A 3 tesla magnetic resonance imaging volumetric analysis of the hippocampal formation: dependence on handedness and age.

BACKGROUND: The hippocampal formation (HF) is one of the most important parts of the brain in the magnetic resonance imaging (MRI) volumetric analysis in various domains, but not completely from all aspects, including the handedness. The aim of our study was to evaluate the possible differences in the volume of the right and left HF among the healthy right-handed and left-handed subjects, and to determine whether the volume differences are age related. MATERIALS AND METHODS: The MRI of this prospective study was performed using T1 fast field echo (FFE) sequence. The 124 subsequent coronal slices (thickness 1.5 mm) were performed in each participant. The obtained HF volumes were normalised and statistically compared. Volunteers comprised 30 persons aged 22.0 years, 12 of whom were the left-handed, and 30 persons aged 75.2 years on average, 9 of whom were the left-handed. RESULTS: The right and left HF volumes averaged 2.986 cm3 and 2.858 cm3 in the right-handed, and 2.879 cm³ and 3.020 cm³ in the left-handed young volunteers, as well as 2.728 cm³ and 2.650 cm³ in the right-handed, and 2.617 cm³ and 2.780 cm³ in the left-handed elderly persons. The HF volume ratios in the young left-handed participants showed a significant left-greater-than-right asymmetry. A significant difference was also noticed within the right-to-left volume ratios of the right- and left-handed young and elderly participants. The latter reduction in the HF volume within the aged group can be interpreted as a slight atrophy of the HF. CONCLUSIONS: There is a significant difference in the volumes of the left and right HF of the left-handed young participants. The age related HF volume differences were proven between the groups of the young and elderly volunteers. The obtained data should be included into the future MRI studies of the HF volumes in various clinical domains.

8-Iso-prostaglandin F2α as a potential biomarker in patients with unipolar and bipolar depression.

OBJECTIVE: Previous studies have shown that the disturbance of redox homeostasis plays a role in the pathogenesis of mood disorders. It is currently unclear whether oxidative stress parameters can be used as biomarkers (state vs. trait). The aim of the present study was to investigate oxidative stress markers in patients with major depressive disorder (MDD) and bipolar disorder (BP) in acute depressive episodes and remission, and healthy individuals. PATIENTS AND METHODS: Thirty-two patients with a diagnosis of MDD, 32 patients with a diagnosis of BP and 32 matched healthy controls were included in the study. We measured the serum levels of markers of oxidative damage, including 8-hydroxy-2'-deoxyguanosine (8-OHdG), 8-Iso-prostaglandin F2α (8-iso-PGF2α; 8-isoprostane), and malondialdehyde (MDA), and also serum activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), and glutathione reductase (GR) in both acute and remission phase, and in control group. RESULTS: After controlling for the effects of age, sex, body mass index, and smoking status, serum 8-iso-PGF2α levels were significantly higher in both patient groups compared to controls, regardless of disease phase. The activities of GPX and GR were significantly lower in the acute phase in MDD patients compared to controls. Serum GR activity was lower in both acute and remission phase in MDD compared to BP. CONCLUSIONS: Our results suggest that both MDD and BP are associated with a disturbed redox balance with a particularly pronounced increase in serum 8-iso-PGF2α levels in both groups and the presence of glutathione metabolism disorders in MDD patients. Further research is needed to confirm the importance of oxidative stress parameters as potential biomarkers of MDD and BP.

The correlation between lipid peroxidation in different brain regions and the severity of lindane-induced seizures in rats.

The aim of this study was to investigate the dynamics of lipid peroxidation and the possible correlation between lipid peroxidation in different brain regions and behavioral manifestations in lindane-induced seizures in rats. Male Wistar rats were divided into the following groups: 1. control, saline-treated group; 2. dimethylsulfoxide (DMSO)-treated group; 3. lindane-treated group (8 mg/kg), intraperitoneally. Animals were sacrificed 0.5 or 4 h after treatment and the malondialdehyde level and superoxide dismutase (SOD) activity were determined in various brain regions spectrophotometrically. Behavioral changes were classified according to the descriptive scale (0--no response, 1--head nodding, lower jaw twitching; 2--myoclonic body jerks, bilateral forelimb clonus with full rearing; 3--progression to generalized clonic convulsions followed by tonic extension of fore- and hind limbs and tail; 4--status epilepticus). A significant rise in the malondialdehyde level was detected in the cerebral cortex, hippocampus, and thalamus of lindane-treated animals 0.5 and 4 h after administration (P < 0.05). SOD activity (total and mitochondrial) was significantly decreased in the hippocampus and the cortex of lindane-treated animals at both time points (P < 0.05). An initial fall in SOD activity was detected in the thalamus 4 h after lindane administration (P < 0.05). A positive correlation between seizure severity and the malondialdehyde level was found in the hippocampus at both time points (P < 0.01). These results suggest that lipid peroxidation may contribute to the neurotoxic effects of lindane in early acute lindane intoxication and that behavioral manifestations correlate with lipid peroxidation in the hippocampus of lindane-treated rats.

Acetylcholinesterase Activity in the Mongolian Gerbil Brain after Acute Poisoning with Aluminum.

The aim of the present study was to evaluate the acetylcholinesterase activity in the brain of adult gerbils (Meriones unguiculatus) treated with aluminum. AlCl3 x 6H2O was given "per os" in the amount of 3.7 g/kg body weight. The animals were killed 24, 48, 72 and 96 hours after the treatment. The activities of acetylholinesterase in the mitochondrial and microsomal fractions of cortex, hippocampus and thalamus as well as plasma levels of aluminum were measured. Acetylcholinesterase activity was significantly reduced in the mitochondrial and microsomal fraction of all investigated structures. Decrease of the enzyme activity was observed in the first 24 hours, and it was most prominent 48 hours after the administration of aluminum in the mitochondrial fractions when the activity of the enzyme was 31%, 29% and 18.9% of the control value, and after 24 hours in the microsomal fractions when the activity of the enzyme was 43%, 48% and 32% of the control value in the cortex, hippocampus and thalamus, respectively. 96 hours after the administration of aluminum the activity of the enzyme was 63%, 57% and 31% of the value in the control group in mitochondrial, and 100%, 80% and 73% of the control value in microsomal fractions in cortex, hippocampus and thalamus. Plasma levels of aluminum were significantly elevated 24 hours after administration of aluminum. After 48 hours the values were doubled in comparison with the control, 72 hours later plasma concentrations of aluminum were decreased, and after 96 hours they reached the value in the control group. We can conclude that a single oral dose (LD50) of aluminum causes the changes in the brain acetylcholinesterase activity. The changes are still present when the aluminum concentration in plasma is normalized.