(PatriotWise.com) — A new study suggests that the mood changes common with Alzheimer’s disease could be partially fueled by inflammation of the brain, Live Science reported.
It is believed that Alzheimer’s is caused by a gradual buildup of the proteins amyloid-beta and tau in the brain, which leads to nerve damage, brain cell death, and symptoms of cognitive decline and mood swings. However, emerging research suggests that brain inflammation may also lead to the development of Alzheimer’s.
In a study published last month in JAMA Network Open, researchers provide what they believe is the first solid evidence that Alzheimer’s neuropsychiatric symptoms are directly linked to immune cells called microglia, which, when activated, cause inflammation in response to disease or injury.
Evidence suggests that when activated, microglia interact with amyloid-beta and tau proteins, which could influence the progression of the disease.
According to the study, researchers found the first evidence that mood swings in Alzheimer’s patients are directly linked to the activation of microglia.
According to a statement from the study’s lead author, University of Pittsburgh post-doctoral researcher Dr. Chrstiano Aguzzoli, symptoms like agitation, anxiety, irritability, and depression are some of the most difficult Alzheimer’s symptoms to treat. The study shows that brain inflammation could be responsible for those neuropsychiatric symptoms, he said.
The researchers recruited 70 subjects with no symptoms of cognitive decline as well as 39 subjects who were either showing early signs of memory loss or dementia caused by Alzheimer’s and assessed if the subjects displayed any mood changes common with Alzheimer’s disease.
The researchers used brain scans to look for signs of microglial activation and an accumulation of the amyloid-beta and tau proteins.
The subjects with cognitive impairment were more likely to have a buildup of the amyloid-beta and tau proteins. However, the subjects with more severe neuropsychiatric symptoms showed a greater level of microglial activation and significant signs of inflammation than subjects with milder neuropsychiatric symptoms.
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