The effect of dietary coconut in tauopathies causing dementia
Alzheimer’s disease (AD) and Frontotemporal dementia (FTD) are the two most common forms of dementia. As tau neuropathology can be exhibited in both AD and FTD they belong to a group of neurodegenerative diseases called tauopathies, where underlying pathology is characterised by increased expression of abnormally hyperphosphorylated protein tau, its deposition and aggregation into neurofibrillary tangles. Despite numerous clinical trials and ongoing research, there are no curative, disease modifying or preventative treatments available for either AD or FTD at present, and their treatments are mainly limited to symptomatic management. Therefore, patients and caregivers have turned to adapting alternative approaches such as specialised diets. Coconut oil, being a naturally occurring ketogenic ingredient that can be easily and cost-effectively integrated into one’s diet have been strongly promoted by the media. However, quality evidence from laboratory-based research or randomised, placebo-controlled clinical trials are lacking. In this study, the cognitive domains of spatial learning and memory were analysed using the Morris Water Maze (MWM) swim path strategies of TAU58/2 mice and wild-type controls who were fed specialised diets consisting of coconut-derived or lard-derived fat compared to control mice fed a standard chow diet. Immunofluorescent staining of post-mortem brain sections of these mice and statistical analysis of staining intensities were performed to determine the extent of tau neuropathology and neuroinflammation in the hippocampus. The results of the MWM swim path analysis revealed that transgenic mice fed with the coconut fat diet displayed significantly higher hippocampal-dependent cognitive behaviour (swim patterns) compared to the other two diet cohorts stipulating that incorporation coconut fat into one's diet may be beneficial in retaining learning and memory in AD and FTD. Although no difference between immunofluorescent staining intensities of antibodies against microglia (IBA1) and astrocytes (GFAP) was observed, the findings of this study indicate that there is a need to explore other avenues regarding neuroinflammation.