Newly published research concludes that inflammation in our 40s and 50s might be linked with increased brain shrinkage decades later. The ties between inflammation and dementia grow stronger.
As the population becomes steadily older, the number of people living with dementia is increasing. In 2006, 26.6 million people worldwide had Alzheimer’s disease, which is the most common form of dementia. By 2050, that figure is expected to quadruple. To put that into perspective, that equates to 1 in 85 people.
There are currently drugs available to treat dementia, but they are only able to reduce symptoms. There is no cure.
One of the major problems facing researchers is that dementia takes many years to develop, and, during this development phase, there are often little or no symptoms. This means that dementia is nearly always caught at an advanced stage. It is therefore difficult to work backward in order to understand the exact causes.
Certain risk factors are known — for instance, individuals who have one copy of the apolipoprotein E (ApoE) e4 gene are at an increased risk of Alzheimer’s disease, as are people who smoke and those with high blood pressure and diabetes — but these do not provide the full picture.
One growing area of interest for dementia researchers is inflammation. Some scientists believe that inflammation earlier on in life could set up a cascade of events that, over time, might lead to brain shrinkage and dementia.
Inflammation has been linked to cardiovascular disease, diabetes, and cancer. Its relationship with depression has also recently come to light. If inflammation can have consequences for brain function, it is possible that it could have a long-term impact on the structure of the brain, too.
Previous research has already suggested a link between inflammation in midlife and dementia as an older adult. For example, a study of 1,050 people as part of the Honolulu-Asia Aging Study concluded:
“These data support the view that inflammatory markers may reflect not only peripheral disease, but also cerebral disease mechanisms related to dementia, and that these processes are measurable long before clinical symptoms appear.”
Most recently, researchers from Johns Hopkins University School of Medicine in Baltimore, MD, set up a study to examine this potential relationship. Their findings are due to be published this week in the journal Neurology.
The team — which was led by Keenan Walker, Ph.D. — measured the levels of five biomarkers for inflammation in the blood, such as white blood cell count. Their study included 1,633 participants, who were aged 53, on average. After an average of 24 years, their brains were scanned and they completed a range of memory tests.
When compared with people who showed no increased markers for inflammation, those with three or more elevated levels had 5 percent lower brain volume in areas of the brain associated with Alzheimer’s disease, including the hippocampus.
According to Dr. Walker, one standard deviation increase in overall inflammation score in midlife impacts brain volume decades later to the same extent as having one copy of the ApoE e4 allele.
In fact, each standard deviation increase was linked to a reduction in hippocampal volume of 110 cubic millimeters. Other areas involved in Alzheimer’s were reduced by as much as 532 cubic millimeters.
“These results suggest that inflammation in midlife may be an early contributor to the brain changes that are associated with Alzheimer’s disease and other forms of dementia.”
Keenan Walker, Ph.D.
When the memory tests — which involved the participants memorizing 10 words — were analyzed, the researchers found that those with three or more elevated markers had a significant deficit. Those without markers managed an average of 5.5, and those with increased marker levels remembered just five.
Dr. Walker explains the importance of these findings, saying, “Because the processes that lead to brain cell loss begin decades before people start showing any symptoms, it is vital that we figure out how these processes that happen in middle age affect people many years later.”
The study does have some limitations, though. For instance, the biomarkers were only measured at one point in time, so it was not possible to ascertain whether or not the inflammation was chronic.
However, the findings do match up with other studies in a similar vein. The relationship between inflammation and dementia is slowly being strengthened.