User:Jlw17e/sandbox

The page I am editing is Neuroinflammation, the section on The Role in Neurodegenerative Disease. The section is not up to date with the latest research and needs to be edited to be more thorough. I am specifically working on the paragraph on Alzheimer's Disease. The last sentence in this paragraph had [needed citation], so I found a recent citation to support that sentence and added it. I also moved some sentences around and changed the wording to make the paragraph flow better and make it less choppy.

Alzheimer's Disease[edit source] Jlw17e edits
Alzheimer's disease (AD) has historically been characterized by two major hallmarks: neurofibrillary tangles and amyloid-beta plaques. Neurofibrillary tangles are insoluble aggregates of tau proteins, and amyloid-beta plaques are extracellular deposits of the amyloid-beta protein. Current understanding leads scientists to believe that AD pathology goes beyond these two typical hallmarks. Recent research suggests that a significant portion of neurodegeneration in Alzheimer's is due to neuroinflammation. Microglia and astrocytes are two cell types that are involved in inflammation in AD. Activated microglia are seen in abundance in post-mortem AD brains. Current thought is that in the presence of inflammatory cytokine-activated microglia cannot phagocytoseamyloid-beta, which may contribute to plaque accumulation as opposed to clearance. Additionally, the inflammatory cytokine IL-1β is upregulated in AD and is associated with decreases of synaptophysin and consequent synaptic loss. Further evidence that inflammation is associated with disease progression in AD is that persons that take non-steroidal anti-inflammatory drugs (NSAIDs) regularly have been associated with reduced AD later in life.