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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. |
- Archer, Trevor, 1949, et al.
(författare)
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Functional consequences of iron overload in catecholaminergic interactions: the Youdim factor
- 2007
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Ingår i: Neurochemical Research. - : Springer Science and Business Media LLC. - 0364-3190 .- 1573-6903. ; 32:10, s. 1625-1639
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Forskningsöversikt (refereegranskat)abstract
- The influence of postnatal iron overload upon implications of the functional and interactive role of dopaminergic and noradrenergic pathways that contribute to the expressions of movement disorder and psychotic behaviours in mice was studied in a series of experiments. (1) Postnatal iron overload at doses of 7.5 mg/kg (administered on Days 10–12 post partum) and above, invariably induced a behavioural syndrome consisting of an initial (1st 20–40 min of a 60-min test session) hypoactivity followed by a later (final 20 min of a 60-min test session) hyperactivity, when the mice were tested at adult ages (age 60 days or more). (2) Following postnatal iron overload, subchronic treatment with the neuroleptic compounds, clozapine and haloperidol, dose-dependently reversed the initial hypoactivity and later hyperactivity induced by the metal. Furthermore, DA D2 receptor supersensitivity (as assessed using the apomorphine-induced behaviour test) was directly and positively correlated with iron concentrations in the basal ganglia. (3) Brain noradrenaline (NA) denervation, using the selective NA neurotoxin, DSP4, prior to administration of the selective DA neurotoxin, MPTP, exacerbated both the functional (hypokinesia) and neurochemical (DA depletion) effects of the latter neurotoxin. Treatment with L-Dopa restored motor activity only in the animals that had not undergone NA denervation. These findings suggest an essential neonatal iron overload, termed “the Youdim factor”, directing a DA–NA interactive component in co-morbid disorders of nigrostriatal-limbic brain regions.
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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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