It has been suggested that inflammatory processes may play a role in the development of Alzheimerâ??s disease (AD), and that nonsteroidal anti-inflammatory drug treatments may provide protection against the onset of AD. In the current study male Wistar rats were trained in two-lever operant chambers under an alternating lever cyclic-ratio ratio (ALCR) schedule. When responding showed no trends, subjects were divided into groups. One group was bilaterally injected into the CA3 area of the hippocampus with 5 Î¼l of aggregated Î²-amyloid (AÎ²) suspension, and one group was bilaterally injected into the CA3 area of the hippocampus with 5 Î¼l of sterile saline. Subgroups were treated twice daily with 0.1 ml (40 mg/kg) ibuprofen administered orally. The results indicated that chronic administration of ibuprofen protected against detrimental behavioural effects following aggregated AÎ² injections. Withdrawal of ibuprofen treatment from aggregated AÎ²-injected subjects produced a decline in behavioural performance to the level of the non-treated aggregated AÎ²-injected group. Ibuprofen treatment reduced the numbers of reactive astrocytes following aggregated AÎ² injection, and withdrawal of ibuprofen resulted in an increase of reactive astrocytes. These results suggest that induced inflammatory processes may play a role in AD, and that ibuprofen treatment may protect against some of the symptoms seen in AD.
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