Here researchers add more evidence to the existing stack of studies linking inflammation to the pace of neurodegeneration, with a focus on white matter damage in the brain in this case. Like raised blood pressure, inflammation is a mediating mechanism that transforms the low-level molecular damage at the root of aging into high-level organ dysfunction and structural damage throughout the body. Chronic inflammation is one of the major reasons why excess visceral fat tissue and exposure to particulates such as smoke are so harmful to long term health. Even the healthy and trim amongst us are faced with the steady rise of inflammation with age, driven by processes such as the accumulation of senescent cells and their inflammatory signals, and the progressive dysfunction of the immune system that is known as inflammaging. The more that can be done to keep chronic inflammation at bay, the better off we are.
"We found that individuals who had an increase in inflammation during midlife that was maintained from mid to late life have greater abnormalities in the brain's white matter structure, as measured with MRI scans. This suggests to us that inflammation may have to be chronic, rather than temporary, to have an adverse effect on important aspects of the brain's structure necessary for cognitive function." Researchers have long gathered evidence that chronic inflammation and the biochemicals associated with it may damage the brain. C-reactive protein, an inflammatory factor made in the liver, for example, already has become a marker for chemical damage to heart and blood vessel tissue indicative of heart attack. So far, however, studies linking inflammation to brain abnormalities have not looked at these factors and features over an extended period of time in the same population.
In the new study, researchers took data from the atherosclerosis risk in communities (ARIC) study that looked at brain structure and integrity, as well as a marker of inflammation over a 21-year period spanning middle age to late life. Specifically, the investigators focused on and compared data on 1,532 participants recruited from 1987 to 1989. At the final visit, participants were an average age of 76. Over the course of the ARIC study, each participant had five visits with study coordinators, averaging every three years. At the last visit, each participant underwent an MRI of their brain to examine evidence of damage to so-called white matter - the part of the brain responsible for transmitting messages. Damaged white matter appears superwhite on a scan, similar to overexposure on a photograph, and was measured using an automated program.
At visits 2, 4 and 5, the researchers took blood samples to measure for high-sensitivity C-reactive protein, a standard measure of inflammation throughout the body. Those with levels below 3 milligrams per liter were considered to have low inflammation, whereas those with 3 or more milligrams per liter of C-reactive protein were considered to have elevated inflammation. Even after adjusting for demographics and cardiovascular disease risk, the researchers found that the 90 people who transitioned from low to persistently elevated C-reactive protein during midlife, indicating increasing inflammation, showed the greatest damage to the white matter in the brain. Because their findings overall showed that increasing and chronic inflammation were associated with the most damage to white matter, there is more reason to infer a cause and effect relationship between growing and persistent inflammation and evidence of dementia.