Medical News Today: Brain structure may play key role in psychosis

New research finds that having a larger choroid plexus, which is a vital brain structure, could be involved in psychosis.
brain illustration
Research finds clues about psychosis in a brain structure that scientists have not yet fully studied.

Variations in the structure of the choroid plexus, which produces cerebrospinal fluid (CSF), could play a key role in psychosis.

A team that Dr. Paulo Lizano — of the Beth Israel Deaconess Medical Center in Boston, MA — led has now investigated this vital structure.

In doing so, they found that there could be a link between its size and the development of psychosis.

The choroid plexus and its product, CSF, are crucial parts of the neurological system. CSF helps cushion the brain within the skull, and the choroid plexus forms a barrier between the brain and the CFS, which helps filter out toxins and keeps blood components from entering the brain.

It also allows some molecules to pass through, including those involved with the immune system.

This study — which now appears in the American Journal of Psychiatry — involved three groups of people: participants with a diagnosis of psychosis, one of their first degree relatives, and people with no history of psychosis (the controls).

Each participant underwent a structural MRI brain scan, and the researchers found that the volume of the choroid plexus was larger in those who had psychosis.

They also found that the volume of the choroid plexus among first degree relatives was larger than that of the controls but smaller than that of those with psychosis.

Additional findings

However, these were not the only significant findings from the group with psychosis.

The researchers also found that larger choroid plexus volume correlated with reduced gray matter, smaller amygdala volume, lower cognitive scores, larger ventricle volume, and lower levels of neural connectivity.

Although they cannot yet say with certainty, the researchers believe that these findings could also offer clues as to the pathology of psychosis.

The team also found that people with an enlarged choroid plexus had high levels of a signaling cell associated with the immune system, called interleukin 6 (IL-6).

IL-6 can cross the barriers between the brain, blood, and CSF. The results are noteworthy; the team explains that people who have schizophrenia and bipolar disorder often have higher levels of IL-6. Dr. Lizano and colleagues conclude:

Our findings suggest the involvement of the choroid plexus across the psychosis spectrum, with a potential mechanism involving the neuro-immune system, which functions in regulating the brain and interacting with the body’s immune and inflammatory systems.”

What is psychosis?

According to the National Institute of Mental Health, psychosis refers to a group of conditions that affect the mind when someone experiences a “loss of contact with reality.”

During a psychotic episode, a person’s thoughts and perceptions are disturbed. They may find it difficult to understand what is real and what is not.

Some symptoms of psychosis include:

  • delusions, or false beliefs
  • hallucinations, such as seeing or hearing things that others do not
  • incoherent speech
  • inappropriate behavior

Experts say that there is no single cause of psychosis. It can be a symptom of a mental health condition such as schizophrenia. There are also several other potential causes, including some medical conditions, drug and alcohol use, certain prescription medications, and sleep deprivation.

There were some scientific discussions in the 1920s about the possible role of the choroid plexus in schizophrenia or bipolar disorder. However, there had not been much specific research on the topic before this study.

Although much more research is still necessary, this study suggests that there is probably a link between an enlarged choroid plexus and psychosis.

Medical News Today: How might obesity affect the brain?

The link between obesity and the brain is a fascinating topic that scientists have only recently begun to explore. New research adds important pieces to the puzzle.
scientist looking at brain scans
Researchers have used MRI scans to examine the brains of people living with obesity.

From the size and functionality of the brain to specific neuronal circuits, recent studies have brought to light important aspects of the connection between obesity and the brain.

For instance, researchers published a study earlier this year that found a link between obesity around the stomach area and smaller brain size — specifically, lower gray matter volume.

The findings of another recent study showed that the brain’s prefrontal cortex — an area that is important for complex thinking, planning, and self-control — is less active in people who tend to overeat, which may lead to obesity and weight gain.

Finally, research that appeared only last month identified an array of neurons that can curb overeating when they become active.

A new study now adds to this mounting body of evidence, shedding further light on the connection between obesity on the one hand and differences in brain structure and form on the other.

Dr. Ilona A. Dekkers, from the Leiden University Medical Center in the Netherlands, led a team of researchers who used cutting-edge MRI scanning technology to understand the link between obesity and brain structure.

Dr. Dekkers and team reported smaller gray matter volumes in people with obesity, thus solidifying previous research findings. They also found connections with the brain’s form and structure, called its morphology.

The researchers published their findings in the journal Radiology.

More body fat, less gray matter volume

Dr. Dekkers and her colleagues decided to investigate how obesity might affect the brain because previous studies had found a higher risk of cognitive decline and dementia among people with obesity.

So, the scientists examined brain scans from over 12,000 people who took part in the United Kingdom Biobank Imaging study. The brain imaging techniques that the team used in the study offered insights into the participants’ gray and white matter.

Describing the brain in very broad terms, this central processing unit consists of an “outer cortex of gray matter and an inner area housing tracts of white matter.”

The gray matter is packed with neurons, whereas white matter primarily consists of nerve projections called axons and glial cells.

In the current study, according to Dr. Dekkers, the team found that “having higher levels of fat distributed over the body is associated with smaller volumes of important structures of the brain, including gray matter structures that are located in the center of the brain.”

“Interestingly, we observed that these associations are different for men and women, suggesting that gender is an important modifier of the link between fat percentage and the size of specific brain structures,” she adds.

Specifically, men with obesity had lower gray matter volume both overall and in certain reward-processing circuits and brain structures that deal with movement.

For women with obesity, an increased amount of body fat only correlated with lower matter volume in a region called the globus pallidus, which is a brain area that plays a role in voluntary movement.

In both men and women, there was a correlation between a larger amount of body fat and the chance of small changes occurring in the brain’s white matter.

Obesity and the brain: Is inflammation key?

“Our study shows that very large data collection of MRI data can lead to improved insight into exactly which brain structures are involved in all sorts of health outcomes, such as obesity,” says Dr. Dekkers.

The scientist ventures some opinions on the possible implications of the study. Less gray matter could mean fewer neurons, she says, and white matter changes could affect the communication between neurons.

Also, previous studies have linked gray matter volume with “food-reward circuitry,” so the changes in gray matter could make it hard for people to control their eating behaviors, she suggests. However, she also cautions that more research is necessary to strengthen this conclusion.

Dr. Dekkers also points out that according to previous studies, obesity-related inflammation can affect brain tissue. This low-grade inflammation could, therefore, explain the study’s recent findings.

“For future research, it would be of great interest whether differences in body fat distribution are related to differences in brain morphological structure, as visceral fat is a known risk factor for metabolic disease and is linked to systemic low-grade inflammation,” says Hildo Lamb, Ph.D., the study’s senior author.

Medical News Today: How ketamine can change the brain to fight depression

New research in mice, which the National Institutes of Health supported, shows how ketamine can alter brain circuits, quickly redressing depression-like symptoms.
researchers looking at brain scans
Ketamine stimulates the regrowth of dendritic spines in the prefrontal cortex, according to a new animal study.

Previous studies have shown that ketamine — an anesthetic — can rapidly reduce severe symptoms of major depressive disorder, particularly the occurrence of suicidal thoughts.

However, researchers are still unsure how this substance acts in the brain to fight off depression or how to maintain its therapeutic effects in the long run.

For this reason, a team of investigators from the University of Tokyo in Japan, Stanford University in California, and Weill Cornell Medicine in New York, NY, recently set out to understand more about how ketamine fights depression in the brain by studying its effect in mouse models.

This research received support from the National Institutes of Health (NIH), who describe the work as “basic research” that “is foundational to advancing new and better ways to prevent, diagnose, and treat disease.”

The study authors report their findings in a scientific paper that appears in the journal Science.

Ketamine and brain circuitry

“Ketamine is a potentially transformative treatment for depression, but one of the major challenges associated with this drug is sustaining recovery after the initial treatment,” explains Dr. Conor Liston, one of the researchers behind the study.

To find out how ketamine works in the brain and identify the mechanisms that reduce depression symptoms, the researchers worked with mice that presented behaviors indicative of depression.

More specifically, the team focused on dendritic spines. These are small protrusions on dendrites, which are brain cell extensions that help the neurons “communicate” among themselves. The dendritic spines are the parts that receive the stimuli that other neurons send out.

The researchers studied the dendritic spines in the prefrontal cortex of the mice’s brains both before and after they exposed some of the rodents to a source of stress. They found that the mice demonstrating depression-like behaviors after experiencing the stressor lost dendritic spines more quickly than the control mice. Moreover, these mice had reduced formation of new dendritic spines.

The team also saw that exposing experimental mice to stress led to poorer connectivity and coordination of neural activity in the prefrontal cortex. These changes, the researchers explain, relate to typical behaviors in depression, which occur in response to stress.

When the researchers treated these mice with ketamine, they found that the animals regained functional connectivity and normal neuron activity in the prefrontal cortex, and they no longer displayed behaviors consistent with depression.

At 24 hours after receiving just one dose of ketamine, the rodents that the team had confronted with a source of stress did not show depression-like symptoms. Brain scans also revealed an increase in the formation of fully functional dendritic spines.

The authors make a distinction between these findings. Mice that received ketamine, they explain, showed behavioral improvements within 3 hours of treatment, but they only experienced new dendritic spine formation between 12 and 24 hours after the treatment.

“Our results suggest that interventions aimed at enhancing synapse formation and prolonging their survival could be useful for maintaining the antidepressant effects of ketamine in the days and weeks after treatment,” Dr. Liston notes.

‘Additional insights could guide advances’

Although the researchers admit that they will have to conduct more studies to understand the exact mechanisms at play, they believe, based on their current findings, that the formation of new dendritic spines may occur thanks to the fact that ketamine boosts brain activity in the prefrontal cortex.

The researchers also found that dendritic spines are likely to play an important role in maintaining the remission of depression-like symptoms in mice. When the team tried selectively removing newly grown dendritic spines in the mice’s brains, the rodents started expressing depression-related behaviors once again.

Dr. Janine Simmons, who leads the National Institute of Mental Health’s Social and Affective Neuroscience Program — and who did not contribute to the current study — explains why conducting new research into the workings of ketamine in the brain is important.

“Ketamine,” she notes, “is the first new antidepressant medication with a novel mechanism of action since the 1980s. Its ability to rapidly decrease suicidal thoughts is already a fundamental breakthrough.”

Additional insights into ketamine’s longer-term effects on brain circuits could guide future advances in the management of mood disorders.”

Dr. Janine Simmons

Adolescent brain development impacts mental health, substance use

Adolescent brain development impacts mental health, substance use. Advances in understanding adolescent brain development may aid future treatments of mental illness a…. #Adolescent #brain #development #impacts #mental #health #substance #use .

Adolescent brain development impacts mental health, substance use.
Advances in understanding adolescent brain development may aid future treatments of mental illness a….
#Adolescent #brain #development #impacts #mental #health #substance #use .

The Adolescent Brain – Substance Use, Depression, and Recovery | Ann Arbor District Library

Important features of brain development exist during the adolescent period, and this developmental phase matters when we talk about adolescent depression and substance use. Understanding these developmentally specific features of depression and substance use helps with parental monitoring, understanding, responding…

Important features of brain development exist during the adolescent period, and this developmental phase matters when we talk about adolescent depression and substance use. Understanding these developmentally specific features of depression and substance use helps with parental monitoring, understanding, responding effectively to youth, as well as knowing more about what to expect and how to discern when more help is needed. It is common for parents to wonder, “are they just being a moody teenager?” or “isn’t it normal to experiment with alcohol or drugs during adolescence?” Sometimes parents are unsure which condition, substance use or mental illness, is primary or what needs to be treated first.

In order to address these and other dilemmas in relation to dual diagnosis in adolescence, The University of Michigan Depression Center and the Ann Arbor District Library present a Bright Nights community forum entitled, “The Adolescent Brain: Substance Use, Depression, and Recovery”.