Dementia is a broad category of brain diseases. These are characterised by loss of memory, reasoning, and sometimes personality and behaviour changes. The most common form of dementia is Alzheimer's Disease (AD), histopathologically recognised by extracellular plaques of amyloid-13 (AI3) and intracellular inclusions of neurofibrillary tangles composed of hyperphosphorylated tau. Another common form of dementia is Frontotemporal dementia with parkinsonism- linked to chromosome 17 (FTDP-17), associated with hyperphosphorylated tau. Animal models of these diseases are important in furthering the understanding of dementia. Anatomical and pharmacological lesion studies have demonstrated that the perirhinal (PRh) cortex is essential for recognition memory; failure of this particular form of memory is often an early indicator of AD. Moreover, the PRh cortex can express a form of long-term depression (LTD) that is thought to underlie recognition memory. Aβ has been found to cause dendritic degeneration and to disrupt both synaptic plasticity and working memory in the hippocampus. The present study aims to examine LTD in the PRh cortex during acute oligomeric Aβ42 pre-treatment, mimicking early stages of Aβ pathology in AD. Furthermore, the effects of AI3 pretreatment on intrinsic neuronal firing and plasticity were investigated. Aβ profoundly inhibited a form of NMDAR-dependent LTD. AI3 also altered the firing frequency of mAChR-dependent persistent activity, a cellular correlate to working memory. However, Aβ did not alter any intrinsic neuronal properties, suggesting that acute AI3 application preferentially affects synapses. Recognition memory and LTD in the PRh cortex were investigated in a FTDP-17 model mouse, Tg4510. This model overexpresses a mutant hyperphosphorylated Tau and exhibits profound neuron loss alongside behavioural and memory deficits. The present study found that recognition memory is impaired in Tg4510 mice alongside a deficit in mAChR-dependent LTD in the PRh cortex. Donepezil, a cholinesterase inhibitor, can ameliorate the effect of hyperphosphorylated tau on LTD in the PRh cortex. Interestingly, the LTD examined in this 8-10 month old mouse model was found to be dependent on a different mechanism compared to the 4-5 week old mice used previously. These data explore the neurophysiological characteristics of neurons in layer 111111 of the PRh cortex and provide evidence of the deleterious effects of two pathological molecules involved in AD and tauopathies.