Methamphetamine Dependence Is Associated With Neurocognitive Impairment in the Initial Phases of Abstinence

Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, School of Medicine, USA.
Journal of Neuropsychiatry (Impact Factor: 2.82). 02/2003; 15(2):215-20. DOI: 10.1176/appi.neuropsych.15.2.215
Source: PubMed


This study documented the association between neurocognitive impairment and methamphetamine dependence in a sample of 27 methamphetamine-dependent individuals who achieved 5 to 14 days of continuously monitored abstinence and in 18 control subjects. Methamphetamine-dependent individuals performed significantly worse than control subjects on neurocognitive measures sensitive to attention/psychomotor speed, on measures of verbal learning and memory, and on executive systems measures sensitive to fluency. These findings are the first to demonstrate that methamphetamine dependence is associated with impairments across a range of neurocognitive domains in a sample of users whose abstinence was continuously monitored with the use of urine screening.

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    • "METH users also present with deficits in learning, motor ability, and working memory tests (Cherner et al., 2010). Neurocognitive deficits occur not only in individuals currently using METH (Simon et al., 2000) but can also persist long after METH is discontinued (4 days to 7 months) (Kalechstein et al., 2003, 2009; Gonzalez et al., 2004; Hoffman et al., 2006; Cherner et al., 2010; Casaletto et al., 2014). Among the different types of neurocognitive deficits caused by METH abuse, METH-associated neurocognitive deficits are greater for episodic memory, executive functions, information processing speed, and motor skills and lesser for attention, working memory , and verbal fluency (Scott et al., 2007). "
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    ABSTRACT: Previous studies have demonstrated that methamphetamine (METH) abuse leads to memory deficits and these are associated with relapse. Furthermore, extensive evidence indicates that nicotine (NIC) prevents and/or improves memory deficits in different models of cognitive dysfunction and these nicotinic effects might be mediated by hippocampal or cortical nicotinic acetylcholine receptors (nAChRs). The present study investigated whether NIC attenuates METH-induced novel object recognition (NOR) deficits in rats and explored potential underlying mechanisms. Adolescent or adult male Sprague-Dawley rats received either NIC water (10-75 μg/ml) or tap water for several weeks. METH (4 x 7.5 mg/kg/injection) or saline was administered either before or after chronic NIC exposure. Novel object recognition was evaluated 6 d after METH or saline. Serotonin transporter function and density, and α4β2 nAChR density were assessed on the following day. Chronic NIC intake via drinking water beginning during either adolescence or adulthood attenuated the NOR deficits caused by a high-dose METH administration. Similarly, NIC attenuated METH-induced deficits in NOR when administered after METH treatment. However, NIC did not attenuate the serotonergic deficits caused by METH in adults. Conversely, NIC attenuated METH-induced deficits in α4β2 nAChR density in the hippocampal CA1 region. Furthermore, NIC increased α4β2 nAChR density in the hippocampal CA3, dentate gyrus and perirhinal cortex (PRh) in both saline- and METH-treated rats. Overall, these findings suggest that NIC-induced increases in α4β2 nAChRs in the hippocampus and PRh might be one mechanism by which NOR deficits are attenuated by NIC in METH-treated rats. © The Author 2015. Published by Oxford University Press on behalf of CINP.
    The International Journal of Neuropsychopharmacology 07/2015; DOI:10.1093/ijnp/pyv073 · 4.01 Impact Factor
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    • "They were 55% less likely to be arrested for a new crime and 53% less likely to have had their probation revoked. These results are even more impressive in light of the participants’ criminal histories and their heavy, chronic exposure to methamphetamine, which can impair aspects of cognitive function [on project HOPE, see (81); on the effects of methamphetamines, see (82–86)]. "
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    ABSTRACT: From Brainwashed: The Seductive Appeal of Mindless Neuroscience by Sally Satel and Scott Lilienfeld, copyright © 2013. Reprinted by permission of Basic Books, a member of The Perseus Books Group. The notion that addiction is a “brain disease” has become widespread and rarely challenged. The brain-disease model implies erroneously that the brain is necessarily the most important and useful level of analysis for understanding and treating addiction. This paper will explain the limits of over-medicalizing – while acknowledging a legitimate place for medication in the therapeutic repertoire – and why a broader perspective on the problems of the addicted person is essential to understanding addiction and to providing optimal care. In short, the brain-disease model obscures the dimension of choice in addiction, the capacity to respond to incentives, and also the essential fact people use drugs for reasons (as consistent with a self-medication hypothesis). The latter becomes obvious when patients become abstinent yet still struggle to assume rewarding lives in the realm of work and relationships. Thankfully, addicts can choose to recover and are not helpless victims of their own “hijacked brains.”
    Frontiers in Psychiatry 01/2013; 4:141. DOI:10.3389/fpsyt.2013.00141
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    • "Animal studies also found that acute low-dose amphetamine, METH or cocaine could facilitate memory performance (Kennedy et al., 2010; Wood et al., 2007), especially the consolidation of memory (Iñiguez et al., 2011; Wiig et al., 2009). Memory impairment was also detected in both humans and rodents which had been exposed to METH (Belcher et al., 2007; Kalechstein et al., 2003; Nordahl et al., 2003; Simon et al., 2000; Vorhees et al., 2009). "
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    ABSTRACT: Drugs of abuse modulated learning and memory in humans yet the underlying mechanism remained unclear. The extracellular signal-regulated kinase (ERK) and the transcription factor cAMP response element-binding protein (CREB) were involved in neuroplastic changes associated with learning and memory. In the current study, we used a Morris water maze to examine the effect of methamphetamine (METH) on different processes of spatial memory in mice. We then investigated the status of ERK and CREB in the hippocampus and prefrontal cortex (PFC). We found that 1.0 mg/kg dose of METH facilitated spatial memory consolidation when it was injected immediately after the last learning trial. In contrast, the same dose of METH had no effect on spatial memory retrieval when it was injected 30 min before the test. Furthermore, 1.0 mg/kg dose of METH injected immediately after retrieval had no effect on spatial memory reconsolidation. Activation of both ERK and CREB in the hippocampus was found following memory consolidation but not after retrieval or reconsolidation in METH-treated mouse groups. In contrast, activation of both ERK and CREB in the PFC was found following memory retrieval but not other processes in METH-treated mouse groups. These results suggested that METH facilitated spatial memory consolidation but not retrieval or reconsolidation. Moreover, activation of the ERK and CREB signaling pathway in the hippocampus might be involved in METH-induced spatial memory changes.
    Neuropharmacology 11/2012; 67. DOI:10.1016/j.neuropharm.2012.10.020 · 5.11 Impact Factor
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