scholarly journals Serum levels of resistin and its relationship with some pro-inflammatory cytokines in a cohort of Egyptian patients with Alzheimer's disease

2020 ◽  
Vol 1 (3-4) ◽  
pp. 100054
Author(s):  
Eman Zaki Azzam ◽  
Dalia Elneily ◽  
Nany Elgayar ◽  
Amr Elfatatry ◽  
Marwa Saad
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Inflammatory Cytokines ◽  
Serum Levels ◽  
Egyptian Patients ◽  
Pro Inflammatory Cytokines

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.

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 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.

Effects of SORL1 Gene on Alzheimer's Disease. Focus on Gender, Neuropsychiatric Symptoms and Pro-Inflammatory Cytokines

2013 ◽  
Vol 10 (2) ◽  
pp. 154-164 ◽  
Author(s):  
Paolo Olgiati ◽  
Antonis Politis ◽  
Diego Albani ◽  
Serena Rodilossi ◽  
Letizia Polito ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Inflammatory Cytokines ◽  
Neuropsychiatric Symptoms ◽  
Sorl1 Gene ◽  
Disease Focus ◽  
Pro Inflammatory Cytokines

Pro-inflammatory cytokines in Alzheimer’s disease

Psychiatriki ◽  
2016 ◽  
Vol 27 (4) ◽  
pp. 264-275 ◽  
Author(s):  
E.C. Stamouli ◽  
◽  
A.M. Politis
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Inflammatory Cytokines ◽  
Pro Inflammatory Cytokines

scholarly journals Immunomodulatory sphingosine-1-phosphates as plasma biomarkers of Alzheimer’s disease and vascular cognitive impairment

2020 ◽  
Vol 12 (1) ◽  
Author(s):  
Xin Ying Chua ◽  
Yuek Ling Chai ◽  
Wee Siong Chew ◽  
Joyce R. Chong ◽  
Hui Li Ang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Cell Line ◽  
Inflammatory Cytokines ◽  
Vascular Cognitive Impairment ◽  
Cerebrovascular Diseases ◽  
Ongoing Research ◽  
Primary Astrocytes ◽  
Pro Inflammatory Cytokines

Abstract Background There has been ongoing research impetus to uncover novel blood-based diagnostic and prognostic biomarkers for Alzheimer’s disease (AD), vascular dementia (VaD), and related cerebrovascular disease (CEVD)-associated conditions within the spectrum of vascular cognitive impairment (VCI). Sphingosine-1-phosphates (S1Ps) are signaling lipids which act on the S1PR family of cognate G-protein-coupled receptors and have been shown to modulate neuroinflammation, a process known to be involved in both neurodegenerative and cerebrovascular diseases. However, the status of peripheral S1P in AD and VCI is at present unclear. Methods We obtained baseline bloods from individuals recruited into an ongoing longitudinal cohort study who had normal cognition (N = 80); cognitive impairment, no dementia (N = 160); AD (N = 113); or VaD (N = 31), along with neuroimaging assessments of cerebrovascular diseases. Plasma samples were processed for the measurements of major S1P species: d16:1, d17:1, d18:0, and d18:1, along with pro-inflammatory cytokines interleukin (IL)-6, IL-8, and tumor necrosis factor (TNF). Furthermore, in vitro effects of S1Ps on cytokine expression were also studied in an astrocytoma cell line and in rodent primary astrocytes. Results Of the S1Ps species measured, only d16:1 S1P was significantly reduced in the plasma of VaD, but not AD, patients, while the d18:1 to d16:1 ratios were increased in all cognitive subgroups (CIND, AD, and VaD). Furthermore, d18:1 to d16:1 ratios correlated with levels of IL-6, IL-8, and TNF. In both primary astrocytes and an astroglial cell line, treatment with d16:1 or d18:1 S1P resulted in the upregulation of mRNA transcripts of pro-inflammatory cytokines, with d18:1 showing a stronger effect than d16:1. Interestingly, co-treatment assays showed that the addition of d16:1 reduced the extent of d18:1-mediated gene expression, indicating that d16:1 may function to “fine-tune” the pro-inflammatory effects of d18:1. Conclusion Taken together, our data suggest that plasma d16:1 S1P may be useful as a diagnostic marker for VCI, while the d18:1 to d16:1 S1P ratio is an index of dysregulated S1P-mediated immunomodulation leading to chronic inflammation-associated neurodegeneration and cerebrovascular damage.

scholarly journals Electroacupuncture Improves M2 Microglia Polarization and Glia Anti-inflammation of Hippocampus in Alzheimer’s Disease

2021 ◽  
Vol 15 ◽  
Author(s):  
Lushuang Xie ◽  
Yi Liu ◽  
Ning Zhang ◽  
Chenyu Li ◽  
Aaron F. Sandhu ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Inflammatory Response ◽  
Inflammatory Cytokines ◽  
Inflammatory Cytokine ◽  
Cytokine Expression ◽  
Tnf Α ◽  
Microglia Polarization ◽  
Anti Inflammatory ◽  
Pro Inflammatory Cytokines

Background: Alzheimer’s disease (AD) is a neurodegenerative disease characterized by loss of recognition and memory. Neuroinflammation plays pivotal roles in the pathology of AD and affects the progression of the disease. Astrocyte and microglia, as main immune executors in the central nervous system (CNS), participate into the inflammatory response in AD. Glia polarize into different phenotypes during neurodegeneration. Pro-inflammatory glia produce cytokines (IL-1β, TNF-α, and IL-6) resulting into debris aggregates and neurotoxicity. Anti-inflammatory phenotypes produce cytokines (IL-4 and IL-10) to release the inflammation. Electroacupuncture is a useful treatment that has been found to slow the neurodegeneration in animals through experimentation and in humans through clinical trials. The aim of this study was to uncover the mechanisms of glia activation, microglia polarization, and cytokine secretion regulated by electroacupuncture as a treatment for AD.Methods: Twenty male Sprague–Dawley (SD) rats were randomly divided into four groups: Control group (Control), Normal saline group (NS), AD group (AD), and Electroacupuncture group (Acupuncture). The AD and Acupuncture groups were bilaterally injected with Aβ1–42 into the CA1 field of the hippocampus. The Acupuncture group received electroacupuncture stimulation on the acupoint “Baihui” (GV20) for 6 days per week for a total of 3 weeks. The Morris Water Maze (MWM) was used to evaluate learning and memory capacity. Immunofluorescence was used to stain GFAP and Iba1 of the DG and CA1 in the hippocampus, which, respectively, expressed the activation of astrocyte and microglia. The M1 microglia marker, inducible nitric oxide synthase (iNOS), and M2 marker Arginase 1 (Arg1) were used to analyze the polarization of microglia. The pro-inflammatory cytokines (IL-1β, TNF-α, and IL-6), anti-inflammatory cytokines (IL-4 and IL-10), and pathway-molecules (p65 and Stat6) were tested to analyze the glia inflammatory response by immunofluorescence and polymerase chain reaction (PCR).Results: The MWM results showed that electroacupuncture improves the escape latency time and the swimming distance of AD rats. The number of GFAP and Iba1 cells significantly increased in AD rats, but electroacupuncture decreased the cells. The iNOS-positive cells were significantly increased in AD, and electroacupuncture decreased the positive cells. Electroacupuncture elevated Arg1-positive cells in AD rats. Electroacupuncture decreased the glia pro-inflammatory cytokine expression and increased the anti-inflammatory cytokine expression in AD rats. Furthermore, electroacupuncture inhibited the NF-κB pathway molecule (p65) while raising the Stat6 pathway molecule (Stat6).Conclusion: These results provide evidence that electroacupuncture improves the recognition abilities and memory of AD rats. Electroacupuncture inhibits the activation of glia and polarizes microglia toward the M2 phenotype. Electroacupuncture decreased the pro-inflammatory cytokines (IL-1β, TNF-α, and IL-6) and increased the anti-inflammatory cytokines (IL-4 and IL-10). Furthermore, electroacupuncture affects the immune responses through inhibition of NF-κB pathway but activation of Stat6 pathway.

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