Biology subjects

Hermann, N.

Publications and source records attributed to Hermann, N..

3 recordsLinked to original sources

bioRxiv2026

Amygdala metabolic activity on FDG PET is associated with survival, response to immune checkpoint inhibition, and tumor immune signaling in non-small cell lung cancer

Amygdala metabolic activity (AmygAc) measured by [18F]FDG PET has been associated with chronic psychological stress and adverse clinical outcomes, but its relationship with antitumor immunity and treatment response remains incompletely understood. We investigated AmygAc as a host-derived imaging biomarker in non-small cell lung cancer (NSCLC) and examined its association with survival, response to immune checkpoint inhibition (ICI), and the tumor immune microenvironment. Methods: In this multicenter retrospective study, baseline [18F]FDG PET scans from 256 treatment-naive patients with NSCLC were analyzed to quantify AmygAc. Overall survival was assessed in the full cohort, and treatment response was evaluated in 79 patients who subsequently received neoadjuvant ICI therapy. AmygAc was integrated with clinical and tumor-derived imaging parameters. To investigate its biological correlates, tumor tissue from a selected subcohort was analyzed using multiplex immunofluorescence and spatial transcriptomics.

cancer biology↗

bioRxiv2025

Ischemic injury triggers a protective microglial phenotype in models of Aβ pathology

Microglia are highly plastic cells that are capable of integrating subsequent insults. As the majority of Alzheimers Disease (AD) patients also show cerebrovascular pathology, we here aimed to dissect the interactions between AD and ischemic brain injury on the microglial response to amyloid beta (A{beta}) pathology. Surprisingly, we find that ischemic stroke in the presence of cerebral {beta}-amyloidosis results in the generation of a novel neuroprotective microglial phenotype. These microglia drive a rapid accumulation of highly dense A{beta} plaques that exhibit a relatively benign nature and are strikingly similar to A{beta} plaques observed in patients that are resilient to AD pathology. Thus, our data do not only highlight the impact of a co-morbid state of brain ischemia and A{beta} pathology on the microglial phenotype but also identify novel molecular pathways that may serve to promote beneficial microglial functions in AD.

neuroscience↗

bioRxiv2021

Visualizing cell death in live retina: Using calpain activity detection as a biomarker for retinal degeneration

Calpains are a family of calcium-activated proteases involved in numerous disorders. Notably, previous studies have shown that calpain activity was substantially increased in various models for inherited retinal degeneration (RD). In the present study, we tested the capacity of the t-BOC-Leu-Met-CMAC calpain-specific substrate to detect calpain activity in living retina, in organotypic retinal explant cultures derived from wild-type mice, as well as from rd1 and RhoP23H/+ RD-mutant mice. Test conditions were refined until the calpain substrate readily detected large numbers of cells in the photoreceptor layer of RD retina but not in wild-type retina. At the same time, the calpain substrate was not obviously toxic to photoreceptor cells. Comparison of calpain activity with an immunostaining for activated calpain-2 furthermore suggested that individual calpain isoforms may be active in distinct temporal stages of photoreceptor cell death. Notably, calpain-2 activity may be a relatively short-lived event, occurring only towards the end of the cell death process. Finally, our results support the development of calpain activity detection as a novel in vivo biomarker for RD, suitable for combination with non-invasive imaging techniques.

neuroscience↗