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Dysregulation of Porphyromonas gingivalis Agmatine Deiminase Expression in Alzheimer’s Disease

牙龈卟啉单胞菌 胍丁胺 牙周炎 唾液 慢性牙周炎 医学 四氢生物蝶呤 口腔微生物群 免疫学 内科学 疾病 生物 腐胺 生物化学 一氧化氮合酶 一氧化氮
作者
Asma Hamdi,Sana Baroudi,Alya Gharbi,Wafa Babay,Ahmed Baligh Laaribi,Imène Kacem,Saloua Mrabet,Inès Zidi,Naouel Klibi,Riadh Gouider,Hadda‐Imene Ouzari
出处
期刊:Current Alzheimer Research [Bentham Science Publishers]
卷期号:21 (4): 232-241
标识
DOI:10.2174/0115672050327009240808103542
摘要

Background: Alzheimer’s disease (AD) is the most prevalent neurodegenerative disorder, with a significant burden on global health. AD is characterized by a progressive cognitive decline and memory loss. Emerging research suggests a potential link between periodontitis, specifically the presence of oral bacteria such as Porphyromonas gingivalis (P. gingivalis), and AD progression. P. gingivalis produces an enzyme, Agmatine deiminase (AgD), which converts agmatine to N-carbamoyl putrescine (NCP), serving as a precursor to essential polyamines. Recent studies have confirmed the correlation between disruptions in polyamine metabolism and cognitive impairment. Objective: This study aims to investigate the dysregulation of P. gingivalis Agmatine deiminase (PgAgD) in the context of AD. Methods: Saliva samples were collected from a total of 54 individuals, including 27 AD patients and 27 healthy controls. The expression of the PgAgD gene was analyzed using quantitative Real-- Time PCR. Results: The results showed a significant decrease in PgAgD gene expression in the saliva samples of AD patients compared to healthy controls. This downregulation was found in AD patients with advanced stages of periodontitis. Additionally, a correlation was observed between the decrease in PgAgD expression and the 30-item Mini-Mental State Examination (MMSE) score. Conclusion: These findings suggest that measuring PgAgD expression in saliva could be a noninvasive tool for monitoring AD progression and aid in the early diagnosis of patients with periodontitis. Further research is needed to validate our results and explore the underlying mechanisms linking periodontitis, PgAgD expression, and AD pathophysiology.
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