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Dextroamphetamine can enhance working memory and verbal memory consolidation in healthy humans. However, working memory improvements will only result from individuals with suboptimal dopaminergic signaling in the prefrontal cortex (the front part of your brain).
Further, the response is represented by an "inverted U" shaped curve. Too much dopamine will impair performance.
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In nonhuman primates, Dextroamphetamine has been shown to induce "enduring" atrophic changes in the dendritic spines of the prefrontal cortex lasting >3 years post-drug! Additionally, amphetamine sensitization (an augmented psychomotor response to subsequent drug "challenges") is associated with impaired spatial working memory and sustained visual attention. This sucks... big time.
Conclusion:
I am not so sure at this point. Toxicity at therapeutic dosages has not been well studied. There is no consensus in the literature. Adderall may very well help a healthy human perform better on some neuropsychological tests but it seems like this use will be accompanied by a "persistent" deficit. Personally, I wouldn't touch it because sensitization (while it may be reversible with some treatment... probably antipsychotics) could occur to some degree in just a few doses of the drug.
Neuropsychopharmacology. 2007 Apr;32(4):919-31. Epub 2006 Aug 16.
Amphetamine sensitization alters dendritic morphology in prefrontal cortical pyramidal neurons in the non-human primate.
Selemon LD, Begović A, Goldman-Rakic PS, Castner SA.
1Department of Neurobiology, Yale University School of Medicine, New Haven, CT 06520-8001, USA.
[email protected]
Amphetamine (AMPH) sensitization in the nonhuman primate induces persistent aberrant behaviors reminiscent of the hallmark symptoms of schizophrenia, including hallucinatory-like behaviors, psychomotor depression, and profound cognitive impairment. The present study examined whether AMPH sensitization induces similarly long-lasting morphologic alterations in prefrontal cortical pyramidal neurons. Three to 3(1/2) years postsensitization, sensitized, and AMPH-naïve control monkeys were killed. Blocks of prefrontal cortex were Golgi-impregnated for elucidation of pyramidal dendritic morphology in layers II/superficial III (II/IIIs), deep III, and V/VI. In AMPH-sensitized animals as compared to AMPH-naïve controls, pyramidal dendrites in layer II/IIIs exhibited reduced overall dendritic branching and reduced peak spine density (22%) on the apical trunk. Across all layers, the distance from soma to peak spine density along the apical trunk was decreased (126.38+/-7.65 mum in AMPH-sensitized compared to 162.98+/-7.26 microm in AMPH-naïve controls), and basilar dendritic length was reduced (32%). These findings indicate that chronic dopamine dysregulation, consequent to AMPH sensitization, results in enduring, atrophic changes in prefrontal pyramidal dendrites that resemble the pathologic alterations described in patients with schizophrenia and may contribute to the persistence of schizophrenia-like behavioral changes and cognitive dysfunction associated with sensitization. These findings may also provide key insights into the etiologic origin of the pronounced behavioral disturbances and cognitive dysfunction associated with schizophrenia.
Biol Psychiatry. 2005 Apr 1;57(7):743-51.
Amphetamine sensitization impairs cognition and reduces dopamine turnover in primate prefrontal cortex.
Castner SA, Vosler PS, Goldman-Rakic PS.
Department of Psychiatry, Yale University School of Medicine, New Haven, Connecticut 06519, USA.
[email protected]
BACKGROUND: Amphetamine (AMPH) sensitization in monkeys produces long-lasting behavioral changes that model positive (hallucinatory-like behaviors) and negative (psychomotor depression) symptoms of schizophrenia. The extent to which this model produces the core deficit in schizophrenia--working memory impairment--is unknown. METHODS: Two groups of rhesus monkeys were sensitized to AMPH over 6 weeks. In one group, acquisition of cognitive tasks (delayed response, visual discrimination, delayed nonmatch-to-sample) was examined beginning 6+ months postsensitization. The second group was pretrained to stability on delayed response before sensitization. Regional postmortem concentrations of dopamine and its metabolites were examined in tissue from age-matched AMPH-naive and AMPH-sensitized monkeys using high-performance liquid chromatography with electrochemical detection (HPLC-ECD). RESULTS: The AMPH-sensitized monkeys were profoundly impaired in their ability to acquire cognitive tasks compared with AMPH-naïve monkeys. Pretrained monkeys showed impaired delayed response performance for several months following sensitization. Analysis by HPLC revealed that AMPH sensitization significantly reduced dopamine turnover in prefrontal cortex and striatum. CONCLUSIONS: Impairments in the acquisition and performance of spatial delayed response in association with reduced dopamine turnover in prefrontal cortex following AMPH sensitization provide further support for the relevance of this model to both the etiology and the treatment of cognitive dysfunction in schizophrenia.
