Abstract
INTRODUCTION: Alzheimer disease (AD) is a progressive neurodegenerative disease that accounts for 60% of dementia cases worldwide. Despite the lack of concrete information about the prevalence of dysphagia among AD patients, it still significantly impairs their quality of life (QoL). That outcome necessitates more investigations to understand the pathophysiology of this condition and how to manage it. In this study, we examined if AD-associated changes in pharyngeal and tongue muscles could explain dysphagia. METHODS: Fourteen adult male rats were allocated into 2 groups: Group I (control) received distilled water orally, group II (AD) received aluminum chloride (AlCl(3)) (200 mg/kg, per os) and D-galactose (60 mg/kg, subcutaneous) daily for 45 days. Biochemical parameters were conducted, including amyloid beta-peptide (Aβ), histopathological investigation of the hippocampus, tongue, and pharynx, and immune-histochemical expression of brain glial fibrillar acidic protein (GFAP). RESULTS: Our AD model showed marked cognitive impairment, hippocampal oxidative stress, and increased brain Aβ expression (P=0.0003) compared to controls. Dysphagia was confirmed by loss of body weight (P=0.0077) and decreased eating and drinking patterns by 25%-35% in AD versus the control group. Histopathological, immune-histochemical, and biochemical evidence, including increased levels of pharyngeal Aβ (P=0.0017), were detected in AD rats' tongue and pharyngeal muscles. CONCLUSION: Dysphagia in AD can result not only centrally but also due to local involvement of the tongue and pharynx. Further translational studies linking dysphagia to AD pathology will be needed.