Brain Inflammation Collaborative, Inc.

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Pro-inflammatory cytokines are elevated in the brains of suicide victims (1). However, this elevation is not exclusive to a suicidal brain. These immune modulators are similarly elevated in people with major depressive disorder (2), bipolar disorder (3), and schizophrenia (4). Therefore, identifying biomarkers unique to a suicidal brain will help researchers understand and perhaps one day prevent suicide. A 16-year-old researcher might have found one such biomarker. Natasha Kulviwat discovered that a protein called Caludin-5 is significantly elevated in the brain in those who died by suicide. Claudin-5 is like a glue that holds blood vessels together. Claudin-5 is highly expressed in the brain vasculature, but Natasha discovered that this "glue" is unexpectedly expressed by the neurons of suicide victims. While more work is needed to understand how Claudin-5 expression in neurons might impact psychiatric conditions, this work from a talented 16-year-old must be celebrated! We at the Brain Inflammation Collaborative envision a world where the causes of suicide are completely understood, properly diagnosed, and treated. Join our mission by sharing this with your family, friends, and colleagues. Literature Cited: 1. Serafini, G. et al., Int J Environ Res Public Health. 2020 2. Yong-Ku Kim, et al., Prog. Neuro-Psychopharmacol. Biol. Psychiatry. 2016 3. Modabbernia, A., et al., Biol. Psychiatry. 2013 4. Reale, M. et al., Frontiers in Psychiatry. 2021 https://buff.ly/3COma4x

We are helping researchers understand the role inflammation plays in our mental health. Join our mission by sharing this content. #immunopsychiatry

Chronic systemic inflammation is associated with a deterioration in our mental health, including depression (1) and anxiety (2). But why? Mouse studies show that socially stressed mice rapidly increase pro-inflammatory cytokine levels (IL-6, IL-1beta, TNF-alpha) in the blood (3). These cytokines increase the permeability of blood vessels in the amygdala and prefrontal cortex, allowing the cytokines to enter the brain, causing depression-like and anxiety-like symptoms in mice (3,4). Blocking systemic inflammation can rescue these changes in behavior (3,4). Could this partly explain why those suffering from chronic rhinosinusitis have higher odds of depression and anxiety, or is it caused by a neurotransmitter imbalance? We are taking a different approach to ending the mental health epidemic by helping researchers understand how the immune system impacts our brain. We hope this will stimulate the next generation of psychiatric medications to safely and effectively treat mental health conditions in a subpopulation of patients. If this resonates with you, please give it a like and share! Citations: 1. Mac Giollabhui N, Ng TH, Ellman LM, Alloy LB. Mol Psychiatry. Jul 2021 2. Renna, M. O'Tool, M. et al. Depress Anxiety. Sept 2018. 3. Wu X, Ding Z, Fan T, et al. Front Cell Dev Biol. 2022. 4. Dion-Albert L, Cadoret A, Doney E, et al. Jan 10 2022.

Our incredibly talented clinical research associates, Melanie Helvick and Christina Moon discuss our new clinical research platform, Unhide. Unhide is designed to help researchers explore the hidden connections between neuroinflammatory illnesses and mental health conditions. We thank Melanie and Christina for their efforts in bridging the gap between bench science and clinical research! Learn more: https://buff.ly/3ZfkbPv #Unhide #clinicalresearchapp #bridgingthegap

A new study reveals that PANDAS/PANS children with tics and OCD have autoantibodies targeting the dopamine receptor 1 (D1R) while those with Sydenham chorea (whiplash-like movements) have autoantibodies targeting dopamine receptor 2 (D2R). This suggests PANDAS/PANS is an autoimmune disease that can be identified clinically using anti-D1R and D2R autoantibodies as biomarkers. Here is what you need to know... \ Background: Evidence suggests children with PANDAS/PANS have an inflamed basal ganglia (1). This is an area of the brain responsible for: - Motor control - Cognitive functions - Procedural learning - Emotional regulation \ Basal Ganglia: The basal ganglia is also enriched for... you guessed it, dopamine receptors. Could these autoantibodies be partly responsible for PANDAS/PANS and Sydenham chorea symptoms? \ Autoantibodies Activate Dopamine Receptors: The study mapped exactly where autoantibodies bind the dopamine receptors (image below), which were found to activate the dopamine receptors. In other words, the autoantibodies mimicked the effects of dopamine. \ Conclusion: This study supports the idea that PANDAS/PANS should be recognized as an autoimmune condition characterized by autoantibodies that signal in the brain and likely cause basal ganglia encephalitis. We envision a world where PANDAS/PANS is widely understood by physicians, rapidly diagnosed, and treated (without health insurance denials). We are collaborating with study authors Dr. Madeline Cunningham and Dr. Chandra Menendez to identify autoantibody profiles in the saliva of PANDAS/PANS children. This research aims to detect these profiles without using blood and store them in a biobank for further analysis by other researchers in the future. Learn more at unhidenow.org Read the full study here: https://buff.ly/4eqOKWG Citations: 1. Kumar, A. Williams, M. et al. J Child Neurol. 2015 May;30(6):749-56. doi: 10.1177/0883073814543303.

Scientists are engineering electrodes 5x smaller than a human hair's width to try and treat mental health and neurodegenerative diseases (to name a few). Could a medical device be used to treat neurological conditions that are ineffectively managed by pharmaceuticals? Here's what you need to know. \ Background: Biomedical engineers at the University of Cambridge received funding to create electrodes that can "constantly monitor the brain to detect abnormal activity and then correct it more gently when needed." \ Applications: When asked about the clinical applications, Dr. George Malliaras said, "The list is ever expanding, but we're talking about brain and spinal cord injuries, Parkinson's, dementia, depression, OCD, and it's looking promising for rheumatoid arthritis and Type 1 diabetes too." \ How It Would Work: The brain or spinal cord implant would send out small electrical impulses in response to abnormal neuronal activity. \ Technical Challenges: "The electrodes which come out of the implant need to be no bigger than a single neuron. That's five times smaller than the diameter of a human hair," explains Prof Malliaras. They must also ensure the electrodes are large enough for surgical implantation, affordable, and suitable for mass production. \ Depression Treatment Precedence: An experimental surgery was recently performed (with a larger electrical device) to electrically stimulate the brain following detection of abnormal nerve communication. The surgery cured the patient's debilitating depression and suicidal thoughts. Read more here: https://buff.ly/4feUTXb \ Electrical Implants to Target Inflammation: There are devices the size of a fingernail that can also be implanted to turn off the inflammatory reflex in the body by stimulating the vagus nerve. Only 1 milliampere of current for up to 5 minutes can block inflammation for 24-48 hours. Read more here: https://buff.ly/3YHwYZv This is important because systemic inflammation predicts the future onset of depression and other mental health conditions (1). Could electrical device implants supplement ineffective pharmaceutical approaches to treat neuroinflammatory, neurodegenerative, and mental health conditions? If you found this interesting please give it a like and share. Check out our free newsletter for the latest on neuroimmune axis conditions (pinned post). Read the full story about brain implants here:

Inflammation in the brain has the power to warp your thoughts, leading to doubts about reality or your self-worth. This unsettling reality is faced by individuals experiencing a neuroinflammatory illness, whether they are aware of it or not. Rachel bravely shares the story of her mental health battles after being diagnosed with PANS and PANDAS. We at the Brain Inflammation Collaborative envision a world where the causes of mental health conditions from illnesses like #POTS and #PANDAS are widely understood promptly diagnosed and treated. Join us by sharing this content! #OCD #Mentalhealth #Immunopsychiatry

The absence of vitamin D accelerates the aging of the thymus, increasing the prevalence of autoimmunity, according to a new study. \ Background - The Thymus and Autoimmunity: T cells are made in the thymus, a lymphoid organ at the base of the neck. To ensure new T cells do not confuse self-antigens with non-self antigens (causing autoimmunity), a special cell type called medullary thymic endothelial cells (mTEC) express a vast array of genes from other tissues in the body, such as the: - cardiovascular system - respiratory system - nervous system - ...everywhere If a new (naive) T cell reacts with antigens (molecules that elicit an immune response) expressed in the mTECs, it is deleted to prevent autoimmunity. \ The Aged Thymus: As we age, the thymus makes fewer T cells increasing our susceptibility to developing: - autoimmunity - infections - cancer The aged thymus also becomes less efficient at deleting autoreactive T cells because the mTECs reduce the expression of genes found elsewhere in the body, like the brain. Researchers found what might slow this aging... vitamin D. \ Vitamin D: Researchers discovered that mice genetically unable to make the biologically active form of vitamin D have a thymus that has undergone accelerated aging. They discovered that vitamin D, a vitamin made in the body from sun exposure (and other sources), allows the array of genes from other tissues to be expressed by the medullary thymic ECs. \ Conclusion: While this has yet to be verified in humans, the study suggests vitamin D supplementation could slow the aging of our thymus and prolong our health span. This is a good reminder to make sure you and your young children get adequate amounts of vitamin D especially since the winter months have arrived. We are on a mission to inform health professionals and patients that chronic inflammation from most autoimmune diseases can impact your brain health and mental health. If you found this content informative, please give it a like and share!

A SARS-CoV-2 infection increases your risk of developing a mental health condition like depression, mood disorder, or psychotic disorder, according to yet another study. \ Study Details: Medical records from the UK Biobank were assessed to determine the relationship between a SARS-CoV-2 infection and a mental health diagnosis. \ Cohort: Individuals with no history of mental health complications 2 years before the study were included and followed for 1 year following their first infection. - 301,398 uninfected controls - 19,353 SARS-CoV-2-infected cases \ Study Findings: People with a SARS-CoV-2 infection had an increased risk (%) of developing: - sleep disorder (47%) - mood disorder (44%) - anxiety disorder (63%) - alcohol use disorder (51%) - depressive episodes (46%) A SARS-CoV-2 infection was also associated with an increased risk (%) of being prescribed: - SSRIs (60%) - opioids (39%) - antipsychotics (199%) - antidepressants (57%) - benzodiazepines (70%) - mood stabilizers (41%) Those who were not fully vaccinated had an increased risk (%) of: - (any) psychiatric diagnosis (85%) - (any) psychotropic prescription (72%) Those who were fully vaccinated had had no significant change in mental health our prescription outcomes. \ Conclusion: This is yet another robust retrospective cohort study suggesting that SARS-CoV-2 infection can damage our physical and mental health. The infected cohort included those with and without a Long COVID diagnosis. We at the Brain Inflammation Collaborative are on a mission to help researchers understand why SARS-CoV-2 infection profoundly impacts our mental health by remotely connecting researchers with pediatric and adult long COVID cohorts (unhidenow.org). Let us know what you think about this study. Does it seem accurate to you? Please give this a like and share if you know anyone who had a mental health setback following a SARS-CoV-2 infection. Read the full study here: https://buff.ly/4hEwewE #LongCOVID #mentalhealth