The influence of tau and inflammation on hippocampal neuron function

In the past AD research has focused on amyloid pathology, using
models such as APP transgenic mice to model the disease, which unfortunately has failed to result in the development of
any successful pharmacological treatments, likely due to the amyloid hypothesis being flawed. More recent literature
indicates the main factor underlying the progression of AD pathology may be Tau hyper-phosphorylation rather than AB.
It seems that the presence of Tau protein is a prerequisite for impairment of cognition in APP Tg mice, suggesting a
predominant role for Tau in impaired neuronal signalling. Also, I am keen to investigate the role that other non-neuronal
cell types might have in AD pathology. During my undergraduate degree I have gained an appreciation for the
importance of non-neuronal cells in the CNS for maintaining tissue homeostasis and potentially for maintaining healthy
cell signalling. The effect of glial impairment in slice culture could be of interest