scholarly journals The NALP3 inflammasome is involved in the innate immune response to amyloid-β

2008 ◽  
Vol 9 (8) ◽  
pp. 857-865 ◽  
Author(s):  
Annett Halle ◽  
Veit Hornung ◽  
Gabor C Petzold ◽  
Cameron R Stewart ◽  
Brian G Monks ◽  
...  
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Amyloid Β ◽  
Innate Immune ◽  
Nalp3 Inflammasome

scholarly journals ApoE facilitates the microglial response to amyloid plaque pathology

2018 ◽  
Vol 215 (4) ◽  
pp. 1047-1058 ◽  
Author(s):  
Jason D. Ulrich ◽  
Tyler K. Ulland ◽  
Thomas E. Mahan ◽  
Sofie Nyström ◽  
K. Peter Nilsson ◽  
...  
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Amyloid Β ◽  
Amyloid Plaque ◽  
Innate Immune ◽  
Fluorescent Imaging ◽  
Amyloid Pathology ◽  
Plaque Deposition ◽  
The Impact ◽  
Deficient Mice

One of the hallmarks of Alzheimer’s disease is the presence of extracellular diffuse and fibrillar plaques predominantly consisting of the amyloid-β (Aβ) peptide. Apolipoprotein E (ApoE) influences the deposition of amyloid pathology through affecting the clearance and aggregation of monomeric Aβ in the brain. In addition to influencing Aβ metabolism, increasing evidence suggests that apoE influences microglial function in neurodegenerative diseases. Here, we characterize the impact that apoE has on amyloid pathology and the innate immune response in APPPS1ΔE9 and APPPS1-21 transgenic mice. We report that Apoe deficiency reduced fibrillar plaque deposition, consistent with previous studies. However, fibrillar plaques in Apoe-deficient mice exhibited a striking reduction in plaque compaction. Hyperspectral fluorescent imaging using luminescent conjugated oligothiophenes identified distinct Aβ morphotypes in Apoe-deficient mice. We also observed a significant reduction in fibrillar plaque–associated microgliosis and activated microglial gene expression in Apoe-deficient mice, along with significant increases in dystrophic neurites around fibrillar plaques. Our results suggest that apoE is critical in stimulating the innate immune response to amyloid pathology.

scholarly journals Altered Relationship between Soluble TREM2 and Inflammatory Markers in Young Adults with Down Syndrome

2019 ◽  
Author(s):  
Grace E. Weber ◽  
Katherine Koenig ◽  
Maria Khrestian ◽  
Yvonne Shao ◽  
Elizabeth D. Tuason ◽  
...  
Keyword(s):  
Immune Response ◽  
Young Adults ◽  
Down Syndrome ◽  
Innate Immune Response ◽  
Exploratory Study ◽  
Inflammatory Markers ◽  
Amyloid Β ◽  
Innate Immune ◽  
Control Group ◽  
The Relationship

AbstractIndividuals with Down syndrome (DS) develop Alzheimer’s disease (AD) - related neuropathology, characterized by amyloid plaques with amyloid β (Aβ) and neurofibrillary tangles with tau accumulation more frequently and at an earlier age than their neurotypical counterparts. Peripheral inflammation and the innate immune response are elevated in DS. Triggering receptor expressed in myeloid cells 2 (TREM2) genetic variants are risk factors for AD and other neurodegenerative diseases. A soluble cleavage product of TREM2 (sTREM2) has been described as elevated in AD cerebrospinal fluid and positively correlates with Aβ and cognitive decline. There is relatively little information about TREM2 in DS. The objective of this study was to examine the relationship between sTREM2 and inflammatory markers in DS, prior to the development of dementia symptoms. Since TREM2 plays a role in the innate immune response and has been associated with dementia, the hypothesis of this exploratory study was that young adults with DS pre-dementia (n=15, mean age 29.5 years) would exhibit a different relationship between sTREM2 and inflammatory markers in plasma, compared to neurotypical, age-matched controls (n=16, mean age 29.6 years). Indeed, young adults with DS had significantly elevated plasma sTREM2 and inflammatory markers. In addition, in young adults with DS, sTREM2 correlated positively with 24 of the measured cytokines, while there were no significant correlations in the control group. Hierarchical clustering of sTREM2 and cytokine concentrations also differed between the group with DS and controls, supporting the hypothesis that its function is altered in people with DS pre-dementia. This exploratory study provides a basis for future studies investigating the relationship between TREM2 and the broader immune response pre-dementia.

Oral Immune Activation by Disgust and Disease-Related Pictures

2015 ◽  
Vol 29 (3) ◽  
pp. 119-129 ◽  
Author(s):  
Richard J. Stevenson ◽  
Deborah Hodgson ◽  
Megan J. Oaten ◽  
Luba Sominsky ◽  
Mehmet Mahmut ◽  
...  
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Innate Immune Response ◽  
Negative Control ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Immune Markers ◽  
Before And After ◽  
Secondary Analyses ◽  
Image Set

Abstract. Both disgust and disease-related images appear able to induce an innate immune response but it is unclear whether these effects are independent or rely upon a common shared factor (e.g., disgust or disease-related cognitions). In this study we directly compared these two inductions using specifically generated sets of images. One set was disease-related but evoked little disgust, while the other set was disgust evoking but with less disease-relatedness. These two image sets were then compared to a third set, a negative control condition. Using a wholly within-subject design, participants viewed one image set per week, and provided saliva samples, before and after each viewing occasion, which were later analyzed for innate immune markers. We found that both the disease related and disgust images, relative to the negative control images, were not able to generate an innate immune response. However, secondary analyses revealed innate immune responses in participants with greater propensity to feel disgust following exposure to disease-related and disgusting images. These findings suggest that disgust images relatively free of disease-related themes, and disease-related images relatively free of disgust may be suboptimal cues for generating an innate immune response. Not only may this explain why disgust propensity mediates these effects, it may also imply a common pathway.

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