Amphetamine dependence refers to a state of psychological dependence on a drug in the amphetamine class. Stimulants such as amphetamines and cocaine do not cause physical dependence.Signs of amphetamine intoxication manifest themselves in euphoria, hypersexuality, tachycardia, diaphoresis, and intensifications of the train of thought, speech, and movement. Over time, neurodegenerative changes become apparent in the form of altered behavior, reduced cognitive functions, and signs of neurological damage, such as a decrease in the levels of dopamine transporters (DAT) and serotonin transporters (SERT) in the brain. Amphetamine use within teenagers can have lasting effects on their brain, in particular the prefrontal cortex. Amphetamine use is rising among students due to the ability to easily access prescribed stimulants like Adderall. Also, in case of chronic use, vegetative disorders soon occur such as bouts of sweating, trouble sleeping, tremor, ataxia and diarrhea; the degradation of the personality takes place relatively slowly. Tolerance is expected to develop with regular substituted amphetamine use. When substituted amphetamines are used, drug tolerance develops rapidly. Amphetamine dependence has shown to have the highest remission rate compared to cannabis, cocaine, and opioids. Severe withdrawal associated with dependence from recreational substituted amphetamine use can be difficult for a user to cope with. Long-term use of certain substituted amphetamines, particularly methamphetamine, can reduce dopamine activity in the brain. For amphetamine dependent individuals, psychotherapy is currently the best treatment option as no pharmacological treatment has been approved.
In 2014, Gambetti P., Zou W.Q., and coworkers found that approximately 54% of mice inoculated with VPSPr brain homogenates exhibited histopathologic lesions and 34% harbored abnormal PrP similar to that of VPSPr on the first passage but no prion disease was detected on the second passage,[10] suggesting that the infectivity of the pathological PrP from VPSPr is lower compared to that from the most common sporadic CJD. See also
Creutzfeldt–Jakob disease

References
8. Xiao X, Yuan J, Haïk S, Cali I, Zhan YA, Moudjou M, Li B, Laplanche JL, Laude H, Langeveld J, Gambetti P, Kitamoto T, Kong Q, Brandel JP, Cobb BA, Petersen RB & Zou WQ. Glycoform-selective prion formation in sporadic and familial forms of prion disease. PLoS ONE, 2013; 8:e58786. 9. Zou, WQ, Gambetti P, Xiao X, Yuan J, Langeveld J & Pirisinu L. Prions in variably protease-sensitive prionopathy: An update. Pathogens 2013; 2(3): 457-471. 10. Notari S, Xiao X, Espinosa JC, Cohen Y, Qing L, Aguilar-Calvo P, Kofskey D, Cali I, Cracco L, Kong Q, Torres JM, Zou W & Gambetti P. Transmission characteristics of variably protease-sensitive prionopathy. Emerg Infect Dis 2014, 20:2006-14. External links

Caroline Parkinson (13 August 2010). "Brain disease could affect more people, research finds". BBC News.