OS02.5.A Alzheimer-type neuropathological changes in glioblastoma-adjacent cortex

Abstract Background Glioblastoma (GBM) is an aggressive type of brain cancer that prevalent and fatal in the elderly. Age not only most common risk factor for but also neurodegenerative diseases, previous studies have indicated excess co-occurrence both diseases. Here, we aim to map Alzheimer (AD)-related pathology GBM-adjacent cortex. Material Methods To this end, screened a cohort 99 individuals with 200 tissue samples comprising tumor adjacent cortex, including longitudinal 13 patients. The were provided by Division Neuropathology Neurochemistry, Medical University Vienna from 2002 2021. location abstracted clinical data where available. All stained A-beta, tau-AT8 NeuN using immunohistochemistry. Whole slide scans segmented protein deposits quantified QuPath. Further statistical analyses conducted R. Tau was recorded as neurofibrillary tangles, neuropil threads, astroglial pathology. Likewise, amyloid assessed plaques and/or cerebral angiopathy (CAA). For proteins, grouped into: absent, mild, moderate, severe. Results In total cohort, median age 67.5 ys (range 20-92 ys), female-to-male ratio 0.68. Overall 44.4 % (n=44/99) showed any A-beta taupathology, which strongly correlated (R=0.26, p= 0.001). Among them, 38.6 (n=17/44) had combined pathology, while 36.4 (n=16/44) displayed pure amyloid-beta, 25 (n=11/44) tau comprised 74.4 (n=29/39) CAA 28.2 (n=11/29). Consistent spatiotemporal evolution AD, tangle load highest temporal lobe (42.9 n=21/49), plaque occipital (62.5 n=5/8). This pattern accentuated patients above 65, it deviated those below 65. Over time, AD-type increased 38.4 (n=5/13) remained stable 53.8 (n=7/13) recurrent tumors. Total cell densities tumor-infiltrated cortex ranged 474 7,540 cells/mm2, being similar across all lobes. Higher density decreased neuronal counts (R= -0.46, p<0.0001) AD-load -0.25, 0.002). Conclusion Collectively, our results establish frequent disease neuropathological changes They prompt further investigation shared pathogenic mechanisms seek raise awareness synergistic effects on cognitive decline.