We aim to highlight the potential of label-free, TPEF metabolic imaging to gain unique insights in the development of Alzheimer’s disease (AD). Using an engineered brain tissue model infected with HSV-1 to induce AD phenotypes, we focus on dynamic changes associated with metabolic function, as reported by both the redox ratio and mitochondrial clustering, and the development of Aβ+ fibrillar plaque like formations (PLFs).
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