No abstract

Dementia is a neurological disorder that is spreading with increasing human lifespan. In this neurological disorder, memory and cognition are declined and eventually impaired. Various factors can be considered as the background of this disorder, one of which is endocrine disorders. Thyroid hormones are involved in various physiological processes in the body; one of the most important of them is neuromodulation. Thyroid disorders, including hyperthyroidism or hypothyroidism, can affect the nervous system and play a role in the development of dementia. Despite decades of investigation, the nature of the association between thyroid disorders and cognition remains a mystery. Given the enhancing global burden of dementia, the principal purpose of this study was to elucidate the association between thyroid disturbances as a potentially modifiable risk factor of cognitive dysfunction. In this review study, we have tried to collect almost all of the reported mechanisms demonstrating the role of hypothyroidism and hyperthyroidism in the pathogenesis of dementia.

Cadmium and lead concentrations were compared in tissues of cutlassfish, Trichiurus lepturus L., its intestinal nematode Hysterothylacium sp. type MB larvae, and in water from the same location in the Sea of Oman. Metal accumulation in hosts, parasites and sea water was measured by ICP-OES. Hysterothylacium larvae from the intestinal lumen and visceral cavity showed much higher metal concentrations than in host tissues or sea water. Statistical analyses revealed no significant differences in metal accumulation between infected and uninfected hosts. Cadmium concentration in the host muscle was lower than in intestine, liver and gonad tissues. The mean concentrations of lead and cadmium in nematodes were 289·03 and 81·5 times higher than in host intestine, 188·4 and 225 times higher than in host muscle, 108·6 and 65·3 times higher than in host gonads, 70·5 and 19·5 times higher than in host liver and 3351 and 148 times higher than in sea water. The results show the value of this and possibly related nematodes as bioindicators of heavy metals and their potential use in environmental studies.

No abstract

The brain reward system consists of the ventral tegmental area that sends its dopaminergic projections to the forebrain, cortical areas, amygdala and largely to the nucleus accumbens (NAc). The present study aims were to investigate the effects of bilateral intra-accumbal microinjection of WIN55,212-2, a CB1 receptor agonist, on the duration of extinction period and reinstatement to morphine by the conditioned place preference (CPP) paradigm in the rat. Forty-six adult male albino Wistar rats received intra-accumbal WIN55,212-2 [p0.5, 1 and 2 mM/0.5 μl dimethyl sulfoxide (DMSO)] injections bilaterally. To induce CPP, morphine (5 mg/kg) was injected subcutaneously over three consecutive days. The results showed that intra-NAc administration of WIN55,212-2 during the extinction period had no effect on its duration but single administration of the1 mM/0.5 μl DMSO dose just before the reinstatement phase significantly attenuated its conditioning score. This is the first time that interactions of opioid and cannabinoid systems by local activation of CB1 receptors in the NAc during extinction and morphine-induced reinstatement were investigated. The CB1 agonist can inhibit and eliminate the reward-associated memory of morphine and the conditioning score in reinstatement but not in the extinction period. Our findings suggest that the extinction period and reinstatement could occur through different mechanisms.