A. Wallace Deckel
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Research Subjects
A. Wallace Deckel has a total of 22 co-authors. Here are the top co-authors by number of shared publications:
- Keith A. Gary
Department of Psychiatry, University of Connecticut Health Center, 263 Farmington Ave., Farmington, CT 06030-6415, USA
3 shared publications Diane Nuttal
Department of Psychiatry, University of Connecticut Health Center, Mail Code 2103, 263 Farmington Avenue, Farmington, CT 06030-2103, USA
2 shared publicationsLarry Arky
2 shared publicationsVictor Hesselbrock
2 shared publicationsVinsee Tang
Department of Psychiatry, University of Connecticut Health Center, Mail Code 2103, 263 Farmington Avenue, Farmington, CT 06030-2103, USA
2 shared publicationsAva Gordinier
1 shared publication
Latest Publications
- 1 June 2002
- Published by Elsevier in Brain Research
- Vol. 939 (1-2) , 76-86
Altered neuronal nitric oxide synthase expression contributes to disease progression in Huntington’s disease transgenic mice
- 1 June 2002
- Published by Elsevier in Brain Research
- Vol. 939 (1-2) , 76-86
Altered neuronal nitric oxide synthase expression contributes to disease progression in Huntington’s disease transgenic mice
- 1 November 2001
- Published by Elsevier in Brain Research
- Vol. 919 (1) , 70-81
Reduced activity and protein expression of NOS in R6/2 HD transgenic mice: effects of l-NAME on symptom progression
- 1 November 2001
- Published by Elsevier in Brain Research
- Vol. 919 (1) , 70-81
Reduced activity and protein expression of NOS in R6/2 HD transgenic mice: effects of l-NAME on symptom progression
- 29 March 2001
- Published by Wiley in Journal of Neuroscience Research
- Vol. 64 (2) , 99-107
Nitric oxide and nitric oxide synthase in Huntington's disease
Nitric oxide (NO) is a biologically active inorganic molecule produced when the semiessential amino acid l‐arginine is converted to l‐citrulline and NO via the enzyme nitric oxide synthase (NOS). NO is known to be involved in the regulation of many physiological processes, such as control of blood flow, platelet adhesion, endocrine function, neurotransmission, neuromodulation, and inflammation, to name only a few. During neuropathological conditions, the production of NO can be either protective or toxic, dependent on the stage of the disease, the isoforms of NOS involved, and the initial pathological event. This paper reviews the properties of NO and NOS and the pathophysiology of Huntington's disease (HD). It discusses ways in which NO and NOS may interact with the protein product of HD and reviews data implicating NOS in the neuropathology of HD. This is followed by a synthesis of current information regarding how NO/NOS may contribute to HD‐related pathology and identification of areas for potential future research. J. Neurosci. Res. 64:99–107, 2001.
- 29 March 2001
- Published by Wiley in Journal of Neuroscience Research
- Vol. 64 (2) , 99-107
Nitric oxide and nitric oxide synthase in Huntington's disease
Nitric oxide (NO) is a biologically active inorganic molecule produced when the semiessential amino acid l‐arginine is converted to l‐citrulline and NO via the enzyme nitric oxide synthase (NOS). NO is known to be involved in the regulation of many physiological processes, such as control of blood flow, platelet adhesion, endocrine function, neurotransmission, neuromodulation, and inflammation, to name only a few. During neuropathological conditions, the production of NO can be either protective or toxic, dependent on the stage of the disease, the isoforms of NOS involved, and the initial pathological event. This paper reviews the properties of NO and NOS and the pathophysiology of Huntington's disease (HD). It discusses ways in which NO and NOS may interact with the protein product of HD and reviews data implicating NOS in the neuropathology of HD. This is followed by a synthesis of current information regarding how NO/NOS may contribute to HD‐related pathology and identification of areas for potential future research. J. Neurosci. Res. 64:99–107, 2001.
- 28 August 2000
- Published by Elsevier in Brain Research
- Vol. 875 (1-2) , 187-195
Dietary arginine alters time of symptom onset in Huntington’s disease transgenic mice
- 28 August 2000
- Published by Elsevier in Brain Research
- Vol. 875 (1-2) , 187-195
Dietary arginine alters time of symptom onset in Huntington’s disease transgenic mice
- 1 July 2000
- Published by Elsevier in Brain Research
- Vol. 872 (1-2) , 258-261
Vasomotor hyporeactivity in the anterior cerebral artery during motor activation in Huntington’s disease patients
- 1 July 2000
- Published by Elsevier in Brain Research
- Vol. 872 (1-2) , 258-261
Vasomotor hyporeactivity in the anterior cerebral artery during motor activation in Huntington’s disease patients
- 1 February 2000
- Published by Elsevier in Progress in Neuro-Psychopharmacology and Biological Psychiatry
- Vol. 24 (2) , 193-206
Increased CBF velocity during word fluency in Huntington's disease patients
- 1 February 2000
- Published by Elsevier in Progress in Neuro-Psychopharmacology and Biological Psychiatry
- Vol. 24 (2) , 193-206
Increased CBF velocity during word fluency in Huntington's disease patients
- 1 June 1997
- Published by Wiley in Alcohol, Clinical and Experimental Research
- Vol. 21 (4) , 631
Effects of 5,7-Dihydroxytryptamine Lesions of the Prefrontal Cortex on Consumption of Sucrose-Ethanol Solutions
- 1 June 1997
- Published by Wiley in Alcohol, Clinical and Experimental Research
- Vol. 21 (4) , 631
Effects of 5,7-Dihydroxytryptamine Lesions of the Prefrontal Cortex on Consumption of Sucrose-Ethanol Solutions
- 1 November 1996
- Published by Wiley in Journal of Clinical Psychology
- Vol. 52 (6) , 639-650
Antisocial personality disorder, childhood delinquency, and frontal brain functioning: EEG and neuropsychological findings
- 1 November 1996
- Published by Wiley in Journal of Clinical Psychology
- Vol. 52 (6) , 639-650
Antisocial personality disorder, childhood delinquency, and frontal brain functioning: EEG and neuropsychological findings
- 1 October 1996
- Published by Wiley in Alcohol, Clinical and Experimental Research
- Vol. 20 (7) , 1173-1178
Behavioral and Cognitive Measurements Predict Scores on the MAST: A 3‐Year Prospective Study
This experiment examined the ability of neuropsychological and behavioral tests of anterior brain functioning to predict changes in alcohol-related behaviors 3 years after the initial evaluation. One hundred four young adult subjects, sixty-six of whom had a positive family history of alcoholism, filled out the Michigan Alcoholism Screening Test (MAST), self-rated the frequency with which they consumed alcohol, and completed a retrospective test of childhood hyperactivity/impulsivity/conduct problems (Wender Behavioral Checklist). Eighty-three of the subjects also completed a neuropsychological battery consisting of cognitive tests of executive functioning (i.e., Trails, Categories Test, Similarities) and motor tests (i.e., TPT, hand dynamometer, finger tapping). Subjects returned to complete the alcohol-related measures during a second testing session 3 years later. Changes in MAST scores, and in alcohol consumption, between the first and second test session were computed, and median splits classified subjects into “high” versus “low” change groups. After factor analysis of the cognitive and behavioral data, hierarchical logistic regression equations assessed the ability of the cognitive and behavioral variables, as well as the presence of a positive family history of alcoholism, to predict future changes in the alcohol outcome measures. Scores from the WENDER behavioral checklist predicted future changes in the MAST scores (p = 0.0026), with more impaired scores associated with higher MAST scores. Tests of executive functioning, in subjects with a positive family history of alcoholism, predicted alcohol consumption (p = 0.033). None of the other predictor variables showed any relationship to the alcohol-related outcome measures.
- 1 October 1996
- Published by Wiley in Alcohol, Clinical and Experimental Research
- Vol. 20 (7) , 1173-1178
Behavioral and Cognitive Measurements Predict Scores on the MAST: A 3‐Year Prospective Study
This experiment examined the ability of neuropsychological and behavioral tests of anterior brain functioning to predict changes in alcohol-related behaviors 3 years after the initial evaluation. One hundred four young adult subjects, sixty-six of whom had a positive family history of alcoholism, filled out the Michigan Alcoholism Screening Test (MAST), self-rated the frequency with which they consumed alcohol, and completed a retrospective test of childhood hyperactivity/impulsivity/conduct problems (Wender Behavioral Checklist). Eighty-three of the subjects also completed a neuropsychological battery consisting of cognitive tests of executive functioning (i.e., Trails, Categories Test, Similarities) and motor tests (i.e., TPT, hand dynamometer, finger tapping). Subjects returned to complete the alcohol-related measures during a second testing session 3 years later. Changes in MAST scores, and in alcohol consumption, between the first and second test session were computed, and median splits classified subjects into “high” versus “low” change groups. After factor analysis of the cognitive and behavioral data, hierarchical logistic regression equations assessed the ability of the cognitive and behavioral variables, as well as the presence of a positive family history of alcoholism, to predict future changes in the alcohol outcome measures. Scores from the WENDER behavioral checklist predicted future changes in the MAST scores (p = 0.0026), with more impaired scores associated with higher MAST scores. Tests of executive functioning, in subjects with a positive family history of alcoholism, predicted alcohol consumption (p = 0.033). None of the other predictor variables showed any relationship to the alcohol-related outcome measures.
- 31 August 1996
- Published by Elsevier in Behavioural Brain Research
- Vol. 78 (2) , 175-182
Behavioral changes in Anolis carolinensis following injection with fluoxetine
- 31 August 1996
- Published by Elsevier in Behavioural Brain Research
- Vol. 78 (2) , 175-182
Behavioral changes in Anolis carolinensis following injection with fluoxetine