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.

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.