a precursor cell decides whether it should turn into an interneuron or into a projection neuron: MEIS2 assists the cellular machinery to activate the genes that are required for a precursor cell to become a projection neuron.

To advance this development, MEIS2 works together with another protein, known as DLX5. When MEIS2 is missing or doesnt function correctly, the development of projection neurons is stalled and a larger fraction of precursor cells turns into interneurons instead. However, MEIS2 cant do the job by itself.

Our experiments show that MEIS2 and DLX5 have to come together at the same time, and in the same cells, explains Christian Mayer.

Only the combination of the two will fully activate the genes that drive projection neuron development.

The importance of this process is underscored by previous reports on a MEIS2 variant that was found in patients with intellectual disabilities and a delayed development. Due to a small change in the MEIS2 gene, a slightly different protein is produced.

The team around Christian Mayer tested this MEIS2 variant in their experiments and found that it leads to a failure to induce the specific genes needed to form projection neurons.

The inability of MEIS2 to activate the genes essential for the formation of projection neurons may contribute to neurodevelopmental disorders, such as those observed in patients with mutations in the gene encoding this protein, says Christian Mayer.

Intrigued by this discovery, the researchers delved into the mechanism by which MEIS2 activates projection neuron specific genes.

Patients with mutations in MEIS2 suffer from a diverse range of effects, like irregularities in digits, impaired lung to brain development, or intellectual disabilities. At a first look, these symptoms have nothing in common, relates Christian Mayer.

This shows, how important it is to understand that genes often have very different roles in different parts of the body.

The genome has millions of non-coding regulatory elements like enhancers, promoters, and insulators. These elements dont actually code for proteins themselves, but they act like switches, controlling when and where genes turn on and off.

Enhancers, which are part of the genome, are like interpreters in the cell. If MEIS2 and DLX5 are present together, a specific set of enhancers becomes active. It is this specific set of enhancers that induces projection neuron genes in the brain. In other parts of the body, MEIS2 interacts with other proteins to induce different sets of enhancers, explains Christian Mayer.

Recent large-scale whole exome sequencing studies in patients have provided a systematic and highly reliable identification of risk genes for neurodevelopmental disorders.

Future studies focusing on the molecular interactions between the proteins encoded by these risk genes, such as MEIS2, will pave the way for a comprehensive understanding of the biological mechanisms underlying neurodevelopmental disorders.

Author: Marius Bruer Source: Max Planck Institute Contact: Marius Bruer Max Planck Institute Image: The image is credited to Neuroscience News

Original Research: Open access. Spatial enhancer activation influences inhibitory neuron identity during mouse embryonic development by Christian Mayer et al. Nature Neuroscience

Abstract

Spatial enhancer activation influences inhibitory neuron identity during mouse embryonic development

The mammalian telencephalon contains distinct GABAergic projection neuron and interneuron types, originating in the germinal zone of the embryonic basal ganglia. How genetic information in the germinal zone determines cell types is unclear.

Here we use a combination of in vivo CRISPR perturbation, lineage tracing and ChIPsequencing analyses and show that the transcription factor MEIS2 favors the development of projection neurons by binding enhancer regions in projection-neuron-specific genes during mouse embryonic development.

MEIS2 requires the presence of the homeodomain transcription factor DLX5 to direct its functional activity toward the appropriate binding sites.

In interneuron precursors, the transcription factor LHX6 represses the MEIS2DLX5-dependent activation of projection-neuron-specific enhancers. Mutations ofMeis2result in decreased activation of regulatory enhancers, affecting GABAergic differentiation.

We propose a differential binding model where the binding of transcription factors atcis-regulatory elements determines differential gene expression programs regulating cell fate specification in the mouse ganglionic eminence.

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The Genetic Secrets of Neuron Formation - Neuroscience News

Neuroscience

Big research, little time: Medical neuroscience student wins 3 Minute Thesis finals – Dal News

Last week, 10 graduate students took to the stage to compete in Dals annual 3 Minute Thesis (3MT) competition, with medical neuroscience PhD student Reynaldo Popoli earning this years winning title with his presentation on improving the quality of life for patients living with the neurological disorder ALS.

The 3MT finals, held Tuesday, March 19 in the Dalhousie Student Union Building, challenged competitors to present their research to a non-specialist audience in three engaging minutes or less, using only one static PowerPoint slide as a visual aid.

Five masters and five PhD students shared their research, representing the Faculties of Medicine, Science and Health.

Along with taking home the title of Dals newest 3MT champion after winning over the judging panel, Popoli won a cash prize of $1,000 and the opportunity to represent Dalhousie at the Eastern 3MT regionals at the Institut national de la recherche scientifique in Quebec this June.

I feel incredibly grateful, especially to my colleagues that allowed me to practice my presentation and provided invaluable feedback, he says.

Faculty of Graduate Studies Dean Marty Leonard with Popoli.

Popolis presentation called attention to the devastating impacts of ALS a disease that affects the cells in our bodies that control our muscles. These cells originate in the brain and spinal cord and travel to the muscles, forming connections called neuromuscular junctions. In ALS, the cells withdraw from the muscles, and these connections are left non-functional.

The goal of my research is to understand some of the changes that occur in ALS. More precisely, in the connections between the cells that control our movements and their respective muscles. By understanding these changes, we hope we can use different therapeutic approaches to slow down disease progression and improve symptoms, he says.

Popolis research looks at drugs that help regulate and maintain the integrity of the neuromuscular junction. He has shown that the use of these drugs in ALS make symptoms progress much slower and maintain neuromuscular junctions for longer, allowing for a 10 per cent increase in life expectancy and better quality of life for patients.

My work is far from over, but Im hopeful that with this novel research, well be able to find new treatments for this devastating disease.

Pooyan Moradi, another PhD student in medical neuroscience, and Kaela Trumble, a masters student in rehabilitation research, were also selected as top finalists by the judging panel.

Moradi earned second place and a $500 prize, presenting on the use of artificial intelligence to detect seizures in animals and how this model can be applied to better predict epilepsy in humans who have suffered head injuries.

Pooyan Moradi.

Trumble placed third in the competition and won $250 with a presentation covering the differences in how people develop health problems as they age in relation to heart disease.

Kaela Trumble.

The remaining eight finalists each earned $100 prizes for their inspiring presentations.

Also receiving the most votes for the Peoples Choice Award, biochemistry and molecular biology masters student Dina Rogers captivated the crowd when describing a biological recycling process by which PET plastic can be repurposed into new materials by protein engineering to combat climate change. The award, valued at $500, was generously sponsored by Estelle Joubert, assistant dean of the Faculty of Graduate Studies, and entrepreneur Paul Doerwald.

Dina Rogers.

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This year's 3MT finals opened with a traditional Mi'kma'ki welcome with Elder Ann LaBillois. The event was enthusiastically hosted by CBC reporter and video journalist Brett Ruskin for a sixth time.

Judges for the competition were Dr. Frank Harvey, Dal's provost and vice-president academic, Grace Jefferies-Aldridge, Dals vice-president, people and culture, and Kristan Hines, senior vice-president of corporate and public affairs at NATIONAL Public Relations.

Organized by the Faculty of Graduate Studies, the event served as an opportunity for members of the Dal community and beyond to learn about the impactful work the universitys graduate students are engaged in.

For many of us, the 3 Minute Thesis competition is the highlight of the year at Dalhousie, says Dr. Marty Leonard, dean of the Faculty of Graduate Studies. It challenges students to take what could be very technologically or theoretically complex research or better yet, both and make it accessible and interesting to anyone.

Dalhousie President Dr. Kim Brooks invited the crowd to relish the opportunity to celebrate the extraordinary research happening on campus.

Dal President Kim Brooks.

If you have the privilege of spending time in a university, one of the things you get to do often in your academic life is trace an idea back to its origins, she says. And almost every time you find a new idea, a unique contribution, and you trace it back to its origins, you find a graduate student.

3MT finalists.

Dina Rogers, MSc, Biochemistry and Molecular Biology

Proteins vs. Pollution: A Biochemical Solution to a Brighter Future

Kateryna Rudenko, MES, Environmental Studies

Weaving Mikmaki from Stories We Share

Joy Liu, MSc, Statistics

From Approximate to Accurate: Improving Sea Scallop Meat Weight Estimates in the Bay of Fundy through Statistical Modeling

Reynaldo Popoli, PhD, Medical Neuroscience

How a life changes forever in just 12 months

Kaela Trumble, MSc, Rehabilitation Research

How will your heart age?

Eniko Zsoldos, PhD, Chemistry

Improving Battery Sustainability by Limiting Charging

Divya Rathore, PhD, Physics and Atmospheric Science

Many Shades of Green

Sophie Inkpen, MSc, Kinesiology

Taking Action Through Activity: A Program for Patients with Acquired Brain Injury

Pooyan Moradi, PhD, Medical Neuroscience

Cloudy with a Chance of Epilepsy

Fatemeh Mahdizadeh Karizaki, PhD in Health

Promoting Health and Wellbeing: Access and Inclusion to Childcare and Early Learning for Children with Disabilities in Nova Scotia

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Big research, little time: Medical neuroscience student wins 3 Minute Thesis finals - Dal News