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