Oxidative stress and pro-inflammatory cytokines may act as one of the signals for regulating microRNAs expression in Alzheimer’s disease

2017 ◽  
Vol 162 ◽  
pp. 63-71 ◽  
Author(s):  
Kedar N. Prasad
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Inflammatory Cytokines ◽  
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

Fruitless Wolfberry-Sprout Extract Rescued Cognitive Deficits and Attenuated Neuropathology in Alzheimer’s Disease Transgenic Mice

2018 ◽  
Vol 15 (9) ◽  
pp. 856-868 ◽  
Author(s):  
Shu-Ying Liu ◽  
Shuai Lu ◽  
Xiao-Lin Yu ◽  
Shi-Gao Yang ◽  
Wen Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Oral Administration ◽  
Inflammatory Cytokines ◽  
Therapeutic Potential ◽  
Dot Blot ◽  
Oxidative Stress Biomarkers ◽  
Object Recognition Test ◽  
Aβ Oligomer

Background: Alzheimer’s disease (AD) is a neurodegenerative disease featured by memory loss, neuroinflammation and oxidative stress. Overproduction or insufficient clearance of Aβ leads to its pathological aggregation and deposition, which is considered the predominant neuropathological hallmark of AD. Therefore, reducing Aβ levels and inhibiting Aβ-induced neurotoxicity are feasible therapeutic strategies for AD treatment. Wolfberry has been traditionally used as a natural antioxidant and anti-aging product. However, whether wolfberry species has therapeutic potential on AD remains unknown. Method: The effects of fruitless wolfberry-sprout extract (FWE) on Aβ fibrillation and fibril disaggregation was measured by thioflavin T fluorescence and transmission electron microscope imaging; Aβ oligomer level was determined by dot-blot; Cell viability and apoptosis was assessed by MTT and TUNEL assay. The levels of Aβ40/42, oxidative stress biomarkers and inflammatory cytokines were detected by corresponding kits. 8-month-old male APP/PS1 mice and their age-matched WT littermates were treated with FWE or vehicle by oral administration (gavage) once a day for 4 weeks. Then the cognitive performance was determined using object recognition test and Y-maze test. The Aβ burden and gliosis was evaluated by immunostaining and immunoblotting, respectively. Results: FWE significantly inhibited Aβ fibrillation and disaggregated the formed Aβ fibrils, lowered Aβ oligomer level and Aβ-induced neuro-cytotoxicity, and attenuated oxidative stress in vitro. Oral administration of FWE remarkably improved cognitive function, reduced Aβ burden, decreased gliosis and inflammatory cytokines release, and ameliorated oxidative stress in the brains of APP/PS1 mice. Conclusion: These findings indicate that FWE is a promising natural agent for AD treatment.

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.

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