Adropin increases with swimming exercise and exerts a protective effect on the brain of aged rats.

Adropin is a protein in the brain that decreases with age. Exercise has a protective effect on the endothelium by increasing the level of adropin in circulation. In this study, whether adropin, whose level in the brain decreases with age, may increase with swimming exercise, and exhibit a protective effect was investigated.

Effects of adropin on learning and memory in rats tested in the Morris water maze.

Adropin is a secreted peptide, which is composed of 43 amino acids and shows an effective role in regulating energy metabolism and insulin resistance. Motor coordination and locomotor activity were improved by adropin in the cerebellum. However, it is not known whether adropin administration has an effect on spatial learning and memory.

Neuropeptide-S affects cognitive impairment and depression-like behavior on MPTP induced experimental mouse model of Parkinson’s disease.

Background/aim: The present study proposes to investigate the effect of neuropeptide–S (NPS) on cognitive functions and depression-like behavior of MPTP-induced experimental model of Parkinson’s disease (PD).

Materials And Methods: Three-month-old C57BL/6 mice were randomly divided into three groups as; Control, Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and MPTP + NPS 0.1 nmol (received intraperitoneal injection of MPTP and intracerebroventricular injection of NPS, 0.

Protective mechanism of Syringic acid in an experimental model of Parkinson's disease.

6-Hydroxydopamine (6-OHDA) is a widely used chemical to model Parkinson's disease (PD) in rats. Syringic acid (SA) is a polyphenolic compound which has antioxidant and anti-inflammatory properties. The present study aimed to evaluate the neuroprotective role of SA in a rat model of 6-OHDA-induced PD.

Metformin protects rotenone-induced dopaminergic neurodegeneration by reducing lipid peroxidation.

Background: Metformin, a widely prescribed antidiabetic drug, has been suggested to have a neuroprotective effect on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced neurotoxicity in mice. In this study, we investigated the neuroprotective potential of metformin against rotenone-induced dopaminergic neuron damage and its underlying mechanisms.

Methods: C57BL/6 mice were given saline or rotenone (2.

The effect of docosahexaenoic acid on apelin distribution of nervous system in the experimental mouse model of Parkinson's disease.

Parkinson's disease (PD) is a degenerative disorder of the human central and peripheral nervous systems. n-3 fatty acids docosahexaenoic acid (DHA, C22: 6n-3) and eicosapentaenoic acid (EPA) as well as apelin have anti-inflammatory effects in various cells. At the same time, apelin has anti-oxidative and anti-apoptotic effects.

Neuronal nitric oxide synthase phosphorylation induced by docosahexaenoic acid protects dopaminergic neurons in an experimental model of Parkinson's disease.

Introduction: Docosahexaenoic acid (DHA) has been shown to have beneficial effects on Parkinson's disease (PD). The aim of this study was to investigate if the DHA acts on neurons of substantia nigra (SN) by phosphorylation of neuronal nitric oxide synthase (nNOS) in an experimental mouse model of PD.

Material And Methods: An experimental model of PD was created by intraperitoneal injections (4 × 20 mg/kg) of the neurotoxin 1-methyl-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP).

The protective mechanism of docosahexaenoic acid in mouse model of Parkinson: The role of hemeoxygenase.

Parkinson's disease (PD) is characterized by degeneration of the dopaminergic neurons in substantia nigra (SN). Its major clinical symptoms are tremor, rigidity, bradykinesia and postural instability. Docosahexaenoic acid (DHA) is an essential fatty acid for neural functions that resides within the neural membrane.

The effect of ingested sulfite on active avoidance in normal and sulfite oxidase-deficient aged rats.

The aim of this study was to investigate the possible toxic effects of sulfite on neurons by measuring active avoidance learning in normal and sulfite oxidase (SOX)-deficient aged rats. Twenty-four months of age Wistar rats were divided into four groups: control (C), sulfite-treated group (S), SOX-deficient group (D) and SOX-deficient + sulfite-treated group (DS). SOX deficiency was established by feeding rats with a low molybdenum (Mo) diet and adding 200 ppm tungsten (W) to their drinking water.

The effect of ingested sulfite on visual evoked potentials, lipid peroxidation, and antioxidant status of brain in normal and sulfite oxidase-deficient aged rats.

Sulfite, commonly used as a preservative in foods, beverages, and pharmaceuticals, is a very reactive and potentially toxic molecule which is detoxified by sulfite oxidase (SOX). Changes induced by aging may be exacerbated by exogenous chemicals like sulfite. The aim of this study was to investigate the effects of ingested sulfite on visual evoked potentials (VEPs) and brain antioxidant statuses by measuring superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities.