Alzheimer disease (AD) is a frustrating health disorder agitating millions in this era of modern science and technology. AD is a progressive neurodegenerative disorder that damages the memory and cognitive systems of the body, therefore wrecking normal daily activities as well as the communicative skills of the afflicted person. To this regard special attention is required by our researchers to develop better treatment and by the various political social-assistence agencies to grant more funds and aides to better provide for the patients. Consequently, it is worthwhile to examine the role of anti-acetylcholinesterases in reducing the level of inflammatory markers reported in current literature. As of today, AD patients are treated by acetylcholinesterase inhibitors which prolong cognitive function by increasing synaptic activity. Often, new natural as well as synthetic inhibitors are reported by researchers all around the world although this treatment is only symptomatic and provides modest outcomes to the patients. The recent explanation of the inflammatory pathways involved in AD however, has opened new avenues for researchers to find a cure by thinking from alternative angles that target the cause of the disease rather than the obvious symptoms. To this respect, there are appreciating efforts by various research teams, who are working on expressions of pro-and anti-inflammatory markers in peripheral blood mononuclear cells of AD patients to understand their actual mechanisms. There are several links between inflammation and central nervous system disorders like Alzheimer's, Cancer, Huntington's, Multiple Sclerosis, and Parkinson's while the depth of their relationship depends on the timing and extent of anti- or pro-inflammatory gene expressions.
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