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Involvement of multiple molecular events in methamphetamine‐induced neurodegeneration: evidence from cDNA array analysis
Author(s) -
Cadet J. L.
Publication year - 2002
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.2002.00011.x
Subject(s) - neurodegeneration , meth , neurotoxicity , methamphetamine , programmed cell death , biology , dna damage , caspase , apoptosis , neuroscience , reactive oxygen species , microbiology and biotechnology , pharmacology , genetics , chemistry , medicine , dna , toxicity , pathology , disease , monomer , organic chemistry , acrylate , polymer
Methamphetamine (METH) is a neurotoxic drug of abuse that can cause terminal degeneration. Our laboratory recently showed that METH can also cause widespread apoptosis in the rodent brain. Current concepts of the molecular neurotoxicity of this illicit substance have earlier suggested the participation of reactive oxygen species, inflammatory processes and immediate early genes. Recent cDNA studies in our laboratory have hinted to the possibility that METH‐induced neurodegeneration might also include the participation of cell death might also include the participation of cell death genes such as BAX and BCL‐2. Activation of multiple caspases appears to also occur during METH‐induced neurodegeneration. Furthermore, DNA repair pathways seem to also be involved in attempts to protect against METH‐induced DNA damage. These results will be discussed in terms of the possible involvement of multiple transduction mechanisms in the appearance of METH neurotoxicity.