Cognitive dysfunction and the neurobiology of ageing in cats.

With improvements in nutrition and veterinary medicine the life expectancy of pet cats is increasing. Accompanying this growing geriatric population there are increasing numbers of cats with signs of apparent senility. A recent study suggests that 28 per cent of pet cats aged 11 to 14 years develop at least one geriatric onset behavioural problem, and this increases to over 50 per cent for cats of 15 years of age or older. While behavioural changes may result from systemic illness, organic brain disease or true behavioural problems, the possibility of age-related cognitive dysfunction is often overlooked. Studies have revealed a number of changes in the brains of geriatric cats that showed signs of cognitive dysfunction, and potential causes include vascular insufficiency leading to hypoxia, increased free radical damage and the deposition of beta-amyloid plaques and/or the modification of other proteins. By recognising the importance of behavioural changes in old cats, investigating them fully for potentially treatable medical conditions, and instigating dietary and environmental modifications to meet their changing needs, we can make the lives of our geriatric cats much more comfortable and rewarding.

Long-term homocysteine exposure induces alterations in spatial learning, hippocampal signalling and synaptic plasticity.

Abnormally high levels of homocysteine (HCY) have been linked to neurodegenerative diseases, but it remains unclear whether this is the cause or effect of degenerative processes. Here, we investigated the effects of prolonged HCY exposure on cognitive abilities and physiological parameters by injecting rats daily with either 20 or 200 mg/kg HCY over a period of up to 14 weeks. Notwithstanding a significant weight reduction in the 200 mg HCY group, HCY-exposed animals did not show a behavioural deficit when tested repeatedly (in weeks 1, 3, 5, 7 and 13) in a reference memory version of the water maze. Unexpectedly, some improvement in repeated reversal learning was observed in HCY exposed animals compared to controls. Pre-treatment with HCY for 3 weeks before water maze training did not uncover any cognitive alterations. Increased plasma concentrations of HCY were revealed only for the 200 mg HCY group after 14 weeks of injections, but no evidence for DNA damage was obtained. Immunocytochemically, HCY was detected in the brain after 14 weeks of treatment (both 20 and 200 mg/kg), but not after 5 weeks. Bidirectional changes in basic synaptic transmission and long-term potentiation of hippocampal CA1 pyramidal cells were observed at 5, 7 and 14 weeks in both HCY groups, indicative of complex, multifactorial time- and concentration-dependent changes. Overall, it is concluded that healthy adult rats are able to cope with continuous exposure to HCY. While HCY affects growth and neuronal excitability, this does not precipitate into an immediate impairment of cognitive function.