July 14, 2024

Brain Inflammation Found to be the Cause of Irritability, Agitation, and Anxiety in Alzheimer’s Patients, According to Study

New research suggests that common neuropsychiatric symptoms seen in patients with Alzheimer’s disease, such as irritability, agitation, and anxiety, may stem from brain inflammation rather than the presence of amyloid and tau proteins. This finding adds to the mounting evidence regarding the role of neuroinflammation in the progression of Alzheimer’s and opens up new opportunities for the development of therapies to target the neurological symptoms of the disease.

These neuropsychiatric symptoms are notoriously difficult to treat in patients with Alzheimer’s. They are challenging to control, have no identifiable cause, and make it burdensome for families to care for their loved ones without substantial support. Dr. Cristiano Aguzzoli, the lead author of the study, explains that this research is the first to suggest that brain inflammation could be the culprit behind these symptoms.

Earlier in 2023, scientists from the University of Pittsburgh discovered that excessive brain inflammation is crucial for the initiation of the disease and can predict whether cognitively unimpaired elderly individuals are at a higher risk of developing Alzheimer’s symptoms. Their earlier study hinted at the significance of neuroinflammation in the pathological cascade associated with other key players in Alzheimer’s, including amyloid beta and tau.

The new findings provide strong evidence that brain inflammation directly causes the neuropsychiatric symptoms frequently observed in Alzheimer’s-associated dementias.

For this study, the researchers examined 109 elderly individuals, most of whom did not have cognitive impairments. However, the majority of them tested positive for amyloid and tau proteins.

By assessing levels of neuroinflammation, amyloid beta, and tau through brain imaging and comparing the results with clinical assessments of the severity of neuropsychiatric symptoms, the scientists found a significant association between microglial activation (a key indicator of inflammation) and various neuropsychiatric symptoms, including disturbed sleep and agitation. While the levels of amyloid and tau alone were predictive of these symptoms, neuroinflammation appeared to have an additional impact.

Neuroinflammation was particularly strongly linked to rapid mood swings, from calm to tears or anger, reported by caregivers or family members. This is a common symptom of Alzheimer’s. Individuals whose caregivers experienced higher levels of distress when caring for them also had greater levels of brain inflammation.

This study contributes to the growing body of evidence supporting the role of brain inflammation in the early stages of Alzheimer’s progression when symptoms like excessive irritability tend to manifest. It also suggests that clinical trials targeting neuroinflammation as a preventive therapy for Alzheimer’s could monitor neuropsychiatric symptoms as a way of measuring the effectiveness of the treatment.

On the other hand, drugs specifically designed to target neuroinflammation may help reduce the severity of neuropsychiatric symptoms and alleviate some of the psychological burden experienced by caregivers, thus improving support for patients. Additionally, since both neuroinflammation and neuropsychological abnormalities are observed in other types of dementia, such as Parkinson’s dementia, the researchers are collaborating with scientists worldwide to expand these findings to these diseases as well, according to senior author Dr. Tharick Pascoal.

This study sheds light on the underlying cause of challenging neuropsychiatric symptoms in Alzheimer’s patients and offers promising avenues for the development of targeted therapies. It also emphasizes the importance of considering neuroinflammation as a key player in the progression of the disease and its associated symptoms.

1. Source: Coherent Market Insights, Public sources, Desk research
2. We have leveraged AI tools to mine information and compile it