<b>Region-Specific Alterations in Brain UPE in Alzheimer’s Disease</b>

Alzheimer’s disease (AD) is the most common cause of dementia in the world, and it is marked by deterioration of cognitive functions; the formation of amyloid-β in the brain; and tau, the formation of tau pathology; synaptic degeneration; and local susceptibility, especially in the hippocampus and association cortices. The most common processes identified to cause neuronal injury and disease development are oxidative stress and mitochondrial dysfunction. Ultraweak photon emission (UPE), a spontaneous biophotonic emission in response to oxidative metabolic reactions, has become a possible cellular redox imbalance and neural activity indicator. Since oxidative changes in AD are region-specific, UPE can indicate region-specific neurodegeneration. Nevertheless, existing research on brain UPE in AD is insufficient and primarily focuses on global oxidative indicators, rather than regional patterns. Lack of systematic analysis of the region-specific UPE changes is also a major gap in research. This aims the regional differences in brain UPE in Alzheimer’s, and determine whether they correlate with oxidative imbalance and neuropathological severity. The detection of specific UPE signatures could contribute to the enhanced comprehension of spatial disease heterogeneity and aid in its advancement as a possible functional biomarker of the early disease detection and progression tracking.