scholarly journals Alzheimer's disease and periodontitis - an elusive link

2014 ◽  
Vol 60 (2) ◽  
pp. 173-180 ◽  
Author(s):  
Abhijit N. Gurav
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Inflammatory Cytokines ◽  
Critical Role ◽  
Anaerobic Bacteria ◽  
Systemic Infection ◽  
Low Grade ◽  
Inflammatory Status ◽  
Pro Inflammatory Cytokines

Alzheimer's disease is the preeminent cause and commonest form of dementia. It is clinically characterized by a progressive descent in the cognitive function, which commences with deterioration in memory. The exact etiology and pathophysiologic mechanism of Alzheimer's disease is still not fully understood. However it is hypothesized that, neuroinflammation plays a critical role in the pathogenesis of Alzheimer's disease. Alzheimer's disease is marked by salient inflammatory features, characterized by microglial activation and escalation in the levels of pro-inflammatory cytokines in the affected regions. Studies have suggested a probable role of systemic infection conducing to inflammatory status of the central nervous system. Periodontitis is common oral infection affiliated with gram negative, anaerobic bacteria, capable of orchestrating localized and systemic infections in the subject. Periodontitis is known to elicit a "low grade systemic inflammation" by release of pro-inflammatory cytokines into systemic circulation. This review elucidates the possible role of periodontitis in exacerbating Alzheimer's disease. Periodontitis may bear the potential to affect the onset and progression of Alzheimer's disease. Periodontitis shares the two important features of Alzheimer's disease namely oxidative damage and inflammation, which are exhibited in the brain pathology of Alzheimer's disease. Periodontitis can be treated and hence it is a modifiable risk factor for Alzheimer's disease.

scholarly journals Role of Pro-Inflammatory Cytokines and Vitamin D in Probable Alzheimer's Disease with Depression

2017 ◽  
Vol 8 (3) ◽  
pp. 267 ◽  
Author(s):  
Anindita Banerjee ◽  
Vineet Kumar Khemka ◽  
Debashree Roy ◽  
Aparajita Dhar ◽  
Tapan Kumar Sinha Roy ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Vitamin D ◽  
Inflammatory Cytokines ◽  
Pro Inflammatory Cytokines

TLR4 Gene Expression and Pro-Inflammatory Cytokines in Alzheimer’s Disease and in Response to Hippocampal Deafferentation in Rodents

2018 ◽  
Vol 63 (4) ◽  
pp. 1547-1556 ◽  
Author(s):  
Justin Miron ◽  
Cynthia Picard ◽  
Josée Frappier ◽  
Doris Dea ◽  
Louise Théroux ◽  
...  
Keyword(s):  
Gene Expression ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Inflammatory Cytokines ◽  
Tlr4 Gene ◽  
Pro Inflammatory Cytokines

scholarly journals Microglial ApoD Induced NLRC4 Inflammasome Activation Promotes Alzheimer’s Disease Progression

2021 ◽  
Author(s):  
Yaliang Yu ◽  
Jianzhou Lv ◽  
Dan Ma ◽  
Ya Han ◽  
Yaheng Zhang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Critical Role ◽  
Microglia Activation ◽  
Inflammatory Factors ◽  
Inflammasome Activation ◽  
Cellular Interactions ◽  
Brain Functions ◽  
Chronic Neuroinflammation

Abstract Alzheimer’s disease (AD) is a progressive neurodegenerative disease with no effective therapies. It’s well-known that chronic neuroinflammation plays a critical role in the onset and progression of AD. Proper neuronal-microglial interactions are essential for brain functions. However, as the main existence of immune cells, determining the role of microglia in Alzheimer’s neuroinflammation and the associated molecular basis has been challenging. Herein, the inflammatory factors in the sera of AD patients were detected and the association with microglia activation was analyzed. The mechanism regarding the microglial inflammation was investigated. The IL6 and TNF-α were found to be significantly increased in the AD stage. Further analysis revealed microglia were extensively activated in AD cerebra releasing mounts of cytokines to impair the neural stem cells (NSCs) function. Moreover, ApoD induced NLRC4 inflammasome was activated in microglia, which gave rise to the proinflammatory phenotype. Targeting the microglial ApoD promoted NSCs self-renewal and inhibited neuron apoptosis. These findings demonstrate the critical role of ApoD in microglial inflammasome activation, and for the first time reveal that microglia-induced inflammation suppresses neuronal proliferation. Our studies establish the cellular basis for microglia activation in AD progression, and shed lights on cellular interactions important for AD treatment.

scholarly journals COVID-19 and Obesity: Role of Ectopic Visceral and Epicardial Adipose Tissues in Myocardial Injury

2021 ◽  
Vol 12 ◽  
Author(s):  
Adèle Lasbleiz ◽  
Bénédicte Gaborit ◽  
Astrid Soghomonian ◽  
Axel Bartoli ◽  
Patricia Ancel ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Intensive Care ◽  
Inflammatory Cytokines ◽  
Visceral Adipose Tissue ◽  
Cardiovascular Events ◽  
Low Grade ◽  
Viral Spread ◽  
Visceral Adipose ◽  
Pro Inflammatory Cytokines

In March 2020, the WHO declared coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a global pandemic. Obesity was soon identified as a risk factor for poor prognosis, with an increased risk of intensive care admissions and mechanical ventilation, but also of adverse cardiovascular events. Obesity is associated with adipose tissue, chronic low-grade inflammation, and immune dysregulation with hypertrophy and hyperplasia of adipocytes and overexpression of pro-inflammatory cytokines. However, to implement appropriate therapeutic strategies, exact mechanisms must be clarified. The role of white visceral adipose tissue, increased in individuals with obesity, seems important, as a viral reservoir for SARS-CoV-2 via angiotensin-converting enzyme 2 (ACE2) receptors. After infection of host cells, the activation of pro-inflammatory cytokines creates a setting conducive to the “cytokine storm” and macrophage activation syndrome associated with progression to acute respiratory distress syndrome. In obesity, systemic viral spread, entry, and prolonged viral shedding in already inflamed adipose tissue may spur immune responses and subsequent amplification of a cytokine cascade, causing worse outcomes. More precisely, visceral adipose tissue, more than subcutaneous fat, could predict intensive care admission; and lower density of epicardial adipose tissue (EAT) could be associated with worse outcome. EAT, an ectopic adipose tissue that surrounds the myocardium, could fuel COVID-19-induced cardiac injury and myocarditis, and extensive pneumopathy, by strong expression of inflammatory mediators that could diffuse paracrinally through the vascular wall. The purpose of this review is to ascertain what mechanisms may be involved in unfavorable prognosis among COVID-19 patients with obesity, especially cardiovascular events, emphasizing the harmful role of excess ectopic adipose tissue, particularly EAT.

scholarly journals Associations Between Oral Health Status, Perceived Stress, and Neuropsychiatric Symptoms Among Community Individuals With Alzheimer's Disease: A Mediation Analysis

2022 ◽  
Vol 13 ◽  
Author(s):  
Bing Yang ◽  
Binbin Tao ◽  
Qianyu Yin ◽  
Zhaowu Chai ◽  
Ling Xu ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Oral Health ◽  
Health Behavior ◽  
Inflammatory Cytokines ◽  
Perceived Stress ◽  
Neuropsychiatric Symptoms ◽  
Oral Health Behavior ◽  
Health Related ◽  
Pro Inflammatory Cytokines

Community individuals with Alzheimer's disease (AD) experience oral disease alongside neuropsychiatric symptoms (NPS) with disease progression. Despite growing evidence for the link between oral health and cognitive status, few studies have investigated the associations between oral health and NPS, especially based on individuals' experience of AD. The primary aim of this study was to examine (a) the difference in oral health-related stressors among individuals with AD, mild cognitive impairment (MCI), and subjective cognitive decline (SCD); and (b) the associations of these stressors with NPS under the framework of the stress process model (SPM). A cross-sectional study was conducted among individuals diagnosed with AD (n = 35), MCI (n = 36) or SCD (n = 35), matched for age, sex education, and body mass index (BMI). Multiple regression and mediation model analyses were performed to explore predictors and their relationships with NPS based on the SPM. Data collection comprised four sections: (a) individual context; (b) oral health-related stressors, including dental caries, periodontal status, oral hygiene, the geriatric oral health assessment index (GOHAI), oral salivary microbiota, pro-inflammatory cytokines, and oral health behavior; (c) subjective stressors (i.e., perceived stress [PS]); and (d) NPS. Decayed, missing, and filled teeth (DMFT), missing teeth (MT), loss of attachment (LoA), plaque index (PLI), PS, oral health behavior, GOHAI, pro-inflammatory cytokines, and salivary bacterial composition were significantly different among the three groups; these parameters were poorer in the AD group than SCD and/or MCI group. LoA, PLI, PS, and pain or discomfort in the GOHAI were directly associated with NPS. PLI, LoA, and psychosocial function in the GOHAI indirectly affected NPS, and this relationship was mediated by PS. Individuals with AD reported greater oral health-related stressors. This study identifies direct and indirect associations linking oral health-related stressors and PS with NPS in individuals with AD. Our findings suggest that targeted dental care and oral-related stressor control may be valuable for managing NPS.

scholarly journals New Insights on the Role of Manganese in Alzheimer’s Disease and Parkinson’s Disease

2019 ◽  
Vol 16 (19) ◽  
pp. 3546 ◽  
Author(s):  
Airton Cunha Martins ◽  
Patricia Morcillo ◽  
Omamuyovwi Meashack Ijomone ◽  
Vivek Venkataramani ◽  
Fiona Edith Harrison ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Parkinson’S Disease ◽  
Alzheimer's Disease ◽  
Parkinson's Disease ◽  
Critical Role ◽  
Essential Trace Element ◽  
Neuronal Function ◽  
Therapy Options ◽  
Physiological Processes

Manganese (Mn) is an essential trace element that is naturally found in the environment and is necessary as a cofactor for many enzymes and is important in several physiological processes that support development, growth, and neuronal function. However, overexposure to Mn may induce neurotoxicity and may contribute to the development of Alzheimer’s disease (AD) and Parkinson’s disease (PD). The present review aims to provide new insights into the involvement of Mn in the etiology of AD and PD. Here, we discuss the critical role of Mn in the etiology of these disorders and provide a summary of the proposed mechanisms underlying Mn-induced neurodegeneration. In addition, we review some new therapy options for AD and PD related to Mn overload.

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