Inflammatory Factors may Offer Protection in Alzheimer's Disease

Elevated levels of two chemical mediators of inflammation, known as cytokines, are found to be associated with slower cognitive decline in aging adults, as per a study at the Massachusetts General Hospital (MGH) and the Harvard Aging Brain Study (HABS), published in the journal Alzheimer's & Dementia: The Journal of the Alzheimer's Association.

Alzheimer's disease (AD) is a neurodegenerative disease that leads to gradual memory loss and behavioral changes. It is characterized by the formation of beta-amyloid plaques and neurofibrillary tangles in the brain tissues, almost 20 years before the actual symptoms occur. This further leads to the shrinkage of the brain tissue.

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‘Elevated levels of two chemical mediators of inflammation, known as cytokines, are found to be associated with slower cognitive decline in aging adults. Thus inflammatory factors such as IL-12 and IFN-γ may appear as biomarkers to predict future brain health in cognitively normal people. ’

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Various studies have demonstrated the implication of inflammation to Alzheimer's disease (AD). Yet the present study depicts an unusual finding, which could further help identify healthy people who are at risk for the devastating neurological condition before they have symptoms.

Immune system in Alzheimer's disease

Earlier studies have discovered that most of the AD genes have been linked to immune system dysfunction and elevated levels of certain cytokines. However, a similar role of the immune system in the earliest stage of AD was unclear.

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The present study thereby measured the levels of nine cytokines in the blood to further predict the onset of cognitive decline in 298 healthy people (men and women) from HABS, who were between the ages 50 and 90 years.

All the participants underwent positron emission tomography (PET) brain-imaging scans to look for evidence of amyloid-beta and other changes associated with AD, such as formations called tau tangles.

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"We wanted to know why some people have amyloid in their brain and don't seem to be affected, while other people experience cognitive decline," says study co-senior author Jasmeer Chhatwal, MD, Ph.D., a neurologist at MGH and a HABS co-investigator.

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The study found that people who experienced little cognitive decline had a significant burden of amyloid-beta, and high levels of a pro-inflammatory cytokine called interleukin-12 (IL-12), in their brains.

"However, men and women with elevated levels of amyloid declined more if they had a lower value of IL-12," says lead author Hyun-Sik Yang, MD, a neurologist at Brigham and Women's Hospital and a HABS co-investigator.

The fewer tau tangles are associated with high levels of IL-12. And slower cognitive decline correlated with the elevated levels of another pro-inflammatory cytokine, interferon-gamma (IFN-γ).

The study thereby hypothesizes that the highest levels of inflammation-inducing proteins in the blood protected people against cognitive decline. This might serve as an indication that their immune systems were better "primed" to fight infection and amyloid-beta forms as a result of defense against infection in the brain through the formation of a sticky web for engulfing microbial pathogens.

However, this protection ultimately becomes destructive over time by causing damage to the neurons. Thus IL-12 and IFN-γ may appear as biomarkers to predict future brain health in cognitively normal people.

Source-Medindia