Conference Publication Details
Mandatory Fields
Lucking, EF;Murphy, KH;Burns, DP;Jaisimha, AV;Barry-Murphy, KJ;Dhaliwal, P;Boland, B;Rae, MG;O'Halloran, KD
RESPIRATORY PHYSIOLOGY & NEUROBIOLOGY
No evidence in support of a prodromal respiratory control signature in the TgF344-AD rat model of Alzheimer's disease
2019
July
Validated
1
Optional Fields
CHRONIC INTERMITTENT HYPOXIA OBSTRUCTIVE SLEEP-APNEA SEROTONIN NEURONS BRAIN TAU NEUROINFLAMMATION INFLAMMATION DYSPHAGIA TAUOPATHY PATHOLOGY
55
67
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-beta 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.
10.1016/j.resp.2018.06.014
Grant Details