Prenatal Methamphetamine Exposure Impairs Helping Behaviour in Male Offspring: The Possible Role of miR-223 and NLRP3 Inflammasomes in the Amygdala.

The increasing prevalence of methamphetamine abuse among women, particularly pregnant females, is a global concern. Methamphetamine can readily cross anatomical barriers like the blood-placenta barrier and cause detrimental impacts on the growing fetus. The current research evaluated the effects of prenatal methamphetamine exposure on helping behaviour and neuroinflammatory cascade in the amygdala of male offspring.

Reproductive status of male rat offspring following exposure to methamphetamine during intrauterine life: An experimental study.

Background: Methamphetamine abuse during pregnancy is associated with maternal and fetal adverse outcomes. Methamphetamine induces reproductive damage in adults; however, its effect has not been studied during pregnancy.

Objective: To investigate the effects of methamphetamine exposure during pregnancy on the reproductive system.

Prenatal Methamphetamine Hydrochloride Exposure Leads to Signal Transduction Alteration and Cell Death in the Prefrontal Cortex and Amygdala of Male and Female Rats' Offspring.

In the last decade, there has been a great increase in methamphetamine hydrochloride (METH) abuse by pregnant women that exposes fetus and human offspring to a wide variety of developmental impairments that may be the underlying causes of future psychosocial issues. Herein, we investigated whether prenatal METH exposure with different doses (2 and 5 mg/kg) could influence neuronal cell death and antioxidant level in the different brain regions of adult male and female offspring. Adult male and female Wistar rats prenatally exposed to METH (2 or 5 mg/kg) and/or saline was used in this study.

Geldanamycin Reduces Aβ-Associated Anxiety and Depression, Concurrent with Autophagy Provocation.

Neurodegenerative disorders are generally characterized by abnormal aggregation and deposition of specific proteins. Amyloid beta (Aβ)-associated neurodegenerative disorder is characterized by an oxidative damage that, in turn, leads to some behavioral changes before the establishment of dementia such as depression and anxiety. In the current study, we investigated the effect of heat shock protein 90 inhibitor geldanamycin (GA) administration 24 h before Aβ injection.

Collaboration of geldanamycin-activated P70S6K and Hsp70 against beta-amyloid-induced hippocampal apoptosis: an approach to long-term memory and learning.

One of the neuropathological hallmarks of Alzheimer's disease (AD) is the accumulation of beta-amyloid peptides (Aβ) in senile plaques. Aβ-induced oxidative stress is believed to be responsible for degeneration and apoptosis of neurons and consequent cognitive and memory deficits. Here, we investigated the possible neuroprotective effect of the heat shock protein 90 (Hsp90) inhibitor geldanamycin (GA) against amyloid pathogenesis in adult male Wistar rats.