Inflammation and Alzheimer’s disease —Akiyama 2000

This is an audio summary of the article "Inflammation and Alzheimer’s disease" by Akiyama in 2000. The Alzheimer's disease (AD) brain exhibits inflammation in pathologically sensitive areas with the full complexity of peripheral local inflammatory responses. Inflammation is often sparked in the periphery by degenerating tissue and the formation of extremely insoluble aberrant materials. Similar to this, in the AD brain, inflammatory stimuli include injured neurons, neurites, deposits of the very insoluble amyloid peptide, and neurofibrillary tangles. Local elevation of complement, cytokines, acute phase reactants, and other inflammatory mediators is persistent, distinct, and micro-localized since these stimuli are present from early preclinical to terminal stages of AD. Direct and incidental damage from AD inflammatory mechanisms over a long period of time is likely to greatly aggravate the pathogenic processes that give birth to it. Therefore, it is clear from animal models and early clinical research that AD inflammation plays a key role in the etiology of AD. It should be feasible to create anti-inflammatory strategies that, while they might not be able to cure AD, will probably help reduce the course or postpone the onset of this dreadful condition by better understanding AD's inflammatory and immunoregulatory mechanisms. This is the end of this informational audio track on "Inflammation and Alzheimer’s disease" by Akiyama.

Inflammation and Alzheimer’s disease. (2000, June 15). Inflammation and Alzheimer’s Disease - ScienceDirect. https://doi.org/10.1016/S0197-4580(00)00124-X