Potential anti neuro-inflammatory effect of BioCen-128 in animal models of dementia.

BACKGROUND: BioCen-128 is a new active pharmaceutical ingredient composed of a specific bovine thymic fraction of a polypeptide nature. Positive results of similar thymus extracts have been shown to be effective in delaying the processes associated with aging, immunosenescence and Alzheimer's disease (AD), where the inflammation plays an important role. Because of the anti-inflammatory potential of BioCen-128, the aim of this study was to evaluate the granuloma model induced by a cotton wool implantation and the model induced by intracerebroventricular (ICV) administration of streptozotocin (STZ). METHOD: The experiment was carried out using male OF-1cenp mice weighing 20 ± 2 g. RESULTS: Mice administered BioCen-128 in via the IP route at 5, 10 and 20 mg/kg of corporal weigh showed a decrease in the wet and dry weights of the granuloma, providing evidence of a systemic anti-inflammatory effect. In the ICV model of STZ, the administration of BioCen-128 improved cognitive function. CONCLUSION: These responses suggested an anti-neuroinflammatory effect explainable by the action of thymosin ß4 and thymosin alfa proteins. The results suggested that BioCen-128 could be used in the prevention and treatment of some diseases, for example AD, where neuroinflammation is one of the biological events that take place.

Characterization of aged male BALB/ccenp mice as a model of dementia.

Dementia is defined as cognitive impairment in more than one cognitive area and leads to an abnormal degree of impairment in the ability to remember past events. Among mice models of dementia the most used strains are SAMP8 and C57BL/6. There is no reference to characterizing a model of dementia in naturally aged mice of the BALB/c strain, or to the minimum age at which these animals can be used. The aim of this study was the characterization of aged male BALB/ccenp mice as a model of dementia from the evaluation of behavioural, pathological and biochemical markers. One hundred and twenty mice were used and 10 of these were analysed from 8 to 9 months of age, and every 4 months, in a comparative way to young control animals from 4 to 5 months. At the age of 12-13 months there was cognitive impairment in the animals from the Y-maze and object recognition tests and this impairment was maintained at 16-17 months of age. An increase in oxidative damage to proteins in the brains of aged animals was also found in relation to young animals; as well as a decrease in the concentration of triglycerides. At the age of 16-17 months, a significant decrease in the size of the thymus and brain was obtained. We consider that it's a very useful option to use animals 12-13 months of age where there are symptoms of cognitive deficiency, histopathological and biochemical elements characteristic of dementia.

Age-Related Changes in the Behavior of Apolipoprotein E Knockout Mice.

The knockout mouse model, B6.129P2-Apoetm1Unc is homozygotic for the Apolipoprotein E (ApoE) deletion; thus, it is capable of developing hyperlipidemia and atherosclerosis but ApoE is also a lipid-transport protein abundantly expressed in most neurons in the central nervous system, so these animals could also be models of neurodegenerative diseases. The aim of this study was to determine age-related changes in spontaneous behavior and in learning and memory of Apolipoprotein E knockout mice. Spontaneous behavioral measurements included sleeping pattern, motor coordination and balance by rotarod and open field activity, whereas learning and memory tests included forced alternation in Y-maze, novel object recognition and passive avoidance conditioning. Significant behavioral differences between aged knockout mice and age-matched wild type strain, C57Bl/6 were found in all the behavioral tests, except for the rotarod test. Genetically' modified mice exhibited less huddling contact during sleeping, decreased locomotor activity in novel environments and in learning and memory deficits. These results are consistent with the cognitive impairment and memory loss seen as the earliest clinical symptoms in neurodegenerative disorders such as Alzheimer's disease. The ApoE knockout mice might therefore be an appropriate model for studying the underlying mechanisms involved in behavioral changes caused by neurodegenerative diseases as well as for evaluating new therapies for these pathologies.

Comparison of the Response of Male BALB/c and C57BL/6 Mice in Behavioral Tasks to Evaluate Cognitive Function.

To evaluate several cognitive parameters during the execution of behavioral tasks assessing cognitive function in laboratory animals, the parameters are reported within a range. This situation entails that each laboratory must establish the conditions under which the behavioral task to evaluate the cognitive function can be carried out. C57BL/6 and BALB/c inbred strains are used more often in behavioral studies relating to anxiety, stress, fear and cognitive function. The aim of this work was to compare the behavioral response of mice of the strains BALB/c and C57BL/6 to evaluate memory and learning as cognitive functions. Young male mice, 7-8 weeks of age, from each strain were used. Y maze, object recognition and passive avoidance tasks were performed. Both strains of mice showed differences in the response to the passive avoidance and Y maze task. This study advances knowledge about the baseline behavior of laboratory mice strains and their response during the experimental procedures, which are due to the treatment, genetic influence, procedural differences, genetic background variance, or any combination of these elements.

Influence of several sources and amounts of iron on DNA, lipid and protein oxidative damage during anaemia recovery.

The study was designed to assess the effect of several Fe amounts and sources on haematological parameters, DNA, lipid and protein oxidative damage during the course of Fe-deficiency anaemia recovery. Peripheral DNA damage was assessed using an alkaline comet assay. The brain, liver, erythrocyte and duodenal mucosa lipid peroxidation and protein damage were assessed in control and anaemic rats after Fe repletion with three different sources (FeSO4, haem Fe, and FeSO4 + haem Fe) and amounts (45, 12, and 31 mg Fe/kg diet) of Fe: F diet, H diet or C diet, respectively. After supplying the diets, the haematological parameters studied were recovered; being remarkable is the haemoglobin increase. The DNA damage was lower in rats with the H diet, as revealed by the percentage of DNA in head, tail and Olive tail moment compared in rats with the F (P < 0.001) and C (P < 0.05) diets. Lipid peroxidation was similar in all the tissues, except in the duodenal mucosa which was lower with H and C diets (P < 0.001). The animals fed with C diet showed lower oxidative protein damage in the duodenal mucosa (P < 0.001) and was also lower in the liver and erythrocytes for H and C diets (P < 0.001). No differences were found in the brain under our experimental conditions. In conclusion, Fe supplementation with low doses of haem Fe or combined forms of non-haem and haem Fe (FeSO4 + haem) are efficient in restoring the impaired haematological parameters and prevent the evoked oxidative stress associated with Fe supplements.