| 1. |
- Archer, Trevor, 1949, et al.
(författare)
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affect, motivation, motor, addiction, impulsiveness, distress, exercise
- 2009
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Ingår i: Beyond Neuropsychiatric Diagnotics: Symptoms not Disorders. - Mountain Home, USA. : F.P. Graham Publishing: Mountain Home, USA. ; , s. 477-512
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Bokkapitel (övrigt vetenskapligt/konstnärligt)abstract
- Cognitive symptoms, considered in conjunction both with their regional brain and biomarkers as well as affective, attributional and neurodevelopmental components, demonstate ever-increasing complexity to facilate conceptualization yet, unavoidably, bedevil diagnosis in neuropsychiatry even before considerations of the enigmatic processes in memory, such as executive function and working memory, are draw into the myriads of equations that await remedial interpretations. Prefrontal and limbic regions of the brain are involved in a diversity of expressions of cognition, normal or dysfunctional, at synaptic, intracellular and molecular levels that mobilise a concatenation of signaling entities. Serotoninergic neurotransission at prefrontal regions directs cogntive-affective entities that mediate decision-making and goal-directed behaviour. Clinical, non-clinical and basic studies challenge attempts to consolidate the multitude of evidence in order to obtain therapeutic notions to alleviate the disordered status of the diagnosed and yet-to-be diagnosed individuals. Locus of control, a concept of some utility in health-seeking procedures, is examined in three self-reort studies from the perspective of a cognitive-emotional situation through observations of ordinary, ‘healthy’ young and middle-aged individuals, to assess the predictors of internal and external locus of control. A notion based on high level executive functioning in the dorsolateral prefrontal cortex in individuals characterised by internal locus of control is contrasted with a hypofunctional executive DLPFC, characterising individuals that express an external locus of control, is discussed.
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| 2. |
- Archer, Trevor, 1949, et al.
(författare)
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Attention-Deficit/Hyperactivity Disorder: Focus upon Aberrant N-Methyl-D-Aspartate Receptors Systems
- 2016
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Ingår i: R. M. Kostrzewa & T. Archert (Eds.), Neurotoxin Modeling of Brain Disorders – Life-long Outcomes in Behavioral Teratology, Volume 29 of the series Current Topics in Behavioral Neurosciences.. - Amsterdam : Springer. - 9783319341347 ; , s. 295-311
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Bokkapitel (refereegranskat)abstract
- Attention-deficit/hyperactivity disorder (ADHD) pathophysiology persists in an obscure manner with complex interactions between symptoms, staging, interventions, genes, and environments. Only on the basis of increasing incidence of the disorder, the need for understanding is greater than ever. The notion of an imbalance between central inhibitory/excitatory neurotransmitters is considered to exert an essential role. In this chapter, we first review how the default mode network functions and dysfunction in individuals diagnosed with ADHD. We also present and briefly review some of the animal models used to examine the neurobiological aspects of ADHD. There is much evidence indicating that compounds/interventions that antagonize/block glutamic acid receptors and/or block the glutamate signal during the "brain growth spurt" or in the adult animal may induce functional and biomarker deficits. Additionally, we present evidence suggesting that animals treated with glutamate blockers at the period of the "brain growth spurt" fail to perform the exploratory activity, observed invariably with control mice, that is associated with introduction to a novel environment (the test cages). Later, when the control animals show less locomotor and rearing activity, i.e., interest in the test cages, the MK-801, ketamine and ethanol treated mice showed successively greater levels of locomotion and rearing (interest), i.e., they fail to "habituate" effectively, implying a cognitive dysfunction. These disturbances of glutamate signaling during a critical period of brain development may contribute to the ADHD pathophysiology. As a final addition, we have briefly identified new research venues in the interaction between ADHD, molecular studies, and personality research.
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| 3. |
- Archer, Trevor, 1949, et al.
(författare)
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Drug abuse neurotoxicity: alcohol and nicotine as developmental stressors
- 2013
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Ingår i: Handbook of Neurotoxicity. - : Springer. - 9781461458357 ; , s. 2003-2023
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Bokkapitel (refereegranskat)abstract
- Drugs of abuse have the property of inducing adverse health complications, not least neurotoxicity under conditions where both the environmental conditions and activity states associated with their intake may strongly enhance drug toxicity, thereby causing life-threatening health complications and tragedy for relations and caregivers. While both chronic alcohol and/or nicotine abuse induce a variety of neuropathological effects, including damage to the brain, the extent of damage and disruption observed in the developing brain and CNS is a considerable affliction for the affected individuals. On the basis of laboratory and clinical studies, the potential of chemicals, including therapeutic and abused agents, to induce neurotoxic effects has been assessed, with considerations of abuse drugs neurotoxicity encompassing several factors that may accelerate and complicate prevailing conditions; the type and influence of environmental conditions, the presence of daily habits such as coffee breaks/smoking breaks, nutritional status, and neuroimmune system mobilization. Abuse neurotoxicity at several stages of early development, alcohol neurotoxicity, nicotine neurotoxicity, and combinations of alcohol-nicotine neurotoxicity present a threatening scenario of two compounds, benefitting from legality and availability that nevertheless have such potential for destruction over multiple domains, particularly in the undeveloped brain.
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| 4. |
- Archer, Trevor, 1949, et al.
(författare)
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Epigenetics in neuropsychiatry
- 2011
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Ingår i: Omics : Biomedical Perspectives and Applications / edited by Debmalya Barh, Kenneth Blum, Margaret A. Madigan. - : CRC Press. - 9781439850084 ; , s. 511-532
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Bokkapitel (övrigt vetenskapligt/konstnärligt)abstract
- The notion of epigenetics offers a putative interface between genetic and environmental factors that interact to provide the phenotypic. The impact of the environment on gene expression (epigenetics) and the convergence of genes and environment along common biological pathways induce greater effects than either those of genes or environment in isolation. Transgenerational epigenetic inheritance, i.e. the survival of epigenetic modifications over generations, provides a process through maternal nurturing behavior may affect the development and health of the offspring. Epigenetic operations regulate depressive disorders and schizophrenia spectrum disorders as well as interventional strategies. The present account examines epigenetic influences to inherited characteristics subjected to conditions of prenatal or early-life adversity that produce the eventual expressions of these disorders, and such developmental disorders as Prader-Willi syndrome. The essential role of nutrition is central: epigenetic regulation encompasses alterations of genetic material that do not affect the DNA nucleotide sequence, but rather include DNA methylation patterns, chromatin structure, histone codes, and noncoding small RNAs. Influences such as epigenetic interactions on DNA damage response and DNA repair may yet provide insights facilitating diagnosis and understanding of progression and intervention
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| 5. |
- Archer, Trevor, 1949, et al.
(författare)
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Functional and structural MRI studies on impulsiveness: Attention Deficit/Hyperactive Disorder and Borderline Personality Disorders
- 2012
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Ingår i: Neuroimaging – Cognitive and Clinical Neuroscience/ Edited by Peter Bright. - : InTech. - 9789535106067 ; , s. 205-228
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Bokkapitel (refereegranskat)abstract
- Impulsive behavior is characterized a tendency to initiate behavior without sufficient/adequate consideration of consequences. It typically refers to ill-conceived, premature or inappropriate behavior that may be self-destructive or harmful to other individuals. Pathological impulsiveness is associated with impaired performance on neuropsychological tests of attention and executive function and with neuroimaging evidence for structural and/or functional correlates, particular in frontal lobe regions. Impulsive behavior is a major component of several neuropsychiatric disorders, including schizophrenia, ADHD, substance abuse, bipolar disorder, and borderline and antisocial personality disorders. The notion of impulsiveness incorporates a multidimensional construct consisting of a range of inter-related factors including novelty-seeking and reckless behavior, lack of planning ability and self-control whereby mechanistic relations evolve from its role in initiating action. The construct incorporates motor impulsiveness, inability to tolerate delays, lack of planning and an incapacity for self-control. Impulsiveness, with or without aggressiveness, has been associated with a range of personality disorders and other psychopathologies, with impulse control difficulties often of primary diagnostic importance. the notions of aberrant reward learning, dysregulated response inhibition and pathological hypersensitivity to temporal delays in reinforcement form the essential behavioural endophenotype of impulsiveness that is witnessed in ADHD and BPD, as well as in compulsive gambling, addictive disorders and dopamine dysregulation syndrome. Developmental trajectories of impulsive behaviors and the damaging effects of early-life trauma on brain development bear essential outcome-expectancies for eventual understanding of etiopathogenesis. Structural and functional resonance imaging has served to provide a point of convergence for the resolution of neurobehavioural, epigenetic and neurodevelopmental factors.
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| 6. |
- Archer, Trevor, 1949, et al.
(författare)
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Fusion models and “Fusioning” in Parkinsonism: Protection and Restoration by exercise.
- 2014
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Ingår i: Kostrzewa R.M. (ed). Handbook of Neurotoxicity. - New York : Springer. - 9781461458357 ; , s. 2047-2063
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Bokkapitel (övrigt vetenskapligt/konstnärligt)abstract
- Fusion models, or the “fusioning” of models, of Parkinson’s disease (PD) to attain the sufficiency of disorder etiopathogenesis have spurred the development of laboratory models incorporating neurotoxin treatments in combination with genetic manipulations of animals studied. The present review describes fusion from two directions: (i) through the fusioning of neurotoxin and genetic models, and, It was observed that wheel-running exercise (four 30-min sessions/week) attenuated the motor deficits, both assessed as distance run in the running wheels and as locomotor, rearing and total activity counts in the motor activity test chambers, and the dopamine (DA) loss induced by the DA neurotoxin, MPTP compared with the no exercise MPTP group (one 30-min session/week).
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| 7. |
- Archer, Trevor, 1949, et al.
(författare)
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Pharmacogenomics and Personalized Medicine in Alzheimer’s Disease
- 2013
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Ingår i: Omics for Personalized Medicine. - : Springer. ; , s. 289-308
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Bokkapitel (refereegranskat)abstract
- Alzheimer’s disease (AD) and related dementias, neurodegenerative disorders accompanied by progressive deterioration of cognitive capacity, every-day behavior abilities, and integrity of brain tissue, present an ever- growing, worldwide dilemma due to aging populations confronted by a related neuropathology. The “amyloid cascade hypothesis,” that pathophysiology is driven by the ever-increasing burden of β-amyloid in the brains of afflicted patients, involves a poorly understood orchestration encompassing multitudes of enzymes and signaling pathways arranged in vast and diverse arrays of cellular processes, and vascular considerations all of which are under the control of predictive genes and susceptibility genes that describe genetic and genes x environmental epigenetic interactions. Genetic aspects of these disorders and the intricacies of pharmacogenomics implicated several neurotransmitter pathways, circuits and regional brain developments, and metabolism that reinforce the growing requirements for personalized medicine. The search for individual-based medication, in addition to genomic assay and biomarker identity, seeks to establish a “reregulation” of destructive β-amyloid pathways, an understanding and application of Aβ-linked immunotherapy, the initiation and formulation of pharmacogenetic/pharmacogenomics principles and methodologies, the emergence of the role of apolipoprotein (APOE) in therapeutic endeavor, the assessment and treatment of behavioral and psychological symptoms, the therapies focused upon frontotemporal dementia, and the interventions centered around instrumental activities of daily activities.
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| 8. |
- Archer, Trevor, 1949, et al.
(författare)
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Pharmacogenomics and Personalized Medicine in Mood Disorders
- 2013
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Ingår i: Handbook of Neurotoxicity. - : Springer. - 9781461458357 ; , s. 2181-2205
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Bokkapitel (refereegranskat)abstract
- Neurotoxic vulnerability that putatively contributes to the etiopathogenesis of schizophrenia spectrum disorders encompasses perinatal adversity, genetic linkage, epigenetic disadvantage, and neurodegenerative propensities that affect both symptom domains, positive, negative, and cognitive and biomarkers of the disorder. Molecular and cellular apoptosis/excitotoxicity that culminates in regional brain loss, reductions reelin expression, trophic disruption, perinatal adversity, glycogen kinase-3 dysregulation, and various instances of oxidative stress all influence the final end point. The existence of prodromal psychotic phases, structural-functional aspects of regional neuroimaging, dopamine signal overexpression, and psychosis propensity provide substance for neurodegenerative influences. The pathophysiology of schizophrenia spectrum disorders encompasses the destruction of normal functioning of the neurotrophins, in particular brain-derived neurotrophic factor (BDNF), dyskinesia of necessary ,ovements, and metabolic-metabolomic and proteomic markers. Neurotoxic accidents combined with genetic susceptibility appear to play a role in interfering with normal neurodevelopment or in tissue-destructive neurodegeneration or both, thereby elevating the eventual risk for disorder tendencies and eventual expression
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| 9. |
- Archer, Trevor, 1949, et al.
(författare)
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Pharmacogenomics and Personalized Medicine in Mood Disorders
- 2013
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Ingår i: Omics for Personalized Medicine. - New Delhi : Springer. - 9788132211839 ; :309, s. 309-334
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Bokkapitel (refereegranskat)abstract
- Pharmacogenomics and the search for personalized medicine focus on the attainment of individualized pharmacotherapies that cover genetic variation and target groups of patients that present neurodevelopmental aspects of symptom profiles and biomarkers underlying the pathophysiology of mood disorders. The identification of genetic biomarkers facilitates choice of treatment, prediction of response, and prognosis of outcome over a wide spectrum of symptoms associated with affective states thereby optimizing clinical practice procedures. Several strategies, under development and refinement, show the propensity for derivation of essential elements in the etiopathogenesis of disorder affecting drug efficacy, drug metabolism, and drug adverse effects, e.g., with regard to SSRIs; these include the following: transporter gene expression and genes encoding receptor systems, hypothalamic-pituitary-adrenal axis factors, neurotrophic factors, and inflammatory factors affecting neuroimmune function. Nevertheless, procedural considerations of pharmacogenetics presume the parallel investment of policies and regulations to withstand eventual attempts at misuse thereby ensuring patient integrity
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| 10. |
- Archer, Trevor, 1949, et al.
(författare)
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Pharmacogenomics and Personalized Medicine in Parkinsonism
- 2013
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Ingår i: Omics for Personalized Medicine. Barh D., Dhawan D., Ganguly N. (eds). - New Delhi : Springer. - 9788132211839 ; , s. 265-287
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Bokkapitel (refereegranskat)abstract
- Pharmacogenetic-pharmacogenomic development from a single gene approach to incorporate pathway-based and genome-wide approaches has been benefi tted from the emergence of several parallel technologies, such as genomics, transcriptomics, metabolomics, and proteomics which have contributed to and enhanced significantly propensities for generation and testing of pharmacogenomic hypotheses both paralleled and followed by associated developments in the clinical practice for treating Parkinson’s disease (PD). The notion of “personalized medicine,” incorporating the customization of healthcare, with decisions and practices that suited to each individual patient through application of genetic, biomarker, gene- environment interactive, or other information, involves principles through which drugs, drug combinations, and drug administration properties are optimized for each individual’s unique genetic makeup. The personalized medication of antiparkinsonian drug therapy; the symptomatic and regional disruptions; genetic, epigenetic, and biomarkers of the disorder; and the pharmacogenomics of neuroleptic drug-induced parkinsonism provide outlets for eventual understanding and management. As a case study in personalized medicine in the laboratory, physical exercise combined with the electromagnetic wavelength treated Saccharomyces cerevisiae yeast, Milmed, was demonstrated to abolish the marked hypokinesia induced by the dopamine (DA) neurotoxin, MPTP, as well as the severe loss of DA in the striatal region of the C57/BL6 mice studied. The Exercise-Milmed coadministration induced also a profound increase in brain-derived neurotrophin levels (BDNF) in the mouse parietal cortex region that included the motor cortex
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