Porphyromonas gingivalis 관련 치주질환과 알츠하이머성 치매 간의 기능적 상관관계 연구 Functional Relationship between Porphyromonas Gingivalis-driven Periodontal Disease and Alzheimer's Dementia
- 언어ENG
- URLhttp://db.koreascholar.com/Article/Detail/419343
pp.111-123
Periodontitis, especially in its chronic form, is one of the leading causes of tooth loss, significantly affecting the quality of life in the modern era of aging society. Recent studies have revealed a potential correlation between periodontitis and various systemic diseases, including cardiovascular diseases and Alzheimer’s dementia (AD). With the body of epidemiologic evidence that links these separate disease entities, several lines of hypotheses have been postulated to provide mechanistic understandings that mostly comprises abnormal regulation of immunologic and inflammatory signaling. In this review, we revisit the experimental findings that describe virulence factors derived from Porphyromonas gingivalis, including gingipains and lipopolysaccharides, as well as their roles in the pathophysiology of AD. In addition, we address potential immunologic challenges imposed by this bacterial pathogen contributing to progression of AD.
Ⅰ. INTRODUCTION
Ⅱ. P. gingivalis-induced gingipain as asignificant molecular player to accelerateAlzheimer’s dementia
1. Gingipain as an important exotoxin derivedfrom P. gingivalis
2. Host system damage induced by gingipains
3. Gingipain as a contributing factor toAlzheimer’s dementia
Ⅲ. Expression of pathophysiologic hallmarksof Alzheimer’s dementia influenced bygingipains
1. The β-amyloid plaques as a representativepathophysiologic hallmark of Alzheimer’sdementia
2. Accumulation of the β-amyloid plaquesfacilitated by gingipains
3. Neurofibrillary tangles and its formationinfluenced by gingipains
4. Clinical trials of gingipain inhibitors to treatAlzheimer’s dementia
Ⅳ. Lipopolysaccharide as a significant riskfactor to accelerate Alzheimer’s dementia
1. Lipopolysaccharide as an importantendotoxin derived from P. gingivalis
2. Cellular mechanisms underlyinglipopolysaccharide-induced microglialdamage linked to Alzheimer’s disease
3. A novel hypothesis of LPS-induced myelindamage as a potential link betweenP. gingivalis-derived lipopolysaccharide andAlzheimer’s dementia
Ⅴ. A relationship between immune evasion ofP. gingivalis and Alzheimer’s dementia
1. Immune evasion of infectious pathogensfrom the host innate immunity
2. Complement system as a target of immuneevasion by bacterial pathogens
3. Immune evasion mechanisms of P. gingivalis
4. Evasion of innate immunity by P. gingivalisand Alzheimer’s dementia
Ⅵ. Conclusion
ACKNOWLEDGMENTS
REFERENCES