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Alzheimer’s Disease (AD) leads to progressive memory loss, mood disturbances, and being unable to take care of oneself. For such a severe decrease in quality of life, no current treatments currently halt AD. Major AD theories include unhealthy protein aggregation and dying brain cells, especially the notable “neuronal” type. However, because these explanations have not produced sufficient solutions, we must revise our understanding of AD to more accurately and successfully treat it. Here, summarizing literature in neuroimmunology and biochemistry, it is posited that AD is primarily caused by aging and dysfunction in the brain’s glia, or non-neuronal cells. From recent rodent models and post-mortem investigation of AD patients, studies agree that aging processes naturally accumulate damaging, oxidizing products. This buildup gradually wears down glia; as glia normally support neuronal cells and each other, this further favours accumulation of more damaging oxidants and unhealthy protein aggregation. These aging-dependent processes also create glia subtypes that add to AD pathology; many such subtypes are defined by impaired clearance of protein aggregates, and release molecules that causes pathological inflammation seen in AD. Two major AD glia subtypes are explored: multiple glia subtypes grouped together into a “senescent” label, and a specific “disease-associated” microglia (DAM), or a glia subtype that prematurely kills neuronal cells. As DAM may act as a key switch between pre-symptomatic and clinical AD, modulating these cell types and their induction by aging processes are vital.
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