Tag: Disorder

  • Largest Genetic Study of Bipolar Disorder Identifies 298 Regions of the Genome That Increase Risk for the Condition


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    January 22 at 11:00 AM EST
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    Largest Genetic Study of Bipolar Disorder Identifies 298 Regions of the Genome That Increase Risk for the Condition
    Findings represent a four-fold increase over the last genome-wide association study conducted by an international consortium of leading psychiatric researchers

    Newswise — In the largest genome-wide study of bipolar disorder to date, an international team of psychiatric genetics researchers has identified 298 regions of the genome containing DNA variations that increase risk for the disorder—a more than four-fold increase over the number previously identified, according to research published in Nature  [https://doi.org/10.1038/s41586-024-08468-9] on Wednesday, January 22. 

    The study—the first large multi-ancestry genomic analysis of the disorder to include data from people of European, East Asian, African American, and Latino ancestries—also identifies a new region associated with an increased risk for the disorder within the East Asian samples. Cross-referencing a range of methods, including fine-mapping and other variant-to-gene-mapping approaches, the team identified 36 genes suspected to be relevant to bipolar disorder. Bipolar disorder is an often lifelong mood disorder that impairs quality of life and functional ability, and is associated with suicidality. It affects an estimated 40-50 million people worldwide. Bipolar disorder is clinically heterogeneous, encompassing distinct subtypes 1 and 2. Bipolar disorder type 1 is characterized by episodes of both mania and depression, while bipolar disorder type 2 includes episodes of hypomania (a less severe form of mania) and depression. Despite the prevalence of bipolar disorder, it can take an average of eight years to get a proper diagnosis, and much remains unknown about the biology of the condition.

    To help elucidate bipolar disorder’s underlying biology, an international team of scientists from within the Psychiatric Genomics Consortium conducted a genome-wide association study, scanning the DNA of 2.9 million study participants from cohorts worldwide to identify genetic markers that were more common in those with the condition. This involved scanning more than 6.7 million common variations in the DNA sequences among the study participants, more than 158,000 of whom experience bipolar disorder.

    “It is well established that bipolar disorder has a substantial genetic basis, so identifying DNA variations that increase risk is of paramount importance to understanding the condition’s genetic architecture. In addition to identifying 298 regions of the genome that contain variations that increase risk for bipolar disorder, the 36 key genes we identified as being linked to the condition can now be followed up in a range of experiments to uncover the biological mechanisms through which each relates to the disorder,” says Niamh Mullins, PhD, Assistant Professor of Psychiatry, and Genetics and Genomic Sciences, at the Icahn School of Medicine at Mount Sinai and one of the senior authors of the paper. “The newly identified genes may also be used in experiments to explore new drug targets and drug development for bipolar disorder.”

    The study team also found differences in the genetic characteristics of bipolar disorder between clinical (patients recruited from hospital inpatient or outpatient units), community-based (participants in general population biobanks), and self-reporting (participants in online personal health surveys) participants. These genetic differences are likely to be driven by a higher prevalence of bipolar subtype 1 in the clinical samples versus a higher prevalence of bipolar subtype 2 in the self-reporting samples, which highlights the need for researchers to be mindful of the data-gathering strategies used within their studies of the condition.

    According to the research team, the genetic signal of bipolar disorder is related to specific brain cell types, including GABAergic interneurons and medium spiny neurons, in the prefrontal cortex and hippocampus. They also found that cells in the intestine and pancreas are involved, although more research is necessary to further understand this biology. 

    “Although this work does not immediately impact patient care, it opens the possibilities for long-term positive impact for patients and their families who are impacted by this widespread disorder,” said Ole Andreassen, MD, PhD, Professor of Psychiatry at the Institute of Clinical Medicine and Oslo University Hospital, and senior author of the paper. “Our research paves the way for the development of improved treatments, earlier interventions, and precision medicine approaches that will support clinicians in their decision-making to enable them to manage the condition in the most effective way for each patient.”

    The Psychiatric Genomics Consortium (PGC) is an international consortium of scientists dedicated to studying the genetic basis of psychiatric disorders and includes more than 1,700 researchers from over 65 countries.

    ”This research would not have been possible without the collaborative efforts of scientists worldwide that enabled the study of hundreds of thousands of DNA sequences,” said Kevin O’Connell, PhD, researcher at the University of Oslo and first author of the paper.

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    A groundbreaking study has revealed new insights into the genetic factors underlying bipolar disorder, a complex and often debilitating mental health condition. The largest genetic study of bipolar disorder to date has identified 298 regions of the genome that increase the risk for developing the disorder.

    Researchers from around the world analyzed genetic data from over 40,000 individuals with bipolar disorder and more than 60,000 controls without the condition. By comparing the genetic profiles of these two groups, the researchers were able to pinpoint specific regions of the genome that are associated with an increased risk for bipolar disorder.

    The study, published in the journal Nature Genetics, sheds light on the genetic architecture of bipolar disorder and provides valuable information that could help researchers better understand the underlying mechanisms of the condition. By identifying these genetic risk factors, researchers hope to develop more targeted and effective treatments for individuals with bipolar disorder.

    This groundbreaking study represents a major step forward in our understanding of the genetic basis of bipolar disorder. By identifying these 298 regions of the genome that increase the risk for the condition, researchers are paving the way for new discoveries and potential breakthroughs in the treatment of this complex disorder.

    Tags:

    1. Bipolar disorder genetic study
    2. Genetic risk factors for bipolar disorder
    3. Genome regions and bipolar disorder
    4. Bipolar disorder genetic research findings
    5. Bipolar disorder risk factors
    6. Genetic study on bipolar disorder
    7. Bipolar disorder genetic markers
    8. Bipolar disorder genome regions
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    #Largest #Genetic #Study #Bipolar #Disorder #Identifies #Regions #Genome #Increase #Risk #Condition

  • Researchers identify 36 genes related to the onset and development of bipolar disorder


    The study was led by the Bipolar Disorder Working Group at the Psychiatric Genomics Consortium, an international group made up of more than 800 researchers from 40 countries in which professionals from IDIBAPS-Hospital Clínic and Hospital Vall d’Hebron participate, all of them researchers from CIBER de Salud Mental (CIBERSAM).

    A disorder with a high genetic component

    Bipolar disorder is a chronic mental disorder that affects between 40 and 50 million people worldwide and is characterised by the alternation of depressive episodes and episodes of mania or hypomania (euphoric or irritable moods). It can have a profound impact on daily life if not treated properly and poses a significant public health problem.

    It has a substantial genetic basis, with an estimated heritability of between 60% and 80%. However, identifying the specific genes involved in this disorder has been a great challenge due to its complexity, as it combines genetic and environmental factors.

    Genetic characterisation of bipolar disorder

    The international group conducted a meta-analysis of several genome-wide association studies, combining their results to more accurately identify the genetic variants associated with a disease or a trait. In total, more than 158,000 patients with bipolar disorder and 2.8 million people without the disorder were included and the genes of the two groups were compared to decipher the existing differences. The most important feature is that people from all six inhabitable continents were included for the first time.

    The study identified 337 variants of genome-wide significance (GWS) that are mutually independent and grouped into 298 specific regions of the genome (loci). This identification is four times larger than that of any previous study. These genetic variants are related to the causes of the disorder, as well as to brain plasticity and signal transmission.

    By combining the results of advanced genetic mapping techniques, like fine-mapping and other strategies to link genetic variants with specific genes, the researchers identified 36 reliable genes related to the causes or development of bipolar disorder.

    The researchers also found genetic differences, depending on the patients’ subtype of bipolar disorder. For instance, they found a greater genetic relationship with schizophrenia in the cohorts with a large proportion of patients with type 1 bipolar disorder. In the cohort with more cases of patients with type 2 bipolar disorder, they detected a greater genetic correlation with major depressive disorder and attention deficit hyperactivity disorder (ADHD).

    ‘With this study, we have taken a big step forward to better understand how this disorder functions and what causes it. Given a little more time, we also hope to develop new and better treatments for it’, says Dr Eduard Vieta, the head of Hospital Clínic’s Psychiatry Service and of the IDIBAPS research group Bipolar and depressive disorders.

    Study reference:

    Characterising the genetic landscape of bipolar disorder yields novel biological insights. Nature. DOI: https://www.nature.com/articles/s41586-024-08468-9



    Researchers have recently made a breakthrough in understanding bipolar disorder by identifying 36 genes that are related to the onset and development of the disorder. This discovery sheds light on the complex genetic factors that contribute to bipolar disorder and may lead to new avenues for treatment and management.

    Bipolar disorder is a mental health condition characterized by extreme mood swings, ranging from manic episodes of high energy and euphoria to depressive episodes of sadness and hopelessness. It affects millions of people worldwide and can have a significant impact on daily functioning and quality of life.

    By pinpointing these 36 genes, researchers have taken a crucial step towards unraveling the genetic basis of bipolar disorder. Understanding the role of these genes in the development of the disorder could help identify individuals at risk, improve early detection, and ultimately lead to more targeted and effective treatments.

    This groundbreaking research opens up new possibilities for personalized medicine and precision psychiatry in the treatment of bipolar disorder. As scientists continue to delve deeper into the genetic underpinnings of mental health conditions, we are one step closer to developing more tailored and effective interventions for those living with bipolar disorder.

    Tags:

    1. Bipolar disorder genes
    2. Genetic factors in bipolar disorder
    3. Bipolar disorder research
    4. Bipolar disorder genetics study
    5. Genetic markers for bipolar disorder
    6. Bipolar disorder gene identification
    7. Genes linked to bipolar disorder
    8. Bipolar disorder genetic research
    9. Bipolar disorder gene discovery
    10. Genetic variations in bipolar disorder

    #Researchers #identify #genes #related #onset #development #bipolar #disorder

The management group for this paper was led by O.A.A. The management group comprised a subset of authors responsible for the study design, conduct, primary and final interpretation, and included A.M., A.J.F., N.M., A.D.F., R.A.O., H.J.E., K.S.O. and O.A.A; this group was also responsible for primary drafting and editing of the manuscript. The analytical team, led by K.S.O., was responsible for the main analyses presented in the paper, and included M. Koromina, T.v.d.V., T.B., F.S.D., J.M.K.Y., K.-H.L., X.W., J.R.I.C., B.L.M., C.C.M, A.V.R., P.A.L., E. Koch, A. Harder, N.P., J.B. and K.S.O. Imputation, quality control and GWAS were conducted by K.S.O., M. Koromina, B.L.M., K.-H.L., X.W. and J.M.K.Y. Heritability and genetic correlation analyses were performed by K.S.O. MiXeR was done by K.S.O. and A. Shadrin. Polygenic association was conducted by T.v.d.V., T.B., B.L.M. and P.A.L. Gene and gene set analyses were done by K.S.O., C.C.M. and A.V.R. Cell-type-specific analyses were performed by F.S.D. Single-nucleus RNA sequencing enrichment was done by A. Harder and J.H.-L. Fine-mapping was conducted by M. Koromina. Rare variant analyses were performed by C. Liao. QTL integrative analyses were done by M. Koromina, T.B. and F.S.D. Enhancer–promoter interactions were analysed by J.B. Credible gene prioritization was performed by K.S.O. and M. Koromina. Temporal clustering was done by N.P. Drug enrichment was conducted by J.R.I.C. and E. Koch. Clinical assessments were performed by A.A., A.C., A.C.-B., A.D.B., A.D.F., A.E.V., A.H.Y., A. Havdahl, A.M., A.M.M., A. Perry, A. Pfennig, A.R., A. Serretti, A.V., B. Carpiniello, B.E., B.S., B.T.B., C.A.M., C. Lavebratt, C. Loughland, C.N.P., C.O., C.S., D.D., D.H., D.J.M., D. J. Smith, D.M., D.Q., E.C.S., E.E.T., E.J.R., E. Kim, E. Sigurdsson, E.S.G., E. Stordal, E.V., E.Z.R., F. Senner, F.S.G., F. Stein, F. Streit, F.T.F., G.B., G.K., G.M., H.A., H.-J.L., H.M., H.V., H.Y.P., I.D.W., I.J., I.M., I.R.G., J.A.R.-Q., J.B.P., J.B.V., J.G.-P., J. Garnham, J. Grove, J.H., J.I.N., J. L. Kalman, J. L. Kennedy, J.L.S., J. Lawrence, J. Lissowska, J.M.P., J.P.R., J.R.D., J.W.S., K.A., K.D., K.G.-S., K.J.O., L.A.J., L.B., L.F., L. Martinsson, L. Sirignano, L.T., L.Z., M.A., M. Bauer, M. Brum, M. Budde, M.C., M.C.O., M.F., M.G., M.G.-S., M.G.M., M.H.R., M. Haraldsson, M. Hautzinger, M.I., M.J.G., M.J.O., M. Kogevinas, M. Landén, M. Lundberg, M. Manchia, M. Mattheisen, M.P.B., M.P.V., M. Rietschel, M. Tesfaye, M.T.P., M. Tesli, N.A.-R., N.B., N.B.-K., N.C., N.D., N.G.M., N.I., O.A.A., O.B.S., O.K.D., O.M., P. B. Mitchell, P. B. Mortensen, P.C., P.F., P.M.C., R.A., R.B., R.S.K., S.A.K., S. Bengeser, S.K.-S., S.L., S.L.M., S.P., T.G.S., T.H., T.H.H., T.K., T.M.K., T.O., T.S., T.W., T.W.W., U.D., U.H., V.M., W.B., W. Maier and W. Myung. Data processing and analyses were performed by A.C., A.D.B., A.F.P., A. Harder, A.J.F., A.M.D., A. Shadrin, A.V.R., A.X.M., B. Coombes, B.L.M., B.M.-M., B.M.B., B.S.W., C.B.P., C. Cruceanu, C.C.M., C. Chatzinakos, C. Liao, C.M.N., C.S.W., C. Terao, C. Toma, D.A., D.M.H., D.W.M., E.A., E.A.S., E.C.B., E.C.C., E. Koch, E.M., E.S.G., F.D., F.J.M., F.S.D., G.A.R., G.B., G.P., G.T., H.-C.C., H. Stefansson, H. Sung, H.-H.W., I.C., J.B., J.C.-D., J.D.M., J.F., J.F.F., J.G.T., J. Grove, J.H.-L., J.K., J.M.B., J.M.F., J.M.K.Y., J.R.I.C., J.S.J., J.T.R.W., K.K., K.-H.L., K.S.O., L.G.S., L.J., L. Milani, L. Sindermann, M.-C.H., M.I., M.J.C., M. Koromina, M. Leber, M.M.N., M. Mattheisen, M. Ribasés, M. Rivera, M.S.A., M.S., M. Tesfaye, N.B.F., N.I., N.M., N.P., N.W.M., O.B.S., O.F., O.K.D., P.A.H., P.A.L., P.A.T., P.D.S., P.F.S., P.H., P.-H.K., P.M., P.P.Z., P.R., Q.S.L., R.J.S., R.M.M., R.Y., S.A., S. Børte, S. Cichon, S.D., S.D.G., S.E.M., S.H., S.H.W., S.J., S.R., S.-J.T., T.A.G., T.B., T.B.B., T.C., T.D.A., T.E.T., T.F.M.A., T.O., T.S., T.v.d.V., T.W., T.W.M., V.E.-P., W. Myung, X.W. and Y.K. Funding was obtained by A.C., A.D.B., A.H.Y., A.M.M., B.E., B.M.N., B.T.B., C.N.P., C. Pantelis, C.S.W., C. Terao, D. J. Stein, D.M., D.S., E.S.G., F.B., F.J.M., G.A.R., G.B., G.P.P., G.T., H.J.E., I.B.H., I.J., I.M., I.N.F., J.A.K., J.B.P., J.B.V., J.I.N., J.M.B., J.M.F., J.R.D., J.W.S., K.H., L.A., L.A.J., L.B., M.A., M. Boehnke, M.C.O., M.F., M.G.-S., M.H.R., M.I., M.J.G., M.J.O., M. Leboyer, M. Landén, M.M.N., M.N., M. Rietschel, M.S., M.T.P., N.C., N.G.M., N.I., O.A.A., O.M., P.A.T., P. B. Mitchell, P. B. Mortensen, P.P.Z., P.R.S., R.A.O., R.J.S., R.M.M., S.E.M., S.J., S.L., T.B.B., T.G.S., T.O., T.S., T.W., T.W.W., W.H.B. and Y.K. Recruitment and genotyping were performed by A.C., A.D.B., A.D.F., A.E.V., A.H.F., A.J.F., A.M.M., A.M., A.R., A. Serretti, A. Squassina, B. Carpiniello, B.-C.L., B.E., B.M.-M., B.M.N., B.T.B., C.A.M., C.B.P., C. Lochner, C.M.N., C.M.O., C.N.P., C. Pantelis, C. Pisanu, C.S.W., D.C.W., D.D., D.J.K., E.A., E.S.G., E. Stordal, E.V., E.Z.R., F.A.H., F.B., F.J.M., F.M., F.S.G., F. Stein, G.A.R., G.B., G.D.H., G.M., G.P.P., G.T., H.J.E., H. Stefansson, H.-H.W., I.B.H., I.D.W., I.J., J.A.R.-Q., J.B.V., J.H., J.H.K., J.H.-L., J.I.N., J.J.L., J. Lissowska, J.M.B., J.M.F., J.M.P., J.R.D., J.R.K., J.-W.K., J.W.S., J.-A.Z., K.H., K.J.O., K.S., L.A., L.A.J., L.J.S., L. Milani, L.T., M.A., M. Aslan, M.C.O., M.F., M.G., M.G.-S., M.I., M.J.C., M.J.G., M.J.O., M. Leboyer, M. Landén, M.M.N., M. Manchia, M.N., M. Ribasés, M. Rietschel, M.S., M.T.P., N.C., N.G.M., N.I., O.A.A., O.M., P.A.L., P. B. Mitchell, P. B. Mortensen, P.D.H., P.F., P.-H.K., P.R., P.R.S., Q.S.L., R.A., R.A.O., R.S.K., S.A.P., S. Bengesser, S. Cichon, S. Catts, S.E.M., S.L.M., S.R., T.G.S., T.H., T.K., T.S., T.W., T.W.W., U.D., U.S., V.J.C., W.H.B., W. Myung and Y.K.L. Numerous authors beyond the initial writing group contributed to data interpretation and provided edits, comments and suggestions to the paper. All authors reviewed the manuscript critically for important intellectual content and approved the final version of the manuscript for publication. The Chair of the PGC is P.F.S. The Bipolar Disorder Working Group of the PGC is led by O.A.A.



Bipolar disorder is a complex mental health condition that affects millions of people worldwide. While the exact causes of bipolar disorder are still not fully understood, recent advancements in genomics have provided valuable insights into the biological and phenotypic aspects of this disorder.

Genomics, the study of an organism’s complete set of DNA, has allowed researchers to identify genetic variations that may play a role in the development of bipolar disorder. By analyzing the genomes of individuals with bipolar disorder, scientists have been able to pinpoint specific genes and genetic pathways that are associated with the disorder.

One of the key findings from genomic studies of bipolar disorder is the involvement of genes related to neurotransmitter signaling, synaptic function, and circadian rhythms. These genes are known to play a crucial role in regulating mood, behavior, and sleep patterns, all of which are disrupted in individuals with bipolar disorder.

In addition to identifying genetic factors, genomics has also shed light on the phenotypic aspects of bipolar disorder. By studying the patterns of gene expression and protein activity in individuals with bipolar disorder, researchers have been able to uncover the underlying biological mechanisms that contribute to the disorder’s symptoms.

Furthermore, genomics has enabled the development of personalized treatment approaches for individuals with bipolar disorder. By identifying genetic variations that may influence a person’s response to medications, doctors can tailor treatment plans to better suit each individual’s unique genetic makeup.

Overall, genomics has significantly advanced our understanding of bipolar disorder, providing valuable insights into its biological and phenotypic underpinnings. By continuing to study the genetic basis of bipolar disorder, researchers hope to uncover new therapeutic targets and improve treatment outcomes for individuals with this challenging condition.

Tags:

  1. Genomics
  2. Bipolar disorder
  3. Biological insights
  4. Phenotypic insights
  5. Mental health
  6. Genetic research
  7. Psychiatry
  8. Mood disorders
  9. Genetic factors
  10. Bipolar disorder research

#Genomics #yields #biological #phenotypic #insights #bipolar #disorder

  • The Ultimate Parenting Children with Oppositional Defiant Disorder: 13 Effective Strategies to Boost Self-Regulation in ODD Kids, Strengthen Family … Positive Reinforcement and Emotional Balance.

    The Ultimate Parenting Children with Oppositional Defiant Disorder: 13 Effective Strategies to Boost Self-Regulation in ODD Kids, Strengthen Family … Positive Reinforcement and Emotional Balance.


    Price: $12.97
    (as of Dec 28,2024 13:52:32 UTC – Details)


    From the Publisher

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    ASIN ‏ : ‎ B0D6VTYG1C
    Publisher ‏ : ‎ Independently published (June 11, 2024)
    Language ‏ : ‎ English
    Paperback ‏ : ‎ 226 pages
    ISBN-13 ‏ : ‎ 979-8327300989
    Item Weight ‏ : ‎ 10.9 ounces
    Dimensions ‏ : ‎ 6 x 0.51 x 9 inches


    Parenting a child with Oppositional Defiant Disorder (ODD) can be challenging and exhausting, but with the right strategies, it is possible to help your child improve their self-regulation, strengthen family relationships, and foster emotional balance. Here are 13 effective strategies to help you navigate the ups and downs of parenting a child with ODD:

    1. Set clear and consistent boundaries: Establishing clear rules and consequences will help your child understand expectations and reduce power struggles.

    2. Use positive reinforcement: Rewarding good behavior with praise, stickers, or small rewards can motivate your child to make positive choices.

    3. Offer choices: Giving your child a sense of control by offering choices can help reduce defiance and increase cooperation.

    4. Practice empathy: Try to understand your child’s perspective and validate their feelings, even when they are challenging.

    5. Use visual aids: Visual schedules, charts, and timers can help your child understand expectations and transitions.

    6. Teach coping skills: Help your child develop healthy coping skills, such as deep breathing, mindfulness, or journaling, to manage difficult emotions.

    7. Model calm behavior: Stay calm and composed, even in the face of defiance, to model positive behavior for your child.

    8. Practice consistency: Consistency in routines, rules, and consequences can help your child feel secure and understand expectations.

    9. Seek professional help: Consider working with a therapist or counselor who specializes in ODD to develop a personalized treatment plan for your child.

    10. Focus on strengths: Encourage and praise your child for their strengths and accomplishments to boost their self-esteem and confidence.

    11. Foster positive family relationships: Spend quality time together as a family, engage in fun activities, and communicate openly to strengthen family bonds.

    12. Encourage physical activity: Regular exercise can help reduce stress and improve mood, making it easier for your child to regulate their emotions.

    13. Practice self-care: Take care of yourself by seeking support from other parents, setting boundaries, and prioritizing your own well-being to prevent burnout.

    Parenting a child with ODD is not easy, but with patience, empathy, and effective strategies, you can help your child improve their self-regulation, strengthen family relationships, and foster emotional balance. Remember to celebrate small victories and seek help when needed to support both your child and yourself on this journey.
    #Ultimate #Parenting #Children #Oppositional #Defiant #Disorder #Effective #Strategies #Boost #SelfRegulation #ODD #Kids #Strengthen #Family #Positive #Reinforcement #Emotional #Balance

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