Abstract
Due to the aging population, modern society is facing an increasing prevalence of neurological diseases such as Alzheimer’s disease (AD). AD is an age-related chronic neurodegenerative disorder for which no satisfying therapy exists. Understanding the mechanisms underlying the onset of AD is necessary to find targets for protective treatment. There is growing awareness of the essential role of the immune system in the early AD pathology. Amyloidopathy, the main feature of early-stage AD, has a deregulating effect on the immune function. This is reciprocal as the immune system also affects amyloidopathy. It seems that the inflammatory reaction shows a heterogeneous pattern depending on the stage of the disease and the variation between individuals, making not only the target but also the timing of treatment important. The lack of relevant translational animal models that faithfully reproduce clinical and pathogenic features of AD is a major cause of the delay in developing new disease-modifying therapies and their optimal timing of administration. This review describes the communication between amyloidopathy and inflammation and the possibility of using nonhuman primates as a relevant animal model for preclinical AD research.
Highlights
Alzheimer’s disease (AD) is a serious age-related chronic neurodegenerative disorder that is increasingly common due to an aging population
It was believed that astrocytes actively participate in Aβ clearance [33], but stimulation of tumor necrosis factor (TNF)-α and interferon (IFN)-γ in combination with Aβ have been shown to result in the production of Aβ in astrocytes
Increased levels of prostaglandin E2 (PGE2) are found in ageing and in neurodegenerative diseases [57]. These findings indicate a complex heterogeneous immune response that is dependent on the stage of AD
Summary
Alzheimer’s disease (AD) is a serious age-related chronic neurodegenerative disorder that is increasingly common due to an aging population. This raises the possibility that disturbed APP metabolism affects the spread of tau pathologies from cell to cell in AD, and abnormalities in APP metabolism may cause aggregation of tau This is in association with the fact that people with a triplication of chromosome 21, as seen in Down syndrome, overexpress the APP gene that drive AD pathology in these individuals at a young age [14]. The causality of Aβ accumulation and activation of the immune system is a matter of debate, as chronic inflammation is measured prior to the onset of AD and could induce Aβ accumulation by reactive microglial cells and pro-inflammatory cytokine secretion [23,31,32] Because this relationship is difficult to Vaccines 2021, 9, 388 investigate in humans, animal models can be an important link in learning more about the cause and effects.
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
