amphetamine has been researched along with Cognition Disorders in 45 studies
Amphetamine: A powerful central nervous system stimulant and sympathomimetic. Amphetamine has multiple mechanisms of action including blocking uptake of adrenergics and dopamine, stimulation of release of monamines, and inhibiting monoamine oxidase. Amphetamine is also a drug of abuse and a psychotomimetic. The l- and the d,l-forms are included here. The l-form has less central nervous system activity but stronger cardiovascular effects. The d-form is DEXTROAMPHETAMINE.
1-phenylpropan-2-amine : A primary amine that is isopropylamine in which a hydrogen attached to one of the methyl groups has been replaced by a phenyl group.
amphetamine : A racemate comprising equimolar amounts of (R)-amphetamine (also known as levamphetamine or levoamphetamine) and (S)-amphetamine (also known as dexamfetamine or dextroamphetamine.
Cognition Disorders: Disorders characterized by disturbances in mental processes related to learning, thinking, reasoning, and judgment.
Excerpt | Relevance | Reference |
---|---|---|
"We evaluated the effects of the levo (l) enantiomer of amphetamine sulfate on cognitive function in multiple sclerosis (MS) patients." | 9.13 | Effects of l-amphetamine sulfate on cognitive function in multiple sclerosis patients. ( Benedict, RH; Carpenter, RL; Erlanger, D; Feaster, T; Munschauer, F; Rowe, V; Zarevics, P, 2008) |
"D-Amphetamine improved reactions times on the spatial working memory and Stroop tasks for both individuals with schizophrenia and controls, and improved working memory accuracy in schizophrenia." | 9.11 | Amphetamine improves cognitive function in medicated individuals with schizophrenia and in healthy volunteers. ( Barch, DM; Carter, CS, 2005) |
"As a test of plausibility for the hypothesis that schizophrenia can result from abnormal brain, especially cerebral cortical, development, these studies examined whether, in the rat, disruption of brain development initiated on embryonic day (E) 17, using the methylating agent methylazoxymethanol acetate (MAM), leads to a schizophrenia-relevant pattern of neural and behavioral pathology." | 7.73 | A neurobehavioral systems analysis of adult rats exposed to methylazoxymethanol acetate on E17: implications for the neuropathology of schizophrenia. ( Geyer, MA; Ghajarnia, M; Grace, AA; Jentsch, JD; Moore, H, 2006) |
"Schizophrenia is a serious psychiatric disorder which impacts a broad range of cognitive, behavioural and emotional domains." | 6.44 | The amphetamine-induced sensitized state as a model of schizophrenia. ( Featherstone, RE; Fletcher, PJ; Kapur, S, 2007) |
"Treatment with levetiracetam dose-dependently improved memory performance of the ketamine-exposed rats." | 5.48 | Treatment with levetiracetam improves cognition in a ketamine rat model of schizophrenia. ( Gallagher, M; Koh, MT; Rosenzweig-Lipson, S; Shao, Y, 2018) |
" In the present experiment, prefrontal acetylcholine (ACh) release was measured in attentional task-performing and non-performing rats pretreated with an escalating dosing regimen of amphetamine (AMPH) and following challenges with AMPH." | 5.34 | Toward a neuro-cognitive animal model of the cognitive symptoms of schizophrenia: disruption of cortical cholinergic neurotransmission following repeated amphetamine exposure in attentional task-performing, but not non-performing, rats. ( Brown, H; Bruno, JP; Kozak, R; Martinez, V; Sarter, M; Young, D, 2007) |
"We evaluated the effects of the levo (l) enantiomer of amphetamine sulfate on cognitive function in multiple sclerosis (MS) patients." | 5.13 | Effects of l-amphetamine sulfate on cognitive function in multiple sclerosis patients. ( Benedict, RH; Carpenter, RL; Erlanger, D; Feaster, T; Munschauer, F; Rowe, V; Zarevics, P, 2008) |
"D-Amphetamine improved reactions times on the spatial working memory and Stroop tasks for both individuals with schizophrenia and controls, and improved working memory accuracy in schizophrenia." | 5.11 | Amphetamine improves cognitive function in medicated individuals with schizophrenia and in healthy volunteers. ( Barch, DM; Carter, CS, 2005) |
"As a test of plausibility for the hypothesis that schizophrenia can result from abnormal brain, especially cerebral cortical, development, these studies examined whether, in the rat, disruption of brain development initiated on embryonic day (E) 17, using the methylating agent methylazoxymethanol acetate (MAM), leads to a schizophrenia-relevant pattern of neural and behavioral pathology." | 3.73 | A neurobehavioral systems analysis of adult rats exposed to methylazoxymethanol acetate on E17: implications for the neuropathology of schizophrenia. ( Geyer, MA; Ghajarnia, M; Grace, AA; Jentsch, JD; Moore, H, 2006) |
"L-amphetamine sulfate was associated with improved learning and memory and was well tolerated in this study." | 2.74 | The effects of L-amphetamine sulfate on cognition in MS patients: results of a randomized controlled trial. ( Bear, MF; Benedict, RH; Erlanger, D; Kaushik, T; Morrow, SA; Munschauer, FE; Zarevics, P, 2009) |
"Administration of amphetamine and methamphetamine can elicit psychiatric adverse effects at acute administration, binge use, withdrawal, and chronic use." | 2.52 | Neuropsychiatric Adverse Effects of Amphetamine and Methamphetamine. ( Harro, J, 2015) |
"Schizophrenia is a serious psychiatric disorder which impacts a broad range of cognitive, behavioural and emotional domains." | 2.44 | The amphetamine-induced sensitized state as a model of schizophrenia. ( Featherstone, RE; Fletcher, PJ; Kapur, S, 2007) |
"Treatment with levetiracetam dose-dependently improved memory performance of the ketamine-exposed rats." | 1.48 | Treatment with levetiracetam improves cognition in a ketamine rat model of schizophrenia. ( Gallagher, M; Koh, MT; Rosenzweig-Lipson, S; Shao, Y, 2018) |
"PWZ-029 did not affect recognition memory deficits in social novelty discrimination procedure." | 1.42 | Negative modulation of α₅ GABAA receptors in rats may partially prevent memory impairment induced by MK-801, but not amphetamine- or MK-801-elicited hyperlocomotion. ( Biawat, P; Cook, JM; Joksimović, S; Marković, B; Savić, MM; Stanković, T; Timić Stamenić, T, 2015) |
" In the present experiment, prefrontal acetylcholine (ACh) release was measured in attentional task-performing and non-performing rats pretreated with an escalating dosing regimen of amphetamine (AMPH) and following challenges with AMPH." | 1.34 | Toward a neuro-cognitive animal model of the cognitive symptoms of schizophrenia: disruption of cortical cholinergic neurotransmission following repeated amphetamine exposure in attentional task-performing, but not non-performing, rats. ( Brown, H; Bruno, JP; Kozak, R; Martinez, V; Sarter, M; Young, D, 2007) |
"Fragile X syndrome is an X-linked form of mental retardation including, among others, symptoms such as stereotypic behaviour, hyperactivity, hyperarousal, and cognitive deficits." | 1.32 | Object recognition impairment in Fmr1 knockout mice is reversed by amphetamine: involvement of dopamine in the medial prefrontal cortex. ( Catania, MV; Musumeci, SA; Pascucci, T; Puglisi-Allegra, S; Ventura, R, 2004) |
" The alleviation of the deficit with chronic administration of a DA precursor points to a possible line of treatment for the cognitive effects of developmental lead exposure." | 1.27 | Psychopharmacological investigations of a lead-induced long-term cognitive deficit in monkeys. ( Bowman, RE; Levin, ED; Vuchetich, J; Wegert, S, 1987) |
Timeframe | Studies, this research(%) | All Research% |
---|---|---|
pre-1990 | 9 (20.00) | 18.7374 |
1990's | 2 (4.44) | 18.2507 |
2000's | 16 (35.56) | 29.6817 |
2010's | 17 (37.78) | 24.3611 |
2020's | 1 (2.22) | 2.80 |
Authors | Studies |
---|---|
Lange, HS | 1 |
Vardigan, JD | 1 |
Cannon, CE | 1 |
Puri, V | 1 |
Henze, DA | 1 |
Uslaner, JM | 1 |
Koh, MT | 1 |
Shao, Y | 1 |
Rosenzweig-Lipson, S | 1 |
Gallagher, M | 1 |
Lapish, CC | 1 |
Ahn, KC | 1 |
Chambers, RA | 1 |
Ashby, DM | 1 |
Ahn, S | 1 |
Phillips, AG | 1 |
Lindgren, HS | 1 |
Klein, A | 1 |
Dunnett, SB | 1 |
Talpos, JC | 1 |
Aerts, N | 2 |
Fellini, L | 1 |
Steckler, T | 2 |
Ingallinesi, M | 1 |
Le Bouil, L | 1 |
Biguet, NF | 1 |
Thi, AD | 1 |
Mannoury la Cour, C | 1 |
Millan, MJ | 1 |
Ravassard, P | 1 |
Mallet, J | 1 |
Meloni, R | 1 |
Richetto, J | 1 |
Labouesse, MA | 1 |
Poe, MM | 1 |
Cook, JM | 2 |
Grace, AA | 2 |
Riva, MA | 1 |
Meyer, U | 1 |
Talpos, J | 1 |
Waddell, J | 1 |
Fries, GR | 1 |
Valvassori, SS | 1 |
Bock, H | 1 |
Stertz, L | 1 |
Magalhães, PV | 1 |
Mariot, E | 1 |
Varela, RB | 1 |
Kauer-Sant'Anna, M | 1 |
Quevedo, J | 1 |
Kapczinski, F | 1 |
Saraiva-Pereira, ML | 1 |
Harro, J | 1 |
Timić Stamenić, T | 1 |
Joksimović, S | 1 |
Biawat, P | 1 |
Stanković, T | 1 |
Marković, B | 1 |
Savić, MM | 1 |
Morrow, SA | 2 |
Rosehart, H | 1 |
Linden, J | 1 |
Van de Beeck, L | 1 |
Plumier, JC | 1 |
Ferrara, A | 1 |
Beninger, RJ | 2 |
Forsyth, JK | 1 |
Van Adel, M | 1 |
Reynolds, JN | 1 |
Boegman, RJ | 1 |
Jhamandas, K | 1 |
Kaushik, T | 1 |
Zarevics, P | 2 |
Erlanger, D | 2 |
Bear, MF | 1 |
Munschauer, FE | 1 |
Benedict, RH | 2 |
Advokat, C | 1 |
Barak, S | 1 |
Weiner, I | 1 |
Jones, CA | 1 |
Watson, DJ | 1 |
Fone, KC | 1 |
Redrobe, JP | 1 |
Elster, L | 1 |
Frederiksen, K | 1 |
Bundgaard, C | 1 |
de Jong, IE | 1 |
Smith, GP | 1 |
Bruun, AT | 1 |
Larsen, PH | 1 |
Didriksen, M | 1 |
Hawken, ER | 1 |
Lister, J | 1 |
Winterborn, AN | 1 |
Ichikawa, J | 1 |
Chung, YC | 1 |
Li, Z | 1 |
Dai, J | 1 |
Meltzer, HY | 1 |
Kipnis, J | 1 |
Cohen, H | 1 |
Cardon, M | 1 |
Ziv, Y | 1 |
Schwartz, M | 1 |
Castner, SA | 2 |
Goldman-Rakic, PS | 2 |
Williams, GV | 1 |
Ventura, R | 1 |
Pascucci, T | 1 |
Catania, MV | 1 |
Musumeci, SA | 1 |
Puglisi-Allegra, S | 1 |
Vosler, PS | 1 |
Barch, DM | 1 |
Carter, CS | 1 |
Wonodi, I | 1 |
Cassady, SL | 1 |
Adami, H | 1 |
Avila, M | 1 |
Thaker, GK | 1 |
Moore, H | 1 |
Jentsch, JD | 1 |
Ghajarnia, M | 1 |
Geyer, MA | 1 |
Kozak, R | 1 |
Martinez, V | 1 |
Young, D | 1 |
Brown, H | 1 |
Bruno, JP | 1 |
Sarter, M | 1 |
Guillin, O | 1 |
Abi-Dargham, A | 1 |
Laruelle, M | 1 |
Featherstone, RE | 1 |
Kapur, S | 1 |
Fletcher, PJ | 1 |
Schilt, T | 1 |
de Win, MM | 1 |
Jager, G | 1 |
Koeter, MW | 1 |
Ramsey, NF | 1 |
Schmand, B | 1 |
van den Brink, W | 1 |
Egerton, A | 1 |
Reid, L | 1 |
McGregor, S | 1 |
Cochran, SM | 1 |
Morris, BJ | 1 |
Pratt, JA | 1 |
Munschauer, F | 1 |
Rowe, V | 1 |
Feaster, T | 1 |
Carpenter, RL | 1 |
Lysaker, PH | 1 |
Bell, MD | 1 |
Bioty, SM | 1 |
Zito, WS | 1 |
Vargo, JM | 1 |
Grachek, RA | 1 |
Rockswold, GL | 1 |
Levin, ED | 1 |
Bowman, RE | 1 |
Wegert, S | 1 |
Vuchetich, J | 1 |
Kinsbourne, M | 1 |
Birkmayer, W | 1 |
Angrist, B | 1 |
Sathananthan, G | 1 |
Wilk, S | 1 |
Gershon, S | 1 |
Wender, PH | 1 |
Stiksrud, HA | 1 |
Süllwold, L | 1 |
Dalai, O | 1 |
Strian, F | 1 |
Tucker, GJ | 1 |
Quinlan, D | 1 |
Harrow, M | 1 |
Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
---|---|---|---|---|---|---|---|
A Double-blind Placebo Controlled Study of Mixed-amphetamine Salts, Extended Release (Adderall XR) for Cognitive Impairment in MS[NCT02676739] | Phase 2/Phase 3 | 180 participants (Anticipated) | Interventional | 2016-05-20 | Recruiting | ||
Intranasal Insulin for Improving Cognitive Function in Multiple Sclerosis[NCT02988401] | Phase 1/Phase 2 | 105 participants (Actual) | Interventional | 2017-12-01 | Completed | ||
Pharmacologic Augmentation of Neurocognition and Cognitive Training in Psychosis[NCT02634684] | Phase 2 | 82 participants (Actual) | Interventional | 2014-07-01 | Completed | ||
[information is prepared from clinicaltrials.gov, extracted Sep-2024] |
The BDI-II is a 21-question multiple-choice self-report inventory test for measuring the severity of depression. Scores range from zero to 63; higher scores indicate greater depression. In order to account for all contributed data (even for those who did not complete the study but contributed some post-randomization data in the active study phase), the analyses include the BDI-II scores acquired within the active treatment phase (from baseline to week 24 visit). We then calculated and report the average change per week in the scores. (NCT02988401)
Timeframe: Up to week 24 visit
Intervention | score on a scale (Mean) |
---|---|
Intranasal Insulin 20 International Units | -0.022 |
Intranasal Insulin 10 International Units | -0.019 |
Placebo | -0.045 |
This is a visual, nonverbal test of learning and memory. Scores range from zero to 12; higher is better. In order to account for all contributed data (even for those who did not complete the study but contributed some post-randomization data in the active study phase), the analyses include the BVMT-R delayed recall scores acquired within the active treatment phase (from baseline to week 24 visit). We then calculated and report the average change per week in the score. (NCT02988401)
Timeframe: Up to week 24 visit
Intervention | score on a scale (Mean) |
---|---|
Intranasal Insulin 20 International Units | 0.027 |
Intranasal Insulin 10 International Units | 0.059 |
Placebo | 0.030 |
This is a verbal learning and memory test. Scores range from zero to 16; a higher number is better. In order to account for all contributed data (even for those who did not complete the study but contributed some post-randomization data in the active study phase), the primary analyses include the CVLT-II scores acquired within the active treatment phase (from baseline to week 24 visit). We then calculated and report the average change per week in the score. (NCT02988401)
Timeframe: Up to week 24 visit
Intervention | score on a scale (Mean) |
---|---|
Intranasal Insulin 20 International Units | 0.082 |
Intranasal Insulin 10 International Units | 0.021 |
Placebo | 0.020 |
This test measures phonemic fluency. The test scores the number of words a participant can provide that begin with a specified letter within one minute, such that scores range from zero (worst) to an infinite number (better). Total score is sum of three 60-second trials. In order to account for all contributed data (even for those who did not complete the study but contributed some post-randomization data in the active study phase), the primary analyses include the COWAT scores acquired within the active treatment phase (from baseline to week 24 visit). We then calculated and report the average change per week in the score. (NCT02988401)
Timeframe: Up to week 24 visit
Intervention | score on a scale (Mean) |
---|---|
Intranasal Insulin 20 International Units | 0.090 |
Intranasal Insulin 10 International Units | 0.070 |
Placebo | 0.021 |
This test measures executive functioning, concept formation, and cognitive flexibility. Scores range from zero to 16; higher is better. In order to account for all contributed data (even for those who did not complete the study but contributed some post-randomization data in the active study phase), the analyses include DKEFS correct sort scores acquired within the active treatment phase (from baseline to week 24 visit). We then calculated and report the average change per week in the score. (NCT02988401)
Timeframe: Up to week 24 visit
Intervention | score on a scale (Mean) |
---|---|
Intranasal Insulin 20 International Units | -0.001 |
Intranasal Insulin 10 International Units | 0.027 |
Placebo | 0.002 |
Judgment of Line Orientation Test measures a person's ability to match the angle and orientation of lines in space. Scores range from zero to 30; higher is better. In order to account for all contributed data (even for those who did not complete the study but contributed some post-randomization data in the active study phase), the analyses include JLO data acquired within the active treatment phase (from baseline to week 24 visit). We then calculated and report the average change per week in the score. (NCT02988401)
Timeframe: Up to week 24 visit
Intervention | score on a scale (Mean) |
---|---|
Intranasal Insulin 20 International Units | -0.031 |
Intranasal Insulin 10 International Units | 0.047 |
Placebo | -0.005 |
"The Rao-version of the PASAT evaluates processing speed, working memory, and basic addition skills. Scores range from zero to 60; higher is better. Herein we present 3-second PASAT results (PASAT-3). In order to account for all contributed data (even for those who did not complete the study but contributed some post-randomization data in the active study phase), the analyses include PASAT-3 scores acquired within the active treatment phase (from baseline to week 24 visit). We then calculated and report the average change per week in the SDMT." (NCT02988401)
Timeframe: Up to week 24 visit
Intervention | score on a scale (Mean) |
---|---|
Intranasal Insulin 20 International Units | 0.372 |
Intranasal Insulin 10 International Units | 0.363 |
Placebo | 0.212 |
This task will be performed at five study visits. The SDMT is one of the most commonly used tests to assess processing speed in the MS population and is included in the Minimal Assessment of Cognitive Function in MS (MACFIMS). Higher scores reflect a better outcome (range 0 to 110). In order to account for all contributed data (even for those who did not complete the study but contributed some post-randomization data in the active study phase), the primary analyses include the SDMTs acquired within the active treatment phase (from baseline to week 24 visit). We then calculated and report the average change per week in the SDMT. (NCT02988401)
Timeframe: Up to week 24 visit
Intervention | score on a scale (Mean) |
---|---|
Intranasal Insulin 20 International Units | 0.145 |
Intranasal Insulin 10 International Units | 0.207 |
Placebo | 0.163 |
The sleep questionnaire asks subjects to report various aspects related to their sleep routine. Scores range from zero to 21; higher score indicates worse sleep quality. In order to account for all contributed data (even for those who did not complete the study but contributed some post-randomization data in the active study phase), the analyses include the PSQIs acquired within the active treatment phase (from baseline to week 24 visit). We then calculated and report the average change per week in the score. (NCT02988401)
Timeframe: Up to week 24 visit
Intervention | score on a scale (Mean) |
---|---|
Intranasal Insulin 20 International Units | -0.026 |
Intranasal Insulin 10 International Units | 0.035 |
Placebo | -0.045 |
FAMS is a self-reported health-related quality-of-life instrument for people with multiple sclerosis. Subjects rate six quality-of-life domains: Mobility, Symptoms, Emotional well-being, General contentment, Thinking/fatigue, and Family/social well-being. Scores range from zero to 176; higher scores indicate better health-related quality of life. In order to account for all contributed data (even for those who did not complete the study but contributed some post-randomization data in the active study phase), the analyses include the FAMS scores acquired within the active treatment phase (from baseline to week 24 visit). We then calculated and report the average change per week in the score. (NCT02988401)
Timeframe: Up to week 24 visit
Intervention | score on a scale (Mean) |
---|---|
Intranasal Insulin 20 International Units | 0.056 |
Intranasal Insulin 10 International Units | 0.051 |
Placebo | 0.240 |
An adverse event will be defined as any occurrence or worsening of an undesirable or unintended sign, symptom (or abnormal laboratory test), or disease temporally associated with the use of a medicinal product or intervention, whether or not it is considered related to the product/intervention. We report overall adverse events in the relevant section. Here, we report adverse events that led to study discontinuation. (NCT02988401)
Timeframe: Up to week 24 visit
Intervention | Participants (Count of Participants) |
---|---|
Intranasal Insulin 20 International Units | 3 |
Intranasal Insulin 10 International Units | 2 |
Placebo | 1 |
Fingerstick blood glucose levels were monitored twice within the 90 minutes following the first dose administration of study drug for the first 15 participants. (NCT02988401)
Timeframe: At the baseline visit, monitored twice within the 90 minutes following the first dose administration of study drug
Intervention | mg/dL (Mean) | |
---|---|---|
First timepoint | Second timepoint | |
Intranasal Insulin 10 International Units | 95.8 | 92.2 |
Intranasal Insulin 20 International Units | 97.8 | 88.4 |
Placebo | 90.0 | 87.8 |
The T-score indicates the performance on a neurocognitive battery of tests. Higher score reflects better performance. (NCT02634684)
Timeframe: two visits, 1 week apart, each visit lasting approximately 6 hours
Intervention | standardized T-score (Mean) | |
---|---|---|
placebo | amphetamine | |
Healthy Subjects: 10 mg Amphetamine 1st, Then Placebo | 57.870 | 56.000 |
Healthy Subjects: Placebo 1st, Then 10 mg Amphetamine | 54.476 | 55.476 |
Subjects With Schizophrenia: 10 mg Amphetamine 1st, Then Placebo | 39.895 | 38.105 |
Subjects With Schizophrenia: Placebo 1st, Then 10 mg Amphetamine | 31.895 | 33.842 |
"PPI was assessed with 42 trials of 6 types: 118 dB 40 ms pulse alone (P) & the same P preceded 10, 20, 30, 60, or 120 ms by a prepulse (pp) 16 dB over background. Startle magnitude (SM), habituation, latency & latency facilitation were measured to interpret changes in PPI.~%PPI = 100 x [(SM on P trials) - (SM on pp+P trials)] / SM on P trials. Example:~SM on P trials = 80 units SM on pp+P trials = 30 units %PPI = 100 x (80-30)/80 = 100 x 50/80 = 62.5%~Greater %PPI mean the reflex has been inhibited to a greater extent in the presence of a pp.~%PPI can't exceed 100: when SM on pp+P trials = 0, then %PPI = 100 x (SM on P trials - 0)/SM on P trials = 100 x 1 = 100%.~However, %PPI can theoretically be infinitely negative since SM on pp+P trials could be infinitely large (prepulse facilitiation (PPF)), i.e. SM is potentiated in the presence of a pp. PPF is normal at very short & very long pp intervals, but not within a species-specific physiological range of intervals." (NCT02634684)
Timeframe: two visits, 1 week apart, each visit lasting approximately 6 hours
Intervention | % inhibition of startle (Mean) | |
---|---|---|
Placebo | Amphetamine | |
Healthy Subjects: 10 mg Amphetamine 1st, Then Placebo | 50.626 | 53.029 |
Healthy Subjects: Placebo 1st, Then 10 mg Amphetamine | 50.626 | 45.822 |
Subjects With Schizophrenia: 10 mg Amphetamine 1st, Then Placebo | 41.162 | 39.545 |
Subjects With Schizophrenia: Placebo 1st, Then 10 mg Amphetamine | 22.629 | 32.656 |
"Auditory discrimination learning: Subjects identify direction (up vs. down) of 2 consecutive sound sweeps. Parameters (e.g. inter-sweep interval, sweep duration) are established for subjects to maintain 80% correct responses. On screen and test days, subjects complete 1h of TCT. Analytic software yields the key measures: auditory processing speed (APS) and APS learning. APS is the shortest inter-stimulus interval at which a subject performs to criteria and APS learning is the difference (ms) between the first APS and the best APS of the subsequent trials. A smaller APS reflects better discrimination (i.e., subject correctly identified frequency sweep direction despite a smaller ms gap between stimuli) and a larger ms value for APS learning reflects more learning, i.e., faster APS with repeated trials. Limits for APS are capped at 0-to-1000 ms; values for APS learning are capped at (-) 1000-to-APS." (NCT02634684)
Timeframe: two visits, 1 week apart, each visit lasting approximately 6 hours
Intervention | msec (Mean) | |
---|---|---|
placebo | amphetamine | |
Healthy Subjects: 10 mg Amphetamine 1st, Then Placebo | -2.113 | 29.190 |
Healthy Subjects: Placebo 1st, Then 10 mg Amphetamine | 5.911 | 35.905 |
Subjects With Schizophrenia: 10 mg Amphetamine 1st, Then Placebo | -50.158 | 101.000 |
Subjects With Schizophrenia: Placebo 1st, Then 10 mg Amphetamine | -15.118 | 52.647 |
7 reviews available for amphetamine and Cognition Disorders
Article | Year |
---|---|
Neuropsychiatric Adverse Effects of Amphetamine and Methamphetamine.
Topics: Aggression; Amphetamine; Amphetamine-Related Disorders; Brain; Cognition Disorders; Humans; Mental D | 2015 |
What are the cognitive effects of stimulant medications? Emphasis on adults with attention-deficit/hyperactivity disorder (ADHD).
Topics: Achievement; Adult; Amphetamine; Attention Deficit Disorder with Hyperactivity; Central Nervous Syst | 2010 |
Animal models of schizophrenia.
Topics: Amphetamine; Animals; Antipsychotic Agents; Cognition Disorders; Disease Models, Animal; Female; Hum | 2011 |
Animal models of working memory: insights for targeting cognitive dysfunction in schizophrenia.
Topics: Amphetamine; Animals; Cognition Disorders; Dopamine; Glutamic Acid; Humans; Memory, Short-Term; Mode | 2004 |
Neurobiology of dopamine in schizophrenia.
Topics: Amphetamine; Animals; Brain; Cognition Disorders; Corpus Striatum; Dopamine; Dopamine Plasma Membran | 2007 |
The amphetamine-induced sensitized state as a model of schizophrenia.
Topics: Amphetamine; Animals; Brain; Brain Chemistry; Central Nervous System Stimulants; Cognition Disorders | 2007 |
Minimal brain dysfunction in children. Diagnosis and management.
Topics: Abnormalities, Multiple; Affective Symptoms; Age Factors; Amphetamine; Attention; Attention Deficit | 1973 |
6 trials available for amphetamine and Cognition Disorders
Article | Year |
---|---|
Effects of single dose mixed amphetamine salts--extended release on processing speed in multiple sclerosis: a double blind placebo controlled study.
Topics: Acoustic Stimulation; Adult; Amphetamine; Cognition; Cognition Disorders; Cohort Studies; Delayed-Ac | 2015 |
The effects of L-amphetamine sulfate on cognition in MS patients: results of a randomized controlled trial.
Topics: Adult; Amphetamine; Central Nervous System Stimulants; Cognition; Cognition Disorders; Double-Blind | 2009 |
Amphetamine improves cognitive function in medicated individuals with schizophrenia and in healthy volunteers.
Topics: Adult; Amphetamine; Analysis of Variance; Antipsychotic Agents; Central Nervous System Stimulants; C | 2005 |
Effects of repeated amphetamine administration on antisaccade in schizophrenia spectrum personality.
Topics: Adult; Amphetamine; Brain; Central Nervous System Stimulants; Cognition Disorders; Drug Administrati | 2006 |
Effects of l-amphetamine sulfate on cognitive function in multiple sclerosis patients.
Topics: Adult; Amphetamine; Central Nervous System Stimulants; Cognition; Cognition Disorders; Dose-Response | 2008 |
[10 years of L-DOPA therapy of Parkinson's syndrome].
Topics: Administration, Oral; Amphetamine; Animals; Brain Chemistry; Catecholamines; Clinical Trials as Topi | 1971 |
32 other studies available for amphetamine and Cognition Disorders
Article | Year |
---|---|
Effects of a novel M4 muscarinic positive allosteric modulator on behavior and cognitive deficits relevant to Alzheimer's disease and schizophrenia in rhesus monkey.
Topics: Alzheimer Disease; Amphetamine; Animals; Association Learning; Behavior, Animal; Central Nervous Sys | 2021 |
Treatment with levetiracetam improves cognition in a ketamine rat model of schizophrenia.
Topics: Amphetamine; Animals; Central Nervous System Stimulants; Cognition Disorders; Disease Models, Animal | 2018 |
Selective effects of D- and L-govadine in preclinical tests of positive, negative, and cognitive symptoms of schizophrenia.
Topics: Alzheimer Disease; Amphetamine; Animals; Antipsychotic Agents; Avoidance Learning; Berberine Alkaloi | 2014 |
Nigral 6-hydroxydopamine lesion impairs performance in a lateralised choice reaction time task--impact of training and task parameters.
Topics: Adrenergic Agents; Amphetamine; Analysis of Variance; Animals; Choice Behavior; Cognition Disorders; | 2014 |
A touch-screen based paired-associates learning (PAL) task for the rat may provide a translatable pharmacological model of human cognitive impairment.
Topics: Amphetamine; Animals; Cognition Disorders; Conditioning, Operant; Disease Models, Animal; Dose-Respo | 2014 |
Local inactivation of Gpr88 in the nucleus accumbens attenuates behavioral deficits elicited by the neonatal administration of phencyclidine in rats.
Topics: Amphetamine; Animals; Central Nervous System Stimulants; Cognition Disorders; Discrimination, Psycho | 2015 |
Behavioral effects of the benzodiazepine-positive allosteric modulator SH-053-2'F-S-CH₃ in an immune-mediated neurodevelopmental disruption model.
Topics: Amphetamine; Animals; Benzodiazepines; Central Nervous System Stimulants; Cognition Disorders; Disea | 2015 |
MK-801 and amphetamine result in dissociable profiles of cognitive impairment in a rodent paired associates learning task with relevance for schizophrenia.
Topics: Amphetamine; Animals; Antipsychotic Agents; Central Nervous System Stimulants; Cognition Disorders; | 2015 |
Memory and brain-derived neurotrophic factor after subchronic or chronic amphetamine treatment in an animal model of mania.
Topics: Amphetamine; Amygdala; Animals; Avoidance Learning; Behavior, Animal; Bipolar Disorder; Brain-Derive | 2015 |
Negative modulation of α₅ GABAA receptors in rats may partially prevent memory impairment induced by MK-801, but not amphetamine- or MK-801-elicited hyperlocomotion.
Topics: Amphetamine; Animals; Behavior, Animal; Benzodiazepines; Cognition Disorders; Dizocilpine Maleate; H | 2015 |
Procedural learning as a measure of functional impairment in a mouse model of ischemic stroke.
Topics: Amphetamine; Animals; Body Weight; Cognition Disorders; Disease Models, Animal; Functional Lateralit | 2016 |
Subchronic MK-801 behavioural deficits in rats: partial reversal by the novel nitrate GT 1061.
Topics: Amphetamine; Animals; Behavior, Animal; Central Nervous System Stimulants; Chlormethiazole; Cognitio | 2009 |
The M₁/M₄ preferring agonist xanomeline reverses amphetamine-, MK801- and scopolamine-induced abnormalities of latent inhibition: putative efficacy against positive, negative and cognitive symptoms in schizophrenia.
Topics: Amphetamine; Animals; Antimanic Agents; Behavior, Animal; Cognition Disorders; Dizocilpine Maleate; | 2011 |
Negative modulation of GABAA α5 receptors by RO4938581 attenuates discrete sub-chronic and early postnatal phencyclidine (PCP)-induced cognitive deficits in rats.
Topics: Amphetamine; Animals; Benzodiazepines; Central Nervous System Stimulants; CHO Cells; Cognition Disor | 2012 |
Spontaneous polydipsia in animals treated subchronically with MK-801.
Topics: Age Factors; Amphetamine; Animals; Animals, Newborn; Body Weight; Central Nervous System Stimulants; | 2013 |
Cholinergic modulation of basal and amphetamine-induced dopamine release in rat medial prefrontal cortex and nucleus accumbens.
Topics: Acetylcholine; Adrenergic Uptake Inhibitors; Amphetamine; Animals; Cognition Disorders; Dopamine; Ma | 2002 |
T cell deficiency leads to cognitive dysfunction: implications for therapeutic vaccination for schizophrenia and other psychiatric conditions.
Topics: Amphetamine; Animals; Brain-Derived Neurotrophic Factor; Cognition; Cognition Disorders; Dizocilpine | 2004 |
Object recognition impairment in Fmr1 knockout mice is reversed by amphetamine: involvement of dopamine in the medial prefrontal cortex.
Topics: Amphetamine; Animals; Central Nervous System Stimulants; Cognition Disorders; Discrimination Learnin | 2004 |
Amphetamine sensitization impairs cognition and reduces dopamine turnover in primate prefrontal cortex.
Topics: 3,4-Dihydroxyphenylacetic Acid; Amphetamine; Analysis of Variance; Animals; Behavior, Animal; Centra | 2005 |
A neurobehavioral systems analysis of adult rats exposed to methylazoxymethanol acetate on E17: implications for the neuropathology of schizophrenia.
Topics: Amphetamine; Analysis of Variance; Animals; Behavior, Animal; Brain; Central Nervous System Stimulan | 2006 |
Toward a neuro-cognitive animal model of the cognitive symptoms of schizophrenia: disruption of cortical cholinergic neurotransmission following repeated amphetamine exposure in attentional task-performing, but not non-performing, rats.
Topics: Acetylcholine; Amphetamine; Animals; Attention; Basal Nucleus of Meynert; Central Nervous System Sti | 2007 |
Specific effects of ecstasy and other illicit drugs on cognition in poly-substance users.
Topics: Adolescent; Adult; Amphetamine; Attention; Cannabis; Central Nervous System Stimulants; Cocaine; Cog | 2008 |
Subchronic and chronic PCP treatment produces temporally distinct deficits in attentional set shifting and prepulse inhibition in rats.
Topics: Amphetamine; Animals; Attention; Behavior, Animal; Central Nervous System Stimulants; Cognition Diso | 2008 |
Cognitive impairment and substance abuse history as predictors of the temporal stability of negative symptoms in schizophrenia.
Topics: Adult; Age Factors; Amphetamine; Cocaine; Cognition Disorders; Comorbidity; Diagnosis, Dual (Psychia | 1997 |
Light deprivation soon after frontal brain trauma accelerates recovery from attentional deficits and promotes functional normalization of basal ganglia.
Topics: Amphetamine; Analysis of Variance; Animals; Attention; Basal Ganglia; Behavior, Animal; Brain Injuri | 1999 |
Psychopharmacological investigations of a lead-induced long-term cognitive deficit in monkeys.
Topics: Acetylcholine; Amphetamine; Animals; Behavior, Animal; Cognition Disorders; Dopamine; Haloperidol; L | 1987 |
School problems: diagnosis and treatment.
Topics: Agnosia; Amphetamine; Anxiety; Child; Child, Preschool; Cognition Disorders; Developmental Disabilit | 1973 |
Amphetamine psychosis: behavioral and biochemical aspects.
Topics: Adolescent; Adult; Affect; Alcoholism; Amphetamine; Brain; Cognition Disorders; Delusions; Depressio | 1974 |
[Objective and subjective attention disorders following polyvalent drug abuse].
Topics: Adolescent; Adult; Amphetamine; Barbiturates; Cannabis; Cocaine; Cognition Disorders; Factor Analysi | 1972 |
[Genetic factors in the recurrent confusional psychoses].
Topics: Amphetamine; Bipolar Disorder; Cognition Disorders; Humans; Lysergic Acid Diethylamide; Mental Proce | 1972 |
[Psychopathology of encephalitis of the temporal lobe type (author's transl)].
Topics: Adolescent; Adult; Amphetamine; Cognition Disorders; Diagnosis, Differential; Electroencephalography | 1973 |
Chronic hallucinogenic drug use and thought disturbance.
Topics: Adolescent; Adult; Amphetamine; Cannabis; Chronic Disease; Cognition Disorders; Female; Hallucinogen | 1972 |