| 61. |
- Archer, Trevor, 1949, et al.
(författare)
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Physical exercise as Intervention in Parkinsonism
- 2013
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Ingår i: Handbook of Neurotoxicity. - New York : Springer Science+Business Media. ; , s. 2255-2280
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Bokkapitel (övrigt vetenskapligt/konstnärligt)abstract
- Physical exercise, particularly for individuals with sedentary occupations and independent of activity type, offers probably the most effective health-ensuring policy available. The associations between physical exercise and symptoms/biomarkers of idiopathic Parkinsonism and animal models of Parkinson’s disease (PD), quality of life and self-reliance, disorder progression, and risk factors all support the contention that activity provides for an improved prognosis. In the present treatise, mice treated with the selective dopamine neurotoxin (1-methyl- 4-phenyl-1,2,3,6-tetrahydropyridine, 3 x 30 mg/kg once each week over three weeks), or Vehicle, were given access to running-wheel exercise from the week following the first injection of MPTP onwards: the MPTP-Exercise group received four 30-min sessions in the running wheels (Mondays to Thursdays), whereas the MPTP No-exercise and Vehicle groups received a single session each week (Wednesdays). It was observed that the MPTP+ Exercise group increased the distance run on each Wednesday 30-min session incrementally, whereas the MPTP No-exercise and Vehicle groups remained at the same distance throughout; similarly, during the 10-min test session on Fridays, prior to the tests of motor activity, the MPTP+ Exercise group increased the distance run on each successive occasion but the MPTP No-exercise and Vehicle groups did not. In the tests of spontaneous motor activity, running- wheel exercise over 4 days/week (30 min, Mon.–Thurs.) improved all three parameters of motor activity, locomotion, rearing, and total activity, in the activity test chamber during test weeks 2–7, compared to the MPTP group following the MPTP administration. In the L-Dopa-induced activity test, running-wheel exercise over 4 days/week enhanced locomotor and rearing but not total activity following the subthreshold dose of L-Dopa for the MPTP+Exercise group but not the MPTP No-exercise group. Running-wheel exercise over 4 days/week increased the DA concentrations in the striatum of MPTP+ Exercise mice.
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| 62. |
- Archer, Trevor, 1949, et al.
(författare)
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Physical Exercise Attenuates MPTP-Induced Deficits in Mice
- 2010
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Ingår i: Neurotoxicity research. - : Springer Science and Business Media LLC. - 1029-8428 .- 1476-3524. ; 18:3-4, s. 313-327
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Tidskriftsartikel (refereegranskat)abstract
- Two experiments were performed to investigate the effects of physical exercise upon the hypokinesia induced by two different types of MPTP administration to C57/BL6 mice. In the first, mice were administered either the standard MPTP dose (2 x 20 or 2 x 40 mg/kg, 24-h interval) or vehicle (saline, 5 ml/kg); and over the following 3 weeks were given daily 30-min period of wheel running exercise over five consecutive days/week or placed in a cage in close proximity to the running wheels. Spontaneous motor activity testing in motor activity test chambers indicated that exercise attenuated the hypokinesic effects of both doses of MPTP upon spontaneous activity or subthreshold l-Dopa-induced activity. In the second experiment, mice were either given wheel running activity on four consecutive days (30-min period) or placed in a cage nearby and on the fifth day, following motor activity testing over 60 min, injected with either MPTP (1 x 40 mg/kg) or vehicle. An identical procedure was maintained over the following 4 weeks with the exception that neither MPTP nor vehicle was injected after the fifth week. The animals were left alone (without either exercise or MPTP) and tested after 2- and 4-week intervals. Weekly exercise blocked, almost completely, the progressive development of severe hypokinesia in the MPTP mice and partially restored normal levels of activity after administration of subthreshold l-Dopa, despite the total absence of exercise following the fifth week. In both experiments, MPTP-induced loss of dopamine was attenuated by the respective regime of physical exercise with dopamine integrity more effectively preserved in the first experiment. The present findings are discussed in the context of physical exercise influences upon general plasticity and neuroreparative propensities as well as those specific for the nigrostriatal pathway.
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| 63. |
- Archer, Trevor, 1949, et al.
(författare)
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Physical Exercise Improves Cognition and Health in ADHD
- 2014
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Ingår i: Journal of Novel Physiotherapies. - : OMICS Publishing Group. - 2165-7025. ; 4:3
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Tidskriftsartikel (refereegranskat)abstract
- Attention-Deficit Hyperactive Disorder (ADHD) disrupts normal functioning and health parameters in children and adults with the additional burden of continuing on into adulthood thereby implying marked disadvantages over the individual’s life-span. In this paper we review interventions that incorporate physical exercise programs, independent of specific type of activity or the proportions or endurance/resistence ingredients. These interventions have been found invariably to improve and alleviate symptom profiles, sometimes replacing the traditional treatments. In many cases, the presence of accompanying behavioral disruptions may be alleviated through exercise regimes.
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| 64. |
- Archer, Trevor, 1949, et al.
(författare)
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Physical Exercise Improves Cognition in Brain Disorders: Alzheimer's Disease
- 2015
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Ingår i: Farooqui, T., & Farooqui, A. A. (2015). Diet and Exercise in Cognitive Function and Neurological Diseases. - New Jersey : John Wiley & Sons, Inc.. - 9781118840559 ; , s. 175-181
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Bokkapitel (refereegranskat)abstract
- Physical exercise impacts upon several aspects of psychological and somatic health, cognitive performance, emotional regulation, brain structure and function, and the integrity of a wide range of biomarkers linked to molecular systems important for maintaining neural function and plasticity. Manifestations of the essential beneficial influence upon neurological and neuropsychiatric disorders have been described, as well as in conditions of brain damage and neurodevelopmental disruption. Several studies have addressed the influence of exercise upon expressions of disorders associated with epilepsy and conditions linked to neuroimmune functioning. Evidence from several perspectives has reinforced the notion that exercise intervention ought to be integrated with conventional therapies for the improvement of brain function and resistance to neurodegenerative and neuropsychiatric disorders in addition to offering a complementary non-pharmacological, noninvasive alternative.
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| 65. |
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| 66. |
- Archer, Trevor, 1949, et al.
(författare)
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Restoration of MPTP-induced deficits by Exercise and Milmed® Co-treatment
- 2014
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Ingår i: PeerJ. - : PeerJ. - 2167-8359. ; 2:e531
-
Tidskriftsartikel (refereegranskat)abstract
- 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) induces permanent neurochemical and functional deficits. Following the administration of either two or four injections of the dopamine neurotoxin, MPTP, at a dose of 40 mg/kg, C57/BL6 mice were given access to running-wheels (30-min sessions, four times/week, Monday–Thursday) and treatment with the treated yeast, Milmed® (four times/week, Monday–Thursday), or simply running-wheel exercise by itself, over ten weeks. It was observed that the combination of physical exercise and Milmed® treatment, the MPTP + Exercise + Yeast (MC) group [MPTP + Ex- ercise + Milmed® (MC)], restored spontaneous motor activity markedly by test day 10, restored completely subthreshold L-Dopa-induced activity, and dopamine concentration to 76% of control values, in the condition wherein two adminis- trations of MPTP (2 × 40 mg/kg) were given prior to initiation of exercise and/or Milmed® treatment. Physical exercise by itself, MPTP + Exercise (MC) group, attenuated these deficits only partially. Administration of MPTP four times (i.e., 40 mg/kg, s.c., once weekly over four weeks for a total of 160 mg/kg, MPTP + Exer- cise + Yeast (MC) group [MPTP + Exercise + Milmed® (SC)] and MPTP + Exercise (SC), induced a lesioning effect that was far too severe for either exercise alone or the exercise + Milmed® combination to ameliorate. Nevertheless, these findings indicate a powerful effect of physical exercise reinforced by Milmed® treatment in restoring MPTP-induced deficits of motor function and dopamine neurochemistry in mice.
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| 67. |
- Archer, Trevor, 1949, et al.
(författare)
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Selective Diets for Dementia Disorders
- 2016
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Ingår i: Clinical and Experimental Psychology. - : OMICS Publishing Group. - 2471-2701. ; 2:2
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Tidskriftsartikel (refereegranskat)abstract
- The global incidence of Alzheimer’s disease (AD) is ever-increasing and all current therapies, when effective, remain only symptomatic. Diet, including fruit and vegetable juicing, nutritional supplements, and ketogenic supplements have been found to improve the condition of subjects presenting neurodegenerative disorders. Under various conditions, it is becoming increasing evident that a Mediterranean-type diet supplemented by olive oil and several different forms of physical exercise may improve global cognition. This type of selective diet that has been combined to be augmented by olive oil and soy isoflavone supplements is linked to potential improve memory and learning, as well as several other necessary daily activities, and several biomarkers of brain health and function. There is an ever-growing trend towards guidelines promoting a greater consumption of plant food- based dietary patterns combined with limitations upon the consumption of animal-based food and a plethora of more-or-less specific guidelines have been formulated. Individual-centered strategies that combine interventions to improve physical, cognitive, and psychosocial functioning may offer improvements to lifestyle (e.g., change in diet) that promote cognitive health in the oldest-old.
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| 68. |
- Archer, Trevor, 1949
(författare)
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Stages in the Pathophysiology and Eventual Treatment of Brain Disorders
- 2010
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Ingår i: European J Psychiatry. ; :24, s. 5-8
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Tidskriftsartikel (refereegranskat)abstract
- Staging in neuropsychiatry has been adapted and, to some extent, modified from applications in oncology. The notion of staging has been presented in a forum defined by Strategies for Studying Brain Disorders. McGorry addressed the enduring issue of Diagnostic utility (cf. Palomo et al., 2008) by posing the question, is clinical staging the answer? It seems likely that staging offers a useful strategy to select safe and effective treatments, providing greater refinement, that treatments differ according to stage, as e.g. in cancer, and is more and effective in the early stages. The clinical staging model offers a continuum over disorder liability ranging from increased risk for psychosis or severe mood changes that are symptom-like but currently asymptomatic, at a “0” score, through scores “1a”, “1b”, “2”, “3a”, “3b”, “3c”, and “4”, the severe persistent unremitting illness, with indicative neurobiological and endophenotypical markers, e.g. that hippocampal volume decreases with severity in affective disorders.
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| 69. |
- Archer, Trevor, 1949, et al.
(författare)
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Staging neurodegenerative disorders: structural, regional, biomarker, and functional progressions.
- 2011
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Ingår i: Neurotoxicity research. - : Springer Science and Business Media LLC. - 1476-3524 .- 1029-8428. ; 19:2, s. 211-34
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Tidskriftsartikel (refereegranskat)abstract
- The notion of staging in the neurodegenerative disorders is modulated by the constant and progressive loss of several aspects of brain structural integrity, circuitry, and neuronal processes. These destructive processes eventually remove individuals' abilities to perform at sufficient and necessary functional capacity at several levels of disease severity. The classification of (a) patients on the basis of diagnosis, risk prognosis, and intervention outcome, forms the basis of clinical staging, and (b) laboratory animals on the basis of animal model of brain disorder, extent of insult, and dysfunctional expression, provides the components for the clinical staging and preclinical staging, respectively, expressing associated epidemiological, biological, and genetic characteristics. The major focus of clinical staging in the present account stems from the fundamental notions of Braak staging as they describe the course and eventual prognosis for Alzheimer's disease, Lewy Body dementia, and Parkinson's disease. Mild cognitive impairment, which expresses the decline in episodic and semantic memory performance below the age-adjusted normal range without marked loss of global cognition or activities of daily living, and the applications of longitudinal magnetic resonance imaging, major instruments for the monitoring of either disease progression in dementia, present important challenges for staging concepts. Although Braak notions present the essential basis for further developments, current staging conceptualizations seem inadequate to comply with the massive influx of information dealing with neurodegenerative processes in brain, advanced both under clinical realities, and discoveries in the laboratory setting. The contributions of various biomarkers of disease progression, e.g., amyloid precursor protein, and neurotransmitter system imbalances, e.g., dopamine receptor supersensitivity and interactive propensities, await their incorporation into the existing staging models thereby underlining the ongoing, dynamic feature of the staging of brain disorders.
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| 70. |
- Archer, Trevor, 1949, et al.
(författare)
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Staging neurological disorders: expressions of cognitive and motor disorder.
- 2010
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Ingår i: Neurotoxicity research. - : Springer Science and Business Media LLC. - 1476-3524 .- 1029-8428. ; 18:2, s. 107-11
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Tidskriftsartikel (refereegranskat)abstract
- In neurologic disorders, there are progressive losses in regional brain structural integrity, circuitry, and neuronal process that threaten individuals' ability to express functional capacity at several levels of severity. The classification of (a) patients on the basis of diagnosis, risk prognosis, and intervention outcome forms the basis of clinical staging and (b) laboratory animals on the basis of animal model of brain disorder, extent of insult and dysfunctional expression, provides the components for the clinical staging and preclinical staging, respectively, of the disease state with certain associated epidemiological, biological, and genetic characteristics. The investigation of epigenetics and biomarkers is intrinsic to any analysis of the progressive nature of the neurogenerative disorders, in the present account disorders relating to Alzheimer's disease, Parkinson's disease, depression, and diabetes.
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