Alz scores, on the other hand, did not show any significant correlations between regions in AD samples suggesting that this biomarker is confined to affected brain regions [26] and more specifically related to AD pathogenesis (Fig. 5, S5). Furthermore, the disease biomarkers were fully validated in a hold-out set of samples (Phase 2), which in addition contained some Huntington disease (HD) samples. As shown in Figure S6, BioAge, NdStress, and Inflame were significantly elevated in both AD and HD samples (p<1E–6). In general, these biomarkers reached similar average levels in AD and HD samples in all profiled brain regions. In PFC2, however, the average BioAge reached in HD samples was significantly lower than that of AD samples (p = 1E–17). These biomarkers, therefore, seemed to capture general systemic neurodegenerative processes rather than being specific to AD. The most striking difference between AD and HD samples was reflected in the Alz biomarker, which again was specific to the presence of AD was not significantly elevated in any brain region in HD samples (Fig. 6).
