Campbell Science

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Campbell Science

Post by TimGDixon »

I thought i would share a little about what we plan to do at Campbell. Press releases are so yesterday hahahaha...
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Campbell Neurosciences is committed to establishing a biological basis for diagnosis and treatment of suicide and its causes, including Schizophrenia and other mental health disorders, thereby eliminating the stigma of the disease.

Treating Suicide as a Disease
Campbell Neurosciences is based on leveraging the fact that the second leading cause of death in young people, suicide, is not currently being treated as a disease.

The stigma associated with suicide, as well as contributing factors such as schizophrenia, has inhibited “cure-based” research. Instead, “band aid” solutions which are synthetic versions of mind-altering drugs are being pumped into patients, generating billions for pharmaceutical companies, while only temporarily helping a subset of victims.

The Company has developed the first blood-based marker for suicidal propensity, the Campbell Score™, as well as accumulated patents and data on treatments addressing the cause of mental illnesses causing suicide: neuroinflammation.

Campbell Score™
Psychiatry, despite commanding a $240 billion a year market, is the only branch of medicine that does not directly quantify efficacy of its interventions to its target organ.

The Campbell Score™ provides an objective tool for psychiatrists to know how well their interventions are working before the patient begins to experience psychological manifestations.

By detecting brain inflammation, it is a “stethoscope” for determining severity of mental illnesses associated with increased suicide risk such as schizophrenia, PTSD, and opioid addiction.

Regenerative Psychiatry: Schizophrenia Lead
Mental illnesses associated with suicide, such as schizophrenia, are characterized by inflammation and a reduced ability of stem cells in the brain to function. Patients with schizophrenia have 170 times higher suicide rates as compared to non-schizophrenics.

The Company is focused on utilizing its “regenerative psychiatry” approach to reduce inflammation and restore the ability of brain cells to repair themselves in advanced schizophrenic patients resistant to treatment. Success in this area will allow for expansion into PTSD and opioid addiction, which predispose to suicide and possess similar biological characteristics.

Path to Success Plan

1. Intellectual property dominance of immunology and regenerative medicine space as relates to suicide: Identifying who owns what and filing
patents to cover anything related to suicide and predisposing factors (completed).
2. Sales of Campbell Score™ and TSOI nutraceuticals to psychiatrists paid by “out of pocket” (Q2 2021)
3. FDA registration of Campbell Score™. Requires 200 patient trial, will provide ability to generate revenue or partnership (Q1 2022).
4. Success of “Regenerative Psychiatry” approach in treatment resistant schizophrenics. Using proprietary microbiome modulation, nutraceutical, and stem cells. Success in patients whose only option is ECT will be a paradigm shift in the industry (Q1 2022).
5. Acquisition/IPO. Based on patents, method of diagnosis and pipeline (Q2 2022)
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Re: Campbell Science

Post by fxandres »

Wow this is FANTASTIC more that Fantastic actually. I hope something that can help a Person from Schizophrenia is amazing. Keep me informed on this simply because unfortunately my daughters mother has Schizophrenia. A have papers where they evaluated her and they said she had Schizophrenia and bipolar as well and something else I cannot remember.

It’s troubling knowing her for years since she was 16 and now 30 years old but she mumbles worlds and even acts very strange when I do see her. It’s very very strange something I’ve never seen or heard before from a person so me personally I’d like to help her I don’t know what doctors are giving her now but it’s definitely not working!

You all are on the right path to start changing lots of Lives!!!
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Re: Campbell Science

Post by TimGDixon »

Really sorry to hear about anyone suffering and even sorrier when its close to home. Too many people for too long have endured the wrath of psychiatry which seems to be more concerned with a status quo than to actually do something different. It may seen strange, but people hearing voices in their heads and responding is immunologically mediated and isn't because they are crazy, we're born crazy, turned crazy... they have an immune imbalance that is also closely tied to their gut biome. But as my old friend Ignaz Semmelweiss likes to remind me from time to time - don' overlook the role that the gene (protein) NLRP3 plays in mediating inflammation.

Yes you may have seen much of my research in NLRP3 as it relates to covid-19/sars/cov/cov2 but it also plays a significant role in schizophrenia.
Nod-like receptor pyrin containing 3 (NLRP3) in the post-mortem frontal cortex from patients with bipolar disorder: A potential mediator between mitochondria and immune-activation

Helena Kyunghee Kim 1 , Ana Cristina Andreazza 2 , Nika Elmi 3 , Wenjun Chen 4 , L Trevor Young 5
Affiliations expand
PMID: 26540403 DOI: 10.1016/j.jpsychires.2015.10.015

Mitochondrial complex I dysfunction, oxidative stress and immune-activation are consistently reported in bipolar disorder (BD). Mitochondrial production of reactive oxygen species was recently linked to activation of an inflammatory redox sensor, the nod-like receptor family pyrin domain-containing 3 (NLRP3). Upon its activation, NLRP3 recruits apoptosis-associated speck-like protein (ASC) and caspase-1 to form the NLRP3-inflammasome, activating IL-1β. This study aimed to examine if immune-activation may be a downstream target of complex I dysfunction through the NLRP3-inflammasome in BD. Post-mortem frontal cortex from patients with BD (N = 9), schizophrenia (N = 10), and non-psychiatric controls (N = 9) were donated from the Harvard Brain Tissue Resource Center. Levels of NLRP3, ASC and caspase-1 were measured by western blotting, ELISA and Luminex. While we found no effects of age, sex or post-mortem delay, lower levels of complex I (F2,25 = 3.46, p < 0.05) and NDUFS7, a subunit of complex I (F2,25 = 4.13, p < 0.05), were found in patients with BD. Mitochondrial NLRP3 (F2,25 = 3.86, p < 0.05) and ASC (F2,25 = 4.61, p < 0.05) levels were higher in patients with BD. However, levels of caspase 1 (F2,25 = 4.13, p < 0.05 for both), IL-1β (F2,25 = 7.05, p < 0.01), IL-6 (F2,25 = 5.48, p < 0.05), TNFα (F2,25 = 7.14, p < 0.01) and IL-10 (F2,25 = 5.02, p < 0.05) were increased in both BD and schizophrenia. These findings suggest that immune-activation in the frontal cortex may occur both in patients with BD and schizophrenia, while complex I dysfunction and NLRP3-inflammasome activation may be more specific to BD. ... 2819304163
Increased inflammasome activity in markedly ill psychiatric patients: An explorative study

The aim of this study was to investigate inflammatory perturbations in 40 patients with severe and complex psychiatric disorders by studying the activity of the NLRP3 inflammasome, with a trans-diagnostic approach. Gene expression of CASP1, NLRP3, PYCARD, IL1B, IL1RN, TNF showed a significant increase in the patient group compared to a matched control group. Plasma levels of IL1Ra, IL-18, TNF, IL-6 and CRP were increased in the patient group. Within the patient group, increased gene expression of inflammatory markers correlated with increased disease severity. The findings support the inflammation hypothesis for markedly ill psychiatric patients across diagnostic groups. ... 408136.pdf
The Potential Role of the NLRP3 Inflammasome as
a Link between Mitochondrial Complex I Dysfunction and Inflammation in Bipolar Disorder
Helena Kyunghee Kim,Wenjun Chen, and Ana Cristina Andreazza

Mitochondrial dysfunction and activation of the inflammatory system are two of the most consistently reported findings in bipolar disorder (BD). More specifically, altered levels of inflammatory cytokines and decreased levels of mitochondrial complex I subunits have been found in the brain and periphery of patients with BD, which could lead to increased production of mitochondrial reactive oxygen species (ROS). Recent studies have shown that mitochondrial production of ROS and inflammation may be closely linked through a redox sensor known as nod-like receptor pyrin domain-containing 3 (NLRP3). Upon sensing mitochondrial release of ROS, NLRP3 assembles the NLRP3 inflammasome, which releases caspase 1 to begin the inflammatory cascade. In this review, we discuss the potential role of the NLRP3 inflammasome as a link between complex I dysfunction and inflammation in BD and its therapeutic implications.
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