Investigation of the effect of caffeine on learning dysfunction induced by aluminum or biperiden

The most frequent cause of Dementia, which is a common public health issue, is Alzheimer's Disease. Alzheimer's Disease is characterized by the accumulation of ß-amyloid plaques and the formation of neurofibrillary tangles in various regions of the brain. Many studies have investigated the effects of caffeine on cognitive functions. This study explored the effects of caffeine, an adenosine receptor antagonist, in an experimental Alzheimer's model performed in mice treated with aluminum or biperiden, a selective muscarinic M1 receptor antagonist. For this purpose, the Morris Water Maze test was applied. Additionally, the brain tissues of the subjects were examined histopathologically. In the Morris test, which was repeated four times daily for five days, the control group's time to find the platform decreased starting from the second day compared to the first day. Histopathological examinations in this group did not reveal any cellular damage in the cerebral cortex or ß-amyloid accumulation in the hippocampus. In the biperiden-treated groups, there was no decrease in the time to find the platform. In the aluminum-treated group, a decrease was only observed on the 5th day. Histopathological examinations in the aluminum or biperiden-treated groups revealed ß-amyloid accumulation in the hippocampus and cellular damage in the cortex. In groups treated with caffeine alone or in combination with aluminum or biperiden, no reduction in platform finding time was observed. However, significant reductions in ß-amyloid accumulation and cellular damage were found in the brain tissues of these groups. These findings suggest that not only aluminum but also biperiden causes amyloid accumulation in brain tissues, and that high-dose caffeine use reduces amyloid deposition and cell damage caused by biperiden or aluminum, while impairing learning function. Keywords: Dementia, Alzheimer, aluminium, biperiden, caffein