Cognitive decline associated with Alzheimer's disease (AD) develops when neurons begin to die, which can be caused by inappropriate immune responses and excessive inflammation in the brain triggered by amyloid beta deposits and tau tangles, two hallmarks of the disease.
Also, immune cells outside of the brain, particularly T cells, can enter the brain and worsen AD pathology, but studying this process has been difficult.
In the new study, the team used the model to demonstrate that as Alzheimer's pathology accumulates in the brain, specific types of immune cells called CT8+ T Cells surge into the brain and amplify the destruction caused by neuroinflammation. Enabled by cutting-edge microfluidic technology, this model opens up a window to observe infiltrating peripheral immune cells in action within 3D cell cultures; their interactions with brain cells; and their impact on neuroinflammation and neurodegeneration." "We hope our work contributes to developing a more physiologically relevant human Alzheimer's disease model in a dish," adds co–senior author Doo Yeon Kim, PhD, associate professor of Neurology at MGH.
In addition to observing higher levels of T cells in AD brain models, the team identified a pathway between a chemokine and chemokine receptor that plays a key role in regulating T cell infiltration.The findings could help in identifying new therapeutic targets that slow or halt the infiltration of T cells into the brains of Alzheimer's patients, and potentially reduce the devastating cognitive impacts of the disease.
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