Melatonin Attenuates Methamphetamine-Induced Alteration of Amyloid β Precursor Protein Cleaving Enzyme Expressions via Melatonin Receptor in Human Neuroblastoma Cells

Nopparat, Chutikorn; Boontor, Anuttree; Panmanee, Jiraporn; Govitrapong, Piyarat

doi:10.1007/s12640-022-00522-6

Cited by 5 publications

(1 citation statement)

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“…of meth injected every 12 h for 8 weeks increases amyloid-β protein and amyloid precursor protein levels in the hippocampus of non-transgenic C57Bl/6J mice [102]. Additionally, meth exposure in vitro has also shown increased amyloid-β and hyperphosphorylated tau pathology [102][103][104]. While epidemiological evidence linking meth and AD is lacking, the neurotoxic effect of chronic meth on LC neurons shown in the current report and prior study [42] suggest that a history of meth abuse could be a potential risk factor for AD, and is in need of further investigation.…”

Section: Discussionmentioning

confidence: 99%

Repeated Methamphetamine Administration Results in Axon Loss Prior to Somatic Loss of Substantia Nigra Pars Compacta and Locus Coeruleus Neurons in Male but Not Female Mice

Pilski,

Graves

2023

IJMS

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Methamphetamine (meth) is a neurotoxic psychostimulant that increases monoamine oxidase (MAO)-dependent mitochondrial oxidant stress in axonal but not somatic compartments of substantia nigra pars compacta (SNc) and locus coeruleus (LC) neurons. Chronic meth administration results in the degeneration of SNc and LC neurons in male mice, and MAO inhibition is neuroprotective, suggesting that the deleterious effects of chronic meth begin in axons before advancing to the soma of SNc and LC neurons. To test this hypothesis, mice were administered meth (5 mg/kg) for 14, 21, or 28 days, and SNc and LC axonal lengths and numbers of neurons were quantified. In male mice, the SNc and LC axon lengths decreased with 14, 21, and 28 days of meth, whereas somatic loss was only observed after 28 days of meth; MAO inhibition (phenelzine; 20 mg/kg) prevented axonal and somatic loss of SNc and LC neurons. In contrast, chronic (28-day) meth had no effect on the axon length or numbers of SNc or LC neurons in female mice. The results demonstrate that repeated exposure to meth produces SNc and LC axonal deficits prior to somatic loss in male subjects, consistent with a dying-back pattern of degeneration, whereas female mice are resistant to chronic meth-induced degeneration.

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