Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2017 Aug:155:149-170.
doi: 10.1016/j.pneurobio.2015.09.011. Epub 2015 Oct 9.

Amphetamine-related drugs neurotoxicity in humans and in experimental animals: Main mechanisms

Affiliations
Review

Amphetamine-related drugs neurotoxicity in humans and in experimental animals: Main mechanisms

Rosario Moratalla et al. Prog Neurobiol. 2017 Aug.

Abstract

Amphetamine-related drugs, such as 3,4-methylenedioxymethamphetamine (MDMA) and methamphetamine (METH), are popular recreational psychostimulants. Several preclinical studies have demonstrated that, besides having the potential for abuse, amphetamine-related drugs may also elicit neurotoxic and neuroinflammatory effects. The neurotoxic potentials of MDMA and METH to dopaminergic and serotonergic neurons have been clearly demonstrated in both rodents and non-human primates. This review summarizes the species-specific cellular and molecular mechanisms involved in MDMA and METH-mediated neurotoxic and neuroinflammatory effects, along with the most important behavioral changes elicited by these substances in experimental animals and humans. Emphasis is placed on the neuropsychological and neurological consequences associated with the neuronal damage. Moreover, we point out the gap in our knowledge and the need for developing appropriate therapeutic strategies to manage the neurological problems associated with amphetamine-related drug abuse.

Keywords: 3,4-Methylenedioxymethamphetamine; Dopamine; Ecstasy; MDMA; METH; Methamphetamine; Mouse; Neurodegeneration; Neuroinflammation neurotoxicity; Non-human primate; Rat.

PubMed Disclaimer

Similar articles

Cited by

MeSH terms

Substances