1/12/2024 0 Comments For mac download Danger Scavenger![]() Aβ deposition and tau protein are found in different areas of the brain, leading to synaptic dysfunction, mitochondrial damage, activation of microglia, and neuronal death. The neuropathological hallmarks of AD include extracellular Aβ deposits, intracellular neurofibrillary tangles, and marked inflammation. According to the World Health Organization, more than 35 million people have dementia and this number is expected to increase in the coming years. In this review, we discuss the role of several receptors expressed on microglia in Aβ recognition, uptake, and signaling, and their implications for AD pathogenesis.Īlzheimer’s disease (AD) is a neurodegenerative disorder characterized by a progressive decline in cognitive and functional abilities. The mechanisms through which amyloid deposits provoke an inflammatory response are not fully understood, but it is believed that these receptors cooperate in the recognition, internalization, and clearance of Aβ and in cell activation. Aβ activates microglia through a variety of innate immune receptors expressed on these cells. ![]() In AD, microglia play a dual role in disease progression, being essential for clearing Aβ deposits and releasing cytotoxic mediators. Microglia cells are the resident macrophages of the brain and act as the first line of defense in the central nervous system. However, increasing evidence suggests that inflammation also plays a critical role in the pathogenesis of AD. For many years, research has been focused on Aβ accumulation in senile plaques, as these aggregations were perceived as the main cause of the neurodegeneration found in AD. The hallmarks of AD pathogenesis include deposition of amyloid β (Aβ), neurofibrillary tangles, and neuroinflammation. Alzheimer’s disease (AD) is a major public health problem with substantial economic and social impacts around the world.
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