Programme Lead, MSc/MClinDent in Clinical Periodontology, Faculty of Clinical and Biomedical Sciences, School of Dentistry, University of Central Lancashire, Preston PR1 2HE, UK.
I.R.C.C.S. "Santa Lucia" Foundation, Neurology and Neurorehabilitation Unit, Via Ardeatina, 306, 00179 Rome, Italy.
Int J Environ Res Public Health. 2023 Jan 5;20(2):1007. doi: 10.3390/ijerph20021007.
Alzheimer's disease (AD) is a leading neurodegenerative disease with deteriorating cognition as its main clinical sign. In addition to the clinical history, it is characterized by the presence of two neuropathological hallmark lesions; amyloid-beta (Aβ) and neurofibrillary tangles (NFTs), identified in the brain at post-mortem in specific anatomical areas. Recently, it was discovered that NFTs occur initially in the subcortical nuclei, such as the locus coeruleus in the pons, and are said to spread from there to the cerebral cortices and the hippocampus. This contrasts with the prior acceptance of their neuropathology in the enthorinal cortex and the hippocampus. The Braak staging system places the accumulation of phosphorylated tau (p-tau) binding to NFTs in the locus coeruleus and other subcortical nuclei to precede stages I-IV. The locus coeruleus plays diverse psychological and physiological roles within the human body including rapid eye movement sleep disorder, schizophrenia, anxiety, and depression, regulation of sleep-wake cycles, attention, memory, mood, and behavior, which correlates with AD clinical behavior. In addition, the locus coeruleus regulates cardiovascular, respiratory, and gastrointestinal activities, which have only recently been associated with AD by modern day research enabling the wider understanding of AD development via comorbidities and microbial dysbiosis. The focus of this narrative review is to explore the modes of neurodegeneration taking place in the locus coeruleus during the natural aging process of the trigeminal nerve connections from the teeth and microbial dysbiosis, and to postulate a pathogenetic mechanism due to periodontal damage and/or infection focused on .
阿尔茨海默病（AD）是一种主要的神经退行性疾病，以认知能力下降为主要临床特征。除了临床病史外，它还以两种神经病理学特征性病变为特征；β淀粉样蛋白（Aβ）和神经原纤维缠结（NFTs），在特定解剖区域的大脑死后在组织病理学上被识别。最近，人们发现 NFTs 最初发生在下丘脑核，如脑桥中的蓝斑，据说它们从那里传播到大脑皮质和海马体。这与先前接受它们在脑回和海马体中的神经病理学不同。Braak 分期系统将磷酸化 tau（p-tau）与 NFTs 的结合在蓝斑和其他皮质下核中的积累置于 I-IV 期之前。蓝斑在人体中具有多种心理和生理作用，包括快速眼动睡眠障碍、精神分裂症、焦虑和抑郁、睡眠-觉醒周期的调节、注意力、记忆、情绪和行为，这些都与 AD 的临床行为有关。此外，蓝斑调节心血管、呼吸和胃肠道活动，这些活动最近才通过现代研究与 AD 相关联，从而通过合并症和微生物失调更广泛地了解 AD 的发展。本叙述性综述的重点是探讨在三叉神经连接的自然老化过程中蓝斑发生的神经退行性变模式，以及由于牙周损伤和/或感染而导致的发病机制，重点是。
