Showing posts with label psychiatric disorders. Show all posts
Showing posts with label psychiatric disorders. Show all posts

Sunday, November 20, 2022

Brain Stimulation Could Limit the Impulse to Binge Eat

 

Binge-eating disorder is a major eating disorder in which you habitually consume an abnormal amount of food and feel unable to stop. It is very common to overeat on occasion, but for some, it feels out of control and becomes a regular occurrence. Symptoms associated with the binge-eating disorder include eating rapidly during binge episodes, when you're full or not hungry, alone, and feeling depressed and guilty about your eating.  This disorder may be caused by family history, a past of dieting, and psychological issues such as stress and poor body self-image. There are various psychiatric disorders that relate to a binge-eating disorder such as depression, bipolar disorder, anxiety, and substance use disorders. 

Plenty of medications and cognitive therapies are available to treat binge-eating disorders, but a recent research study has found that deep brain stimulation, used for people with Parkinson's disease, can limit the urge to overeat.  This is, a person who lives with a psychiatric diagnosis like bing-eating disorder may be no more culpable for overeating than a patient with Parkinson's disease is for their tremors. The researchers recorded electrical impulses in a binge-eating patient's nucleus accumbus, a key hub of the brain's reward center, as they ate. It was determined that neurons were firing just before the binge and that these electrical impulses were correlated with the patient's loss of control.  When electrodes were placed in the patient's brains, they regulated aberrant signals, and they no longer felt the uncontrollable eating urges. 

A common medication for a binge-eating disorder is Vyvanse, which alters the balance of chemicals in your brain and increases norepinephrine and dopamine levels. Although, this medication has many side effects that can also increase the severity of this disorder. In addition, the patient may become dependent on the pill and take it in larger amounts than recommended. In so, I think that using a device to regulate aberrant signals in the brain is a much more innovative way to treat patients. The device is simply placed under the scalp, which is invisible to the naked eye and the patient can use it as required until they feel in control of their eating. 




Tuesday, April 19, 2022

Study Discovers Possible Genetic Link to Suicide Attempts

 

A news report from KSAT.com discusses a study done in November 2021 about how suicide attempts have a genetic link to them, and not just a genetic link of mental illness. Unfortunately, suicide is a leading cause of death in America and attempts are even higher than ever. In 2020 alone, 45,000 died by suicide and over a million attempts, meaning that every 11 minutes an American attempts to end their life. While this specific cause of death has been attributed to mental heath and their disorders, researchers at Mount Sinai in New York tried to identify a genetic cause independent of psychiatric disorders, and their findings were unheard of.

The study consisted of a genome-wide study of 500,000 people, 30,000 of which had attempted suicide, which is about 6% of the study's population. This association study was conducted by the International Suicide Genetics Consortium, and focused on looking at similarities among the human genome for those who had attempted suicide. During the study, evidence was found that the suicide attempts were consistent with psychiatric disorders and the genes associated with a higher risk of those diseases, but another result was discovered as well.

Chromosome 7 has had a lot of interest in the medical community as it is the chromosome for cystic fibrosis, polydactyly, deafness, and many other health conditions. The researchers found that there was a region located on Chromosome 7 that contain variants which could increase a person's risk for attempting suicide. The region identified on Chromosome 7 is also linked to non-psychiatric issues like insomnia and risky behaviors. This discovery paves the way for further research into this region as well as a more in-depth look at other chromosomes to determine if there are other genetic variations related to suicide independently of psychiatric disorders.

This study provides a great insight in helping find a scientific way to help prevent suicide. By looking into the genome and finding a specific region that is common in the people who have attempted suicide can lead into possible treatments or even provide a reason as to why certain people are more inclined to attempt suicide. Suicide is a horrible health problem that has affected millions of Americans and it is especially common among teenagers and young adults. This research could possibly help look into the reasoning for that along with mental health resources in order to make sure death by suicide decreases.

Related Articles

Information Regarding Chromosome 7

Suicide Prevention and Mental Health Resources

Wednesday, October 9, 2019

Genetic Study Points to Metabolic Roots of Anorexia Nervosa

Article Link: genetic-study-points-to-metabolic-roots-of-anorexia-nervosa-66159
Supporting Article: researchers-explore-the-genetics-of-eating-disorders-65237

Through the biggest research on anorexia nervosa eating disorders, it was discovered that there are eight different genetic markers for the disorder. There is connection between AN and a locus overlapping six genes on chromosome 12 (Am J Psychiatry, 174:850–58) which is a chromosome that is linked to other disorders such as autoimmune diseases, and diabetes 1. Leading to the confirmation that the disorder has both psychiatric and metabolic origins. The disorder "claims more lives than any other psychiatric disorder. The condition affects up to 2 percent of women and 0.3 percent of men worldwide." psychiatrists have always struggled to find a treatment for the disorder due to its branched causes. 

In a breakthrough discovery, it was found that the disease is linked to the body’s ability to metabolize sugars and fats (insulin-glucose metabolism) and is related to high levels of physical activity. It was also found that characteristic single-nucleotide polymorphisms (SNPs) GABRG genes—which code for receptors involved in neural signaling that anorexia shares with several other psychiatric disorders, such as obsessive compulsive disorder, major depressive disorder and schizophrenia. Researchers have established that AN is 50 percent to 60 percent heritable. How the disorder works is that it allows the body to live without food longer than normal. This helps scientists to understand the disorder more and take metabolism and the patient's family history and genome into consideration when they work on a treatment plan for their patients. 


Genetic Study Points to Metabolic Roots of Anorexia Nervosa
I find these articles interesting as it changes no only the way psychiatrists view the disorder but how the patients, their family, and society views the disorder as well. Finding a biological tie to the disorder allows the patient to feel better about themselves and relieves some of the shame, excessive self-criticism and guilt they experience. It helps the society understand the disease more and know that this is a biological as well as it is a psychiatric disorder and not just a diet that an individual chooses. 

Tuesday, December 13, 2016

MicroRNA: The Cure to Schizophrenia Voices?

Schizophrenia often occurs during late adolescence or early adulthood and is characterized by cognitive problems such as delusions and hallucinations. About 1.1 % of Americans are affected by schizophrenia every year.  Despite schizophrenia being so common and having many treatments, there are still unanswered questions. One question in particular is the origin of auditory hallucinations. 

Researchers at St. Jude Children's Research Hospital have been using mouse models in order to replicate genetic predisposition for schizophrenia. The model that researchers were studying in particular is the 22q11 deletion syndrome, also known as DiGeorge syndrome. By modeling this syndrome, it allows the researchers to observe the development of psychiatric conditions, some of which that lead up to the development of schizophrenia.  


While running the mouse model, scientists have identified microRNAs that can be served as useful for creating new anti-psychotic drugs with reduced side effects. MircoRNAs are non-coding RNA molecules that generally involved in regulating and silencing gene expression. The specific microRNA that is of particular interest to researchers is miR-338-3p. This specific microRNA regulates the manufacture of protein D2 dopamine receptor (DRd2) in which have a major role in auditory hallucinations. According to Dr. Zakharenko, auditory hallucinations that are typical in schizophrenia is related to high levels of Drd2 in the auditory thalamus.

Through the mouse modeling, the researchers have discovered that individuals with 22q11 deletion syndrome are missing Dgcr8 genes in which is essential for the production of microRNAs. Because of the reduction of Dgcr8 genes based on this study, this leads to an increase in DrD2, thus causing auditory hallucinations demonstrated from schizophrenia. Further results have concluded that by replenishing microRNAs, the Drd2 levels decreased thus restoring normal functioning within the auditory thalamus, thus leading to a cure to auditory hallucinations. This is an important breakthrough for anti-psychotic drugs. By using a natural process and the concepts of microRNA, it can serve a new basis for how drugs for treating mental disorders are made. In particular, the benefits of microRNA is that it can lead to more effective interventions with limited side effects. With such an important discovery, this research can pave the way to tacking other mental disorders using the same concept. It will be very interesting to see how this research will progress and be beneficial in terms of psychiatric and medical research.

Wednesday, May 4, 2016

Genetic Variants in Psychiatric Illnesses

Bipolar disorder affects approximately 1-3% of Americans, causing intense mood swings that are very disruptive to the individual.  Recent studies show that variations in two different genes, CACNA1C and CACNB2, are significantly associated with psychiatric conditions such as bipolar disorder, schizophrenia, and major depression.  The CACNA1C gene is known to impact brain function involved in emotion, attention, thinking, and memory. 

Scientists can analyze which genes travel with or segregate with bipolar disorder by a mechanism called exome sequencing.  The trial involves examining the genomes of the individual with bipolar disorder as well as their family members.  In this particular study, researchers found 84 genetic variants that were previously linked to schizophrenia and autism.  Those genetic variants were also considered to be destructive to the gene that is responsible for coding.




It makes perfect sense that psychiatric conditions such as schizophrenia, bipolar disorder, autism, and major depression have similar genes in common.  All of those disorders have similarities in terms of affecting the way we think and feel.  I hope to see more progress in detecting genes responsible for certain psychiatric illnesses in the near future.  

Tuesday, April 12, 2016

Marijuana Addiction Linked to Genetics

Researchers are finding a possible link between certain genes and marijuana dependence. These three genes are also said to have an affect on risk factors for depression, which may mean that the two are linked together. In one study, 14,000 Americans provided information on marijuana use and 18-36% of people reported to be marijuana dependent. Given this information, researchers also looked for genetics variations that were linked to this. One genetic variant was located in a gene that regulates calcium concentrations in blood. Calcium has also been shown to have an affect on opioid dependence. Another one was located in the CSMD1 gene which has also been linked to schizophrenia. While these studies suggest that these genetic variants can lead to marijuana dependence, it is not proven. Further research is needed in order to have a better understanding of the addiction so that drugs can be made to help treat people who are dependent.


I found it interesting that the CSMD1 gene was also associated with schizophrenia, because I have heard that smoking a lot of marijuana can lead to psychiatric disorders, such as schizophrenia. It is important to be cautious about these drugs because no one knows whether or not becoming marijuana dependent is in their genes, so trying it one time can lead to a lifetime of addiction and complications. I also find it interesting that calcium signaling can lead to substance-abuse disorders, because it is not what I would expect. I would like to get genetic testing done so I can see what my risk levels are for these types of disorders as well as other health problems, because a lot can be determined simply from examining your DNA.

Thursday, March 31, 2016

Scientist's Eliminate Core Symptom of Schizophrenia in Mice


Schizophrenia  is a psychiatric disorder that affects more than 20 million people in the world. Eugene Daniels discusses the possible root causes of Schizophrenia in the video from Newsy. As he mentions in the video, people who suffer from Schizophrenia have fewer neural connections than people without the disease. Also, scientists have found that the immune system plays a major role in the development of Schizophrenia. However, in order to effectively treat this psychiatric disorder scientists need to discover the underlying factors that cause this disorder. 

Researchers from Columbia State University and New York State Psychiatric Institute used a chemical compound to fuse and grow new neural connections within the main regions of the brain so that memory loss can be restored. Since memory deficit is a main defining factor in Schizophrenia, their main focus was to discover how it develops on a biological and neurological level. The study involved testing mice with the genetic mutation called 22q11.2 microdeletion which is associated with memory loss. In previous studies, they have found that these microdeletions of 22q11.2 are linked to fewer neural connections in certain areas of the brain which in turn leads to memory deficits. People who express this genetic mutation of 22q11.2 microdeletions have a one in three chance of developing Schizophrenia. Whereas, people who do not express this genetic mutation have a one in 100 chance of developing Schizophrenia. The findings from the study demonstrated that through the restoration of neural connections the effects of memory loss in people with Schizophrenia can be reversed. According to Dr. Gordon (2016), in the mouse models the long neural connections were stunted within the prefrontal cortex and hippocampus which are the regions of the brain associated with memory. This lead researchers to conduct a new study which addressed the issue that the 22q11.2 microdeletion causes the protein Gsk3β to be overactive resulting in stunted growth of the neurons in the areas of the brain responsible for memory. They found that by suppressing the Gsk3β protein the neurons were able to branch out and form strong connections with each other which helps strengthen memory. Through these findings, scientist reveal the potential of the Gsk3β protein in helping to alleviate the symptoms of Schizophrenia. 

Through this scientific discovery, scientists and doctors can use this valuable information to develop more effective treatments for Schizophrenia. Even though Schizophrenia is a complicated disorder and doesn't have a single cause, I think that this discovery can contribute greatly to the scientific research on this disorder and relieve the symptoms from people who are suffering from it.  

Wednesday, March 30, 2016

Hunting the Genetic Signs of Postpartum Depression With an iPhone App


         With mothers and medical providers clamoring for answers about postpartum depression, scientists are starting a major effort to understand the genetic underpinnings of mood disorders that afflict millions of women during and after pregnancy. Researchers led by a University of North Carolina team will use a new iPhone app to recruit women who have had postpartum depression. The team’s theory is that postpartum depression may be distinct, involving genes with more identifiable effects because they act during or soon after pregnancy.
          The free app, PPD ACT, will be offered for this research. “To make sure this is not just a study of iPhone-using people,” Dr. Meltzer-Brody said, iPad versions of the app will be available and patients who want to provide their DNA will “right then and there be offered a spit kit.”This Research Kit software will be used for medical data collection, poses questions about sadness, anxiety or panic after childbirth in an effort to assess whether women have experienced serious postpartum depression. Women with high scores are asked if they want to submit DNA; if so, they will be mailed a kit to donate their saliva. Names and email addresses will be required, Dr. Meltzer-Brody said, but the project will encrypt personal data.

This article caught my attention because postpartum depression is a common everyday issue for women all around the country. This study can help and benefit so many women. I hope to read more about this study in the future. Postpartum depression is a serious illness and the fact that researchers are are starting to understand the genetic underpinnings of mood disorders is such a blessing.

Saturday, January 30, 2016

Scientists Move Closer to Understanding Schizophrenia's Cause


Recently, scientists took a significant step toward finding the cause of schizophrenia, in a study that provides the first rigorously tested insight into the genetics behind any common psychiatric disorder. Schizophrenia is a psychiatric disorder characterized by hallucinations and delusional thinking. Although people who suffer from schizophrenia are prescribed drugs, they only hide some symptoms and do not nearly touch upon the underlying cause. 

The recent findings were published in the journal Nature, which explained that although these findings were a step in the right direction, scientists and researchers are not even close to finding the exact cause, and unfortunately, will not lead to any new treatments. But, this new finding will help scientists and researchers move forward in finding the root cause to this ancient disorder, and does explain some mysteries such as why this disorder usually begins in adolescence. 

Researchers put pieces together by which genetics can increase the risk of developing schizophrenia, and found it was linked to synaptic pruning. Synaptic pruning is a process that happens in the brain which sheds weak or redundant connections between neurons as it matures. This happens in the prefrontal cortex, where thinking and planning happens, and starts during adolescence through early adulthood. Researchers suggest that people who carry genes that accelerate synaptic pruning are at a higher risk of developing schizophrenia. They suspect that synaptic pruning goes awry in people with schizophrenia because studies show they have a diminished number of neural connections in prefrontal areas, as compared to people without schizophrenia. 

The research team was made up by scientists from Harvard Medical School, Boston's Children's Hospital and the Broad Institute, a research center allied with Harvard and the Massachusetts Institute of Technology. The team began by focusing on the human genome MHC which was strongly associated with schizophrenia in previous studies. 

The below "skyline" graphs show the genetic variation associated with schizophrenia from 2011 to 2014, while the MHC looms the highest.


The MHC genome is known to control the body's immune responses, which had given rise to the question if schizophrenia is an autoimmune condition. Using advanced statistical methods, the research team found that the MHC locus contained four common variants of a gene called C4 which produced two kinds of proteins, C4-A and C4-B. The team analyzed 64,000 people and came to the conclusion that people with schizophrenia were more likely to have the overactive form of C4-A than the control subjects. C4-A leads to innapropriate pruning in the critical phase of development. Researchers hope to soon determine an at-risk genetic profile for schizophrenia that will help clarify a prognosis for patients. 

The finding of the C4-A gene leading to innapropriate pruning is an enormous step in the process of finding the cause of schizophrenia, and the researchers are excited about this finding. Although they have a long way to go, it gives them more insight into what can be causing this early psychiatric disorder. 

I believe this finding will give researchers motivation to find out more, because this finding has answered many questions and mysteries. We now know what gene is responsible for how fast synaptic pruning happens, but still are not sure why or how this actually happens. This finding also gives researchers ideas on new medications; possibly medications that can interfere with the pruning process. These findings also reveals why schizophrenia shows itself in young people, because that is when synaptic pruning happens, which is very promising. I am surprised, though, that this article does not talk about non-genetic events and if they can have an effect on schizophrenia. Are researchers leaning more towards schizophrenia as a true genetic disorder? Can traumatic events cause schizophrenia? Or maybe worsen effects after a person already has it? There are still many unanswered questions. Although this study did not reveal the cause of schizophrenia, we are well on our way, and technology will only keep advancing to help us through this process. 

Tuesday, December 15, 2015

Mutation in Shank3 Gene Can Lead to Different Psychiatric Disorders

Diagnosing and treating psychiatric disorders is a complex task, understanding the causes of these diseases is even more intricate and complex.  Neuroscientists at MIT are examining mutations on one gene, Shank3, that has been linked to autism and schizophrenia.  Shank3 encodes for a scaffold protein which organizes hundreds of other proteins found on the post-synaptic cell membrane.  Synapses are structures between neurons that help transmit electrical and chemical signals across the brain and nervous system.  Through ongoing research the scientist found that different mutations on the Shank3 gene, in mice, produce different psychiatric behaviors.  In 2011 scientists found that the absence of the Shank3 protein induced two common behaviors of autism- social avoidance and compulsive, repetitive behavior.  Years earlier, researchers at the University of Montreal found a mutation in the Shank3 gene in patients schizophrenia.



The scientists interested with the current research on Shank3 engineered mice to have the two different mutations of the Shank3 gene; one in which the protein was truncated and caused schizophrenic behavior and the other in which the absence of the Shank3 protein caused autistic behavior.  The mice also shared many common behaviors but also possessed the hallmark behaviors of their respective disorders.  By activating the mutations in different parts of the brain at different stages of development researchers were able to narrow down the brain circuits these mutations effected.  The autism mutation exerted its effects early in development, primarily in the region of the brain known as the striatum, these region is responsible for coordinating motor planning, habitual behavior and motivation.  The schizophrenia mutation exerted its effects later in development, suggesting that the truncated protein can function sufficiently early in development.  However as development continued the truncated proteins interfered with the synapses of the cortex, where executive function occur.

The brain is by far the most complex organ in our bodies, it is remarkable to think that essentially a pile of jelly is responsible for all of the thought, behavior, emotion, and movement that occurs in everyday life.  As if the brain isn't complex enough to understand, psychiatric disorders and the causes of those disorders are equally as complex.  The research being conducted by this group of scientists is aiming to understand the potential cause of these psychiatric orders and to also understand the brain circuits these defective proteins effect in order to tailor treatments for individuals affected by these disorders.  

Wednesday, September 23, 2015

5 Disorders Share Genetic Risk Factors, Study Finds



According to an article published in the New York Times, there are five psychiatric illnesses that share several genetic glitches, which are responsible for pushing the brain along a path toward mental illness. These psychiatric illnesses are bipolar disorder, autism, schizophrenia, major depression and attention deficit hyperactivity disorder. There are other factors that also influence mental illness such as other genetic issues as well as environmental factors. 

This study began in 2007 and included 60,000 people worldwide. Of these 60,000 people who were involved with the study, 33,332 were affected by mental illness and 27,888 that were not. Researchers examined the DNA from each participant searching for any variations. This study found four DNA areas that conferred a slight risk of psychiatric disorders. Two have been identified as genes that are part of the calcium channel. It is not clear what the other two genes are involved in or what they do.

I found this article to be interesting. The study that was preformed did produce good results however, I think further research is still required. Especially on the two genes that researchers are not sure of what their function is, maybe they are the key to creating a better treatment for psychiatric illnesses.

Thursday, November 21, 2013

New Genetic Risk Factor Discovered for Schizophrenia and Bipolar Disorder

  

     A team from The Feinstein Institute for Medical Research have discovered a factor in NDST3 that is likely to lead to schizophrenia and bipolar disorder. The risk factor was isolated using DNA from scizophrenic individuals as well as healty adults. The variant changes only a single letter, but can lead to devastating psychiatric illness. Bipolar and schizophrenia have long been hypothetically linked, and this new discovery combined with others further strengthens that theory (see the second link below).

    These articles resonate with me, since an isolated case of schizophrenia occured in my ancestry. While no one in my immediate family is known to have the disease, it's nice to know that we will eventually be able to test for these defects in our progeny. They are serious conditions, so any insight into their origins and methods is cetainly useful.

http://www.sciencedaily.com/releases/2013/11/131119112815.htm
http://www.sciencedaily.com/releases/2013/08/130811150815.htm

Thursday, April 11, 2013

5 Disorders Share Genetic Factors, Study Finds

On Wednesday, February 28th, the Cross-Disorder Group of the Psychiatric Genomics Consortium published in the Lancet identified the risk of loci with shared effects on five major psychiatric disorders (schizophrenia, bipolar disorder, autism, major depression, and attention deficit hyperactivity disorder). They began to examine genetic data in 19 countries. Researchers say gene variations are only a small risk of psychiatric disease.

The group studied families and identical twins, and found a few abnormal disruptions of chromosomes that were linked to psychiatric disorders. In one set of twins, one twin had schizophrenia while the other had bipolar disorder. Dr. Jonathan Sebat chief of the Beyster Center for Molecular Genomics of Neuropsychiatric Diseases gave his opinion by saying,
“No one had systematically looked at the common variations…in DNA.” “We didn’t know if this was particularly true for rare mutations or if it would be true for all genetic risk.”

In addition, the new study found four DNA regions that presented a small risk of psychiatric disorders. Researchers haven’t yet discovered the risk of the first two DNA regions. The other two regions are part of calcium channels, which are used when neurons send signals to the brain. This is exciting news because there are drugs on the market that block calcium channels. The problem is that the researchers are not sure if it will work and be safe for the consumers.

 

 

 

 

Friday, March 15, 2013

Un Poco Loci: Genetic Ties to Mental Disorders

In their efforts to better understand and more accurately diagnose mental conditions, a recent article from disabilityscoop.com states that researchers discovered that there may be a close genetic link between several psychiatric disorders in what they refer to as genetic “risk factors.” Specifically, the targeted psychiatric disorders included autism spectrum disorder, attention deficit hyperactivity disorder (ADHD), bipolar disorder, major depressive disorder and schizophrenia.

After analyzing the genomes of more than 30,000 people each with one of the these five psychiatric disorders, and almost 28,000 people with no mental health issues, scientists found that single-nucleotide polymorphisms (SNPs) at four loci displayed variations seen in people with the five psychiatric conditions.

Scientists say knowing that these psychiatric conditions share genetic risk factors could help doctors better diagnose  and treat these conditions.
“Our results provide new evidence that may inform a move beyond descriptive syndromes in psychiatry and towards classification based on underlying causes,” said Jordan Smoller of Massachusetts General Hospital who worked on the study."

More information on the actual study can be found at The Lancet.

What I find fascinating about this article is that from outside of the view of genetics these disorders already seem to have some relations to one another. If you have ever met a person with any of these disorders you may see certain parallels in their expressions that mimic other mental disorders. Probably the most obvious at least to myself, would be the sense of confusion all must feel. But to now see these disorders are displayed on shared loci give us a bigger picture on the smallest of scales of genetic disposition rather than just a “loose screw”.