Enhancing performance
Cognitive performance
In 2015, a systematic review and a meta-analysis of high quality clinical trials found that, when used at low (therapeutic) doses, amphetamine produces modest yet unambiguous improvements in cognition, including working memory, long-term episodic memory, inhibitory control, and some aspects of attention, in normal healthy adults; these cognition-enhancing effects of amphetamine are known to be partially mediated through the indirect activation of both dopamine receptor D1 and adrenoceptor α2 in the prefrontal cortex. A systematic review from 2014 found that low doses of amphetamine also improve memory consolidation, in turn leading to improved recall of information. Therapeutic doses of amphetamine also enhance cortical network efficiency, an effect which mediates improvements in working memory in all individuals. Amphetamine and other ADHD stimulants also improve task saliency (motivation to perform a task) and increase arousal (wakefulness), in turn promoting goal-directed behavior. Stimulants such as amphetamine can improve performance on difficult and boring tasks and are used by some students as a study and test-taking aid. Based upon studies of self-reported illicit stimulant use, 5–35% of college students use diverted ADHD stimulants, which are primarily used for enhancement of academic performance rather than as recreational drugs. However, high amphetamine doses that are above the therapeutic range can interfere with working memory and other aspects of cognitive control. Physical performance
Amphetamine is used by some athletes for its psychological and athletic performance-enhancing effects, such as increased endurance and alertness; however, non-medical amphetamine use is prohibited at sporting events that are regulated by collegiate, national, and international anti-doping agencies.
Congenital stromal corneal dystrophy (CSCD) is an extremely rare, autosomal dominant form of corneal dystrophy. Only 4 families have been reported to have the disease by 2009. The main features of the disease are numerous opaque flaky or feathery areas of clouding in the stroma that multiply with age and eventually preclude visibility of the endothelium. Strabismus or primary open angle glaucoma was noted in some of the patients. Thickness of the cornea stays the same, Descemets membrane and endothelium are relatively unaffected, but the fibrils of collagen that constitute stromal lamellae are reduced in diameter and lamellae themselves are packed significantly more tightly. Genetics
CSCD is associated with a mutation in the gene DCN that encodes the protein decorin, located at chromosome 12q22. The disorder is inherited in an autosomal dominant manner, which indicates that the defective gene responsible for a disorder is located on an autosome (chromosome 12 is an autosome), and only one copy of the gene is sufficient to cause the disorder, when inherited from a parent who has the disorder. Diagnosis
Treatment
References
External links
GeneReviews/NCBI/NIH/UW entry on Congenital Stromal Corneal Dystrophy