Methamphetamine (METH) is an illicit psychostimulant that is subject to abuse worldwide. While the modulatory effects of METH on dopamine neurotransmission and its neurotoxicity in the central nervous system are well studied, METH’s effects on modulating microglial neuroimmune functions and on eliciting neuroinflammation to affect dopaminergic neurotoxicity has attracted considerable attention in recent years. The current review illuminates METH-induced neurotoxicity from a neuropathological perspective by summarizing studies reporting microglial activation after METH administration in rodents. Assessing microglial reactivity in terms of the cells’ morphology and immunophenotype offers an opportunity for comprehensive and objective assessment of the severity and nature of METH-induced neuronal perturbations in the CNS and can thus contribute to a better understanding of the nature of METH toxicity. We reach the conclusion here that the intensity of microglial activation reported in the majority of animal models after METH administration is quite modest, indicating that the extent of dopaminergic neuron damage directly caused by this neurotoxicant is relatively minor. Our conclusion stands in contrast to claims of excessive and detrimental neuroinflammation believed to contribute and exacerbate METH neurotoxicity. Thus, our analysis of published studies does not support the idea that suppression of microglial activity with anti-inflammatory agents could yield beneficial effects in terms of treating addiction disorders.

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Background: An electroencephalogram (EEG) is an accepted method in neurophysiology with a wide application. Different types of brain rhythms indicate that simultaneous activity of the brain cortex neurons depend on the person’s mental state. Method: we have focus on reviewing the existing literature pertaining to changes of the brain’s bioelectrical activity that recorded from the scalp in different conditions such as cognition and some mental disorders. Result: The frequency of brain waves may indicate sleep, consciousness, cognition, and some mental disorders. Slow brain waves are seen in some conditions such as sleep, coma, brain death, depression, autism, brain tumors, obsessive–compulsive disorder (OCD), attention deficit hyperactivity disorder (ADHD), and encephalitis, while rapid waves are generally reported in conditions such as epilepsy, anxiety, posttraumatic stress disorder (PTSD), and drug abuse. Conclusion: Increase in the EEG rhythm is a marker of high brain activity that leads to high degrees of consciousness, while slow waves are suggestive of less brain activity. The pattern of EEG rhythm can be an indicator of some mental disorders, too.

Aggregated amyloid beta (Aβ) peptides are believed to play a decisive role in the pathology of Alzheimer's disease (AD). Previous evidence suggested that exercise contributes to the improvement of cognitive decline and slows down pathogenesis of AD; however, the exact mechanisms for this have not been fully understood. Here, we evaluated the effect of a 4-week moderate treadmill exercise on spatial memory via central and peripheral Aβ clearance mechanisms following developed AD-like neuropathology induced by intra-hippocampal Aβ injection in male Wistar rats. We found Aβ-treated animals showed spatial learning and memory impairment which was accompanied by increased levels of amyloid plaque load and soluble Aβ (sAβ), decreased mRNA and protein expression of neprilysin (NEP), insulin degrading enzyme (IDE) and low-density lipoprotein receptor-related protein-1 (LRP-1) in the hippocampus. Aβ-treated animals also exhibited a higher level of sAβ and a lower level of soluble LRP-1 (sLRP-1) in plasma, as well as a decreased level of LRP-1 mRNA and protein content in the liver. However, exercise training improved the spatial learning and memory deficits, reduced both plaque load and sAβ levels, and up-regulated expression of NEP, IDE, and LRP-1 in the hippocampus of Aβ-treated animals. Aβ-treated animals subjected to treadmill exercise also revealed decreased levels of sAβ and increased levels of sLRP-1 in plasma, as well as increased levels of LRP-1 mRNA and protein in the liver. In conclusion, our findings suggest that exercise-induced improvement in both of central and peripheral Aβ clearance are likely involved in ameliorating spatial learning and memory deficits in an animal model of AD. Future studies need to determine their relative contribution.

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