No evidence in support of a prodromal respiratory control signature in the TgF344-AD rat model of Alzheimer’s disease

•Respiratory control is well maintained in 8–11 month old TgF344-AD rats.•Diaphragm and genioglossus muscle activities are similar in WT and TgF344-AD rats.•APP C-terminal fragments are elevated in the TgF344-AD brainstem.•No evidence of tau hyperphosphorylation, Aβ accumulation or neuroinflammation in the TgF344-AD brainstem.•No evidence of a prodromal respiratory control signature in the TgF344-AD rat. Alzheimer’s disease (AD) is a progressive neurodegenerative condition disturbing major brain networks, including those pivotal to the motor control of breathing. The aim of this study was to examine respiratory control in the TgF344-AD transgenic rat model of AD. At 8–11 months of age, basal minute ventilation and ventilatory responsiveness to chemostimulation were equivalent in conscious wild-type (WT) and TgF344-AD rats. Under urethane anesthesia, basal diaphragm and genioglossus EMG activities were similar in WT and TgF344-AD rats. The duration of phenylbiguanide-induced apnoea was significantly shorter in TgF344-AD rats compared with WT. Following bilateral cervical vagotomy, diaphragm and genioglossus EMG responsiveness to chemostimulation were intact in TgF344-AD rats. Amyloid precursor protein C-terminal fragments were elevated in the TgF344-AD brainstem, in the absence of amyloid-β accumulation or alterations in tau phosphorylation. Brainstem pro-inflammatory cytokine concentrations were not increased in TgF344-AD rats. We conclude that neural control of breathing is preserved in TgF344-AD rats at this stage of the disease.