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Hypercapnic ventilatory response (HcVR) is increased in a rat model of Alzheimer's disease

Besides the typical cognitive decline, patients with Alzheimer's disease (AD) develop disorders in the respiratory system such as sleep apnea, shortness of breath and arrhythmias. These symptoms are aggravated with progression of the disease. However, the cause and nature of this disturbance are not well understood. Here, we, used an animal model for sporadic Alzheimer's disease (AD) induced by icv injection of streptozotocin (STZ) (2 mg/kg). We measured ventilation (VE) EEG and EMG during normocapnia, hypercapnia and hypoxia. In addition, we performed Western blot for phosphorylated Tau and β‐amyloid peptide (Aβ) in Locus Coeruleus (LC), Retrotrapezoid nucleus, Raphe Bulbar, Botzinger and Hippocampus and evaluated memory and learning acquisition by using the Barnes maze. STZ treatment promoted memory and learning deficits and an increase of 70% the of Aβ in the LC. STZ treated rats presented an increased HcVR during wakefulness (VE: STZ= 2456.7 ± 261.5 vs VE Vehicle= 1677.4 ±141.8 mL. Kg−1. min−1) and sleep (VE: STZ= (2106.9 ± 261.6 vs VE Vehicle= 1724.1 ± 37.4 mL. Kg−1. min−1). Our data suggest that sporadic AD animals present an increased sensitivity to CO2 possibly due an increased Aβ in the LC.