Abstract
Alzheimer’s disease (AD) is characterized by blood-brain barrier (BBB) breakdown and neuronal cell death related to the deposition of aggregated amyloid-β (Aβ) plaques. A healthy BBB requires tight junctions (TJ) that render high transendothelial electrical resistance (TEER). AD-associated breakdown of the BBB correlates with vascular Aβ deposition, suggesting that aggregated, pathological Aβ can modulate TEER. By coupling this phenomenon with the nucleation-dependent nature of Aβ aggregation, we explore leveraging this cellular response and aggregate amplification for early disease diagnosis via detection of early Aβ aggregates.
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