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- 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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| 2. |
- 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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| 3. |
- 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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