Cognitive decline in Alzheimer’s (AD) arises as neurons die, driven by immune responses and inflammation due to amyloid beta and tau tangles in the brain.
Researchers at Massachusetts General Hospital (MGH) have engineered a 3D model simulating brain-immune cell interactions. This extends their previous work and identifies CT8+ T Cells worsening neuroinflammation as AD progresses.
The team unraveled mechanisms guiding T cell brain entry, lessened damage by blocking these, offering potential Alzheimer’s treatments.
Enabled by microfluidic tech, this model reveals immune-cell actions, aiding Alzheimer’s research. Co-lead author Mehdi Jorfi, PhD, says it provides a physiologically relevant AD model.
MGH’s new model, a 3D human neuroimmune axis, includes neurons, astrocytes, microglia, and immune cells. It replicates disease features in a 3D setting.
Blocking the CXCL10-CXCR3 pathway curbs T cell infiltration and neurodegeneration in AD cultures.
These findings could lead to therapies halting T cell brain entry, countering Alzheimer’s cognitive impact.
Co-lead author Joseph Park, PhD, emphasizes understanding distinct cell behaviors for effective treatments.
The study identifies an accessible T cell drug target outside the brain, a breakthrough considering drug penetration challenges. Senior author Rudolph Tanzi, PhD, highlights the significance.