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.
"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). "
"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)]. "
"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). "
[Show abstract][Hide abstract] 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.
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