Related Experiment Video
Updated: Mar 19, 2026
06:52
Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages
Published on: May 21, 2018
11.3K
Inflammasome Involvement in Alzheimer's Disease
1Department of Oral Biology, Faculty of Dentistry, University of Oslo, Oslo, Norway.
Journal of Alzheimer'S Disease : JAD
|June 18, 2016
Summary
Inflammasomes, particularly NLRP3, may drive Alzheimer's disease (AD) pathogenesis. Bacterial infections might influence NLRP3 activity, potentially worsening AD progression and neuroinflammation.
Area of Science:
- Neuroimmunology
- Infectious Disease
- Neurodegeneration
Background:
- Inflammasomes activate inflammatory cytokines and cell death, crucial for innate immunity.
- Alzheimer's disease (AD) involves amyloid-β and tau pathology, with growing evidence for innate immune system involvement.
- Genome-wide association studies highlight inflammatory genes in AD etiology.
Purpose of the Study:
- To review the potential role of inflammasomes, especially NLRP3, in Alzheimer's disease pathogenesis.
- To explore how specific bacterial infections may influence NLRP3 inflammasome activity and AD progression.
Main Methods:
- Literature review focusing on inflammasome function and AD pathology.
- Analysis of the interplay between microbial triggers, innate immunity, and neuroinflammation in AD.
Main Results:
- The NLRP3 inflammasome is implicated in AD pathogenesis, potentially activated by amyloid-β.
- Certain bacteria may evade immune responses and modulate NLRP3 activity, contributing to AD progression.
Conclusions:
- Inflammasomes, particularly NLRP3, are likely contributors to Alzheimer's disease pathology.
- Bacterial infections represent a potential factor influencing NLRP3 inflammasome activity and AD progression, warranting further investigation.
Related Concept Videos
01:26Alzheimer's Disease: Overview
2.0K
Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ...
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ...
2.0K
03:03Amyloid Fibrils
12.8K
Amyloid fibrils are aggregates of misfolded proteins. Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils.
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining,...
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining,...
12.8K
01:22Alzheimer's Disease: Treatment
1.2K
Alzheimer's Disease (AD), a neurodegenerative disorder, is pathologically identified by amyloid plaques and neurofibrillary tangles composed of tau protein. AD pharmacotherapy aims to manage cognitive symptoms, delay disease progression, and treat behavioral symptoms. The treatment is primarily symptomatic and palliative, with no definitive disease-modifying therapy available. Cholinesterase inhibitors, including donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne), are...
1.2K