In the past, researchers have noted an association between neuroinflammation (inflammation of nervous system tissue) and Alzheimer’s disease. However, researchers often believed that neuroinflammation was more of a result of the disease than it was anything else. According to Medical XPress, this perspective may be changing. In research published in Nature Medicine, a research team from the University of Pittsburgh School of Medicine highlights how neuroinflammation is actually an upstream driver of Alzheimer’s disease development.

Neuroinflammation

To understand this, you must first understand what neuroinflammation actually is. According to a separate and unrelated article published in the Journal of Neurochemistry, neuroinflammation is:

an inflammatory response within the brain or spinal cord…mediated by the production of cytokines, chemokines, reactive oxygen species, and secondary messengers. These mediators are produced by resident CNS glia (microglia and astrocytes), endothelial cells, and peripherally derived immune cells.

Dr. Tharick Pascoal, MD, PhD, one of the lead authors of the Nature Medicine article, explained that this research began as a way to provide better care and outcomes for patients with Alzheimer’s disease. He and his team wanted to understand how amyloid plaques and tau tangles began to accumulate. Although animal studies have shown that microglial activation plays a role, this had not yet been seen in human patients. 

Within this study, the researchers first explored the brains of patients with Alzheimer’s disease, compared to healthy brains, through live imaging. Findings from the study include:

• Neuroinflammation is more common in older individuals than younger individuals, regardless of disease status (“healthy” vs. Alzheimer’s disease). 
• However, neuroinflammation is also seen at a much greater level in those with Alzheimer’s disease and dementia.
• Within this study, researchers used bioinformatics to definitively link microglial activation with the accumulation of amyloid plaques and tau tangles. As a result, researchers highlighted how neuroinflammation caused this process to begin, resulting in Alzheimer’s disease development.

Thus, moving forward, researchers believe that finding ways to target neuroinflammation as a therapeutic option could prevent microglial activation from occurring, thus preventing Alzheimer’s disease from developing or progressing. 

Alzheimer’s Disease (AD)

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder, characterized by brain cell death and degeneration. In the past, doctors have denoted the cause of AD as being a mixture of environmental and lifestyle factors, as well as genetics. Additional risk factors include being female, being older (65+), having a family history of AD, having past head trauma, or having poor sleeping or exercise patterns. AD occurs in stages, with patients being significantly less independent in later stages. Symptoms include:

• Progressively worsening memory loss
• Malnutrition or dehydration
• Frequent falls or fractures
• Appetite loss
• Jumbled speech
• Changes in behavior and personality
• Difficulty making judgments, decisions, or completing familiar tasks
• Loss of preserved skills
• Confusion, forgetfulness, or disorientation