Thyroid Disorders and Development of Cognitive Impairment: A Review Study.

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.

The Positive Effect of MiR1 Antagomir on Ischemic Neurological Disorders Via Changing the Expression of Bcl-w and Bad Genes.

INTRODUCTION: MicroRNAs (miRNAs or miRs) are non-coding RNAs. Studies have shown that miRNAs are expressed aberrantly in stroke. The miR1 enhances ischemic damage, and a previous study has demonstrated that reduction of miR1 level has a neuroprotective effect on the Middle Cerebral Artery Occlusion (MCAO). Since apoptosis is one of the important processes in neural protection, the possible effect of miR1 on this pathway has been tested in this study. Post-ischemic administration of miR1 antagomir reduces infarct volume via bcl-w and bad expression. METHODS: Rats were divided into four experimental groups: sham, control, positive control, and antagomir treatment group. One hour after MCAO surgery, the rats were received intravenously (Tail vein) 0.1 mL Normal Saline (NS), 0.1 mL rapamycin, and 300 pmol/g miR1 antagomir (soluble in 0.1 mL normal saline) in control, positive control, and treatment group, respectively. Twenty-four hours after reperfusion infarct volume was measured. The expression of miR1, bcl-w, and bad were analyzed using real-time PCR in sham, control, and treated groups. RESULTS: Our results indicate that administration of miR1 antagomir reduces infarct volume significantly, it also decreases miR1 and bad expression while increases bcl-w expression. CONCLUSION: Understanding the precise neuroprotective mechanism of miR1 antagomir can make it a proper treatment and an innovative approach for stroke therapy.

Effect of intravenous injection of antagomiR-1 on brain ischemia.

Stroke is one of the leading causes of death in the world, but the underlying molecular mechanism of this disease remains elusive, thus it will be great challenges to finding appropriate protection. MicroRNAs are short, single-stranded, non-coding RNAs and recent studies have shown that they are aberrantly expressed in ischemic condition. Due to the fact that miR-1 has harmful effects on neural damages during brain ischemia, limited miR-1 has been proven to be protective in middle cerebral artery occlusion (MCAO). Here, the possible positive effect of intravenous injection of antagomiR-1 as a post-ischemic treatment on neurological deficits, infarct volume, brain edema and blood-brain barrier (BBB) permeability was evaluated. The rats were divided randomly into three experimental groups, each with 21 animals. MCAO surgery was performed on all groups and one hour later, 0.1 ml normal saline, 0.1 ml rapamycin and 300 pmol/g miR-1 antagomir (soluble in 0.1 ml normal saline), were injected intravenously into control, positive control and treatment group, respectively. After 24 h, neurologic deficits score, infarct volume, brain edema and BBB permeability were measured. The results indicated that post-treatment with miR-1 antagomir significantly improved neurological deficits and reduced infarction volume, brain edema, and BBB permeability. These data proved that there is a positive effects of antagomiR-1 on ischemic neuronal injury and neurological impairment. Due to the fact that microRNAs are able to protect the brain, it would be a promising therapeutic approach to stroke treatment.

The Role of Estrogen Receptors on Spatial Learning and Memory in CA1 Region of Adult Male Rat Hippocampus.

The hippocampal system plays an important role in memory function. Neurohormones like androgens and estrogens that syntheses in hippocampus have an important role in learning and memory. Many biological effects of estrogens in the brain via estrogenic receptors (ERs) are investigated. The current research has conducted to assess the effect of estrogenic receptors on spatial discrimination in rats by using Morris water maze (MWM) task. Adult male rats were bilaterally cannulated into CA1 region of hippocampus and divided in to 9 groups. Different groups received dimethyl sulfoxide (DMSO) 0.5 µl as control groups and different doses of tamoxifen (TAX) as antagonist of ER (0.0625, 0.125 and 0.25µg/0.5µl), propyl pyrazol thiol (PPT) as agonist of ERα (5,10 and 20µg/0.5µl), TAX 0.25µg/0.5µl + PPT 20µg/0.5µl all days 30-35 min before training. Our results have shown TAX (0.25µg/0.5µl), PPT (20µg/0.5µl), TAX (0.25µg/0.5µl) + PPT (20µg/0.5µl) groups significantly increase the escape latency and traveled distance to find invisible platform. Our results indicate that TAX and PPT and also TAX (0.25µg/0.5µl) + PPT (20µg/0.5µl) impaired acquisition of spatial learning and memory. As a consequence, it seems that estrogen modulates memory function via a novel estrogenic mechanism.