Seppi
Bluelighter
- Joined
- Feb 22, 2014
- Messages
- 294
There isn't a single shred of evidence of neurotoxicity as a result of long-term amphetamine (the compound, not the class) use at therapeutic doses in humans and this is not due to a lack of research. E.g., Ricaurte tried to show this, but didn't publish negative results: https://projectreporter.nih.gov/project_info_description.cfm?aid=8429516&icde=0 - that's one of many instances of a study on amphetamine-induced neurotoxicity in humans. Based on 3 meta-analyses/med-reviews (too lazy to link them - see the 3 citations at the end of the first paragraph of this section), both structural and functional neuroimaging studies suggest that, relative to non-medicated controls, amphetamine and MPH induce persistent structural and functional improvements in a few output structures along DA/NE-ergic pathways when used for ADHD. No pathological effects on the brain were noted in those reviews. In a nutshell, current evidence in humans supports a lack of neurotoxicity from long-term amphetamine use at low doses (i.e., those used for treating ADHD).
Might be worth adding that the only positive findings of amphetamine-induced neurodegeneration in humans that I've seen is from 3 primary studies on recreational users. One study that had clear findings of neurodegeneration (IMO, probably neurotoxicity-related) involved participants who took minimum daily doses of 500 mg with an average of ~10 years of recreational use. A related paper and one other study found effects that were analogous to plasticity observed in drug addicts (e.g., borked reward processing and impaired D2 receptor signaling). So, the findings from the last 2 papers might simply be addiction-related neuroplasticity as opposed to a toxicity-related phenomenon.
Might be worth adding that the only positive findings of amphetamine-induced neurodegeneration in humans that I've seen is from 3 primary studies on recreational users. One study that had clear findings of neurodegeneration (IMO, probably neurotoxicity-related) involved participants who took minimum daily doses of 500 mg with an average of ~10 years of recreational use. A related paper and one other study found effects that were analogous to plasticity observed in drug addicts (e.g., borked reward processing and impaired D2 receptor signaling). So, the findings from the last 2 papers might simply be addiction-related neuroplasticity as opposed to a toxicity-related phenomenon.
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