Inflammation and Immune System Activation in Aging: A Mathematical Approach

Nikas, Jason B.

It is worth noting here that various anti-inflammatory drugs have been used in an effort to slow down the progression of neurodegenerative diseases, such as Alzheimer, with various degrees of success 35, 36 . The magnitude of the neuroinflammatory processes in the case of Alzheimer disease or other neurodegenerative diseases, however, cannot be compared to that of the neuroinflammation in the normal aging process; and by virtue of the same argument, the task of . The F 1 uses 7 of the 36 most significant genes as its input variables. Using the expression value of those 7 genes for a particular subject, the F 1 yields the F 1 score of that subject; and, based on the determined cut-off score of 53.450, the F 1 classifies that subject as young if the F 1 score is , 53.450 or as old if the F 1 score is $ 53.450. As can be seen by the overall performance, the F 1 classified correctly all subjects except one old one [sensitivity 5 (24/25) 5 0.96 and specificity 5 (15/15) 5 1.00]. The mean F 1 score of the Y subjects was 45.028 (top of the blue bar) and their standard deviation (whiskers above or below the top of the blue bar) was 4.721. The mean F 1 score of the O subjects was 64.212 (top of the red bar) and their standard deviation (whiskers above or below the top of the red bar) was 6.514. The significance level was set at a 5 0.001 (two-tailed), and the probability of significance for the F 1 was P 5 4.18 3 10 212 (independent t-Test with T-value 5 9.927). The F 1 is parametrically distributed with respect to both groups. The F 1 scores of all 40 subjects are shown in Supplementary Table 3. www.nature.com/scientificreports SCIENTIFIC REPORTS | 3 : 3254 | DOI: 10.1038/srep03254 halting neuronal cell loss during the course of a neurodegenerative disease cannot be compared to that of restoring synaptic plasticity during the course of the normal aging process. It would stand to reason, therefore, that anti-inflammatory treatment strategies may be more successful and efficacious than those employed against the progression of neurodegenerative diseases. Finally, I should point out that, based on increased evidence over the last twenty years or so, neuroinflammation seems to be the common denominator of normal aging and neurodegenerative diseases, such as Alzheimer. Understanding the causal circumstances under which a chronic, low-level neuroinflammatory process can transition to a major neuroinflammation conducive to neuronal degeneration and death would be of paramount importance. According to the latest evidence 37 , even a single substitution mutation on a single inflammation gene might suffice to trigger that transition in a small percentage of the population.