![]() Aβ activates microglia and astrocytes, causing them to clear Aβ via phagocytosis and proteolysis. Aβ monomers are intrinsically disordered and have a propensity to oligomerize and aggregate into Aβ plaques. In the earliest stages of AD, the formation of Aβ occurs due to abnormal cleavage of amyloid precursor protein (APP) by β- and γ-secretases, whereas it is normally cleaved by α- and γ-secretases. The pathogenic hallmarks of AD in the human brain over time. Our goal is to bring attention to potential shared signals presented by the immune system during different conditions that could lead to the development of successful treatments. In this review, the different inflammatory signals associated with AD and its risk factors will be outlined to demonstrate how chronic inflammation may be influencing individual susceptibility to AD. ![]() ![]() Moreover, it is now well accepted that chronic inflammation has an important role in the onset and progression of AD. Although the immune system is one of the body’s key defense mechanisms, chronic inflammation has been increasingly linked with several age-related diseases. Identifying common factors and trends between these conditions could enhance our understanding of AD and lead to the development of more effective treatments. ![]() Although some cases are genetically linked, there are many diseases and lifestyle factors that can lead to an increased risk of developing AD, including traumatic brain injury, diabetes, hypertension, obesity, and other metabolic syndromes, in addition to aging. This has made the disease difficult to characterize and, thus, diagnose. Alzheimer’s disease (AD) is a neurodegenerative disorder, most cases of which lack a clear causative event. ![]()
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