Mar 31, 2009

Methamphetamine toxicity and messengers of death

Brain Research Reviews
Irina N Krasnova, Jean Lud Cadet

Abstract

Methamphetamine (METH) is an illicit psychostimulant that is widely abused in the world. Several lines of evidence suggest that chronic METH abuse leads to neurodegenerative changes in the human brain. These include damage to dopamine and serotonin axons, loss of gray matter accompanied by hypertrophy of the white matter and microgliosis in different brain areas. In the present review, we summarize data on the animal models of METH neurotoxicity which include degeneration of monoaminergic terminals and neuronal apoptosis. In addition, we discuss molecular and cellular bases of METH-induced neuropathologies. The accumulated evidence indicates that multiple events, including oxidative stress, excitotoxicity, hyperthermia, neuroinflammatory responses, mitochondrial dysfunction, and endoplasmic reticulum stress converge to mediate METH-induced terminal degeneration and neuronal apoptosis. When taken together, these findings suggest that pharmacological strategies geared towards the prevention and treatment of the deleterious effects of this drug will need to attack the various pathways that form the substrates of METH toxicity.

Mentioned in this Paper

Striatonigral Degeneration, Infantile (Disorder)
Metabolic Process, Cellular
POLB gene
Serum Albumin Measurement
JUN gene
Larsen Syndrome
JUND gene
Biochemical Pathway
Blood - Brain Barrier Anatomy
Central Nervous System

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