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- Blum, K., et al.
(författare)
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Neuroquantum Theories of Psychiatric Genetics: Can Physical Forces Induce Epigenetic Influence on Future Genomes?
- 2015
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Ingår i: Neuroquantology. - 1303-5150. ; 13:1, s. 90-103
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Tidskriftsartikel (refereegranskat)abstract
- This paper serves to encourage quantum physicists to engage in psychiatric based research on the brain and its functions (i.e., consciousness, memory, attention). By using physics theorems such as Einstein's theory of relativity and the string theory, both physicists and geneticists alike may be able to elucidate potential links between components of the universe and their effects on the human brain. We have outlined some interesting posits including the cosmos' role in evolutionary biology, alpha bonding in biological molecules, and environmentally induced epigenetic effects on genetics. We also explore how physical forces can influence human memory, behavioral traits, and rates of addiction. Impulsiveness is used to exemplify how environmental changes can contribute to epigenetics and its hereditary alterations. We propose the idea of the presence of a "mental universe," where brain functionality like consciousness is a continuum of physically altered pathways. The realization that the universe and all of its precepts remains a mystery is reflected in the lack of a standardized "unified" physics theorem and mathematical equation that can explain universal dimensions (physical and mental), and as such, so is the complex nature of the functionality of the human brain. We provide herein a suggestion to remedy possible confusion, whereby we attempt to show the relationship of brain as a complex quantum-like organ and the impact of epigenetics on behavioral expression.
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| 2. |
- Blum, K., et al.
(författare)
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Common Neurogenetic Diagnosis and Meso-Limbic Manipulation of Hypodopaminergic Function in Reward Deficiency Syndrome (RDS): Changing the Recovery Landscape
- 2017
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Ingår i: Current Neuropharmacology. - : Bentham Science Publishers Ltd.. - 1570-159X .- 1875-6190. ; 15:1, s. 184-194
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Tidskriftsartikel (refereegranskat)abstract
- Background: In 1990, Blum and associates provided the first confirmed genetic link between the DRD2 polymorphisms and alcoholism. This finding was based on an earlier conceptual framework, which served as a blueprint for their seminal genetic association discovery they termed "Brain Reward Cascade." These findings were followed by a new way of understanding all addictive behaviors (substance and non-substance) termed "Reward Deficiency Syndrome" (RDS). RDS incorporates a complex multifaceted array of inheritable behaviors that are polygenic. Objective: In this review article, we attempt to clarify these terms and provide a working model to accurately diagnose and treat these unwanted behaviors. Method: We are hereby proposing the development of a translational model we term "Reward Deficiency Solution System (TM)" that incorporates neurogenetic testing and meso-limbic manipulation of a "hypodopaminergic" trait/state, which provides dopamine agonistic therapy (DAT) as well as reduced "dopamine resistance," while embracing "dopamine homeostasis." Result: The result is better recovery and relapse prevention, despite DNA antecedents, which could impact the recovery process and relapse. Understanding the commonality of mental illness will transform erroneous labeling based on symptomatology, into a genetic and anatomical etiology. WC: 184.
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| 3. |
- Blum, K., et al.
(författare)
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Substance use disorder a bio-directional subset of reward deficiency syndrome
- 2017
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Ingår i: Frontiers in Bioscience-Landmark. - : IMR Press. - 1093-9946 .- 1093-4715. ; 22, s. 1534-1548
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Tidskriftsartikel (refereegranskat)abstract
- This commentary is to inform clinicians challenged with an increase in people seeking treatment for Substance Use Disorder (SUD), that the ninety percent revolving door, is, in part, due to post-withdrawal, untreated neurotoxicity. This impairment attenuates neurotransmitter signaling and compromises resting state functional connectivity, leading to unwanted sequelae including depression, sleep disturbances, sensation seeking, lack of satisfaction and impulsivity. Neuroimaging studies indicate that neurobiological recovery can take years. Like a "double edge sword" SUD has a biological bi-directional (bio-directional) effect on the brain reward circuitry. The acute intake of psychoactive drugs results in heightened dopaminergic activity, while, the opposite, hypodopaminergia occurs following chronic abuse. Individuals with SUD can have a genetic predisposition, compounded by stress and neurotoxically induced, epigenetic insults that impact recovery from protracted abstinence. Follow-up post -short-term recovery usually includes supportive therapies and programs like 12 -steps and other fellowships. However, relapse will usually occur if post -short-term recovery hypodopaminergia is not treated with attempts at epigenetic manipulation of compromised brain neurochemistry using some manner of pro-dopamine regulation.
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| 4. |
- Sharma, Hari Shanker, et al.
(författare)
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Intracerebral administration of neuronal nitric oxide synthase antiserum attenuates traumatic brain injury-induced blood-brain barrier permeability, brain edema formation, and sensory motor disturbances in the rat
- 2006
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Ingår i: Acta neurochirurgica. Supplement. - 0065-1419. ; 96, s. 288-294
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Tidskriftsartikel (refereegranskat)abstract
- The role of nitric oxide (NO) in traumatic brain injury (TBI)-induced sensory motor function and brain pathology was examined using intracerebral administration of neuronal nitric oxide synthase (nNOS) antiserum in a rat model. TBI was produced by a making a longitudinal incision into the right parietal cerebral cortex limited to the dorsal surface of the hippocampus. Focal TBI induces profound edematous swelling, extravasation of Evans blue dye, and up-regulation of nNOS in the injured cerebral cortex and the underlying subcortical areas at 5 hours. The traumatized animals exhibited pronounced sensory motor deficit, as seen using Rota-Rod and grid-walking tests. Intracerebral administration of nNOS antiserum (1 : 20) 5 minutes and 1 hour after TBI significantly attenuated brain edema formation, Evans blue leakage, and nNOS expression in the injured cortex and the underlying subcortical regions. The nNOS antiserum-treated rats showed improved sensory motor functions. However, administration of nNOS antiserum 2 hours after TBI did not influence these parameters significantly. These novel observations suggest that NO participates in blood-brain barrier disruption, edema formation, and sensory motor disturbances in the early phase of TBI, and that nNOS antiserum has some potential therapeutic value requiring additional investigation.
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