My name is Allison Bischoff, and I am a rising senior studying Molecular Genetics at The Ohio State University. At Ohio State, I conduct research as part of Dr. Tamar Gur’s research group, aimed at elucidating the mechanisms by which maternal stress during pregnancy impacts neurodevelopmental and behavioral outcomes in children. My research project aims to determine how stress alters maternal immune response and the gut barrier function, potentially having functional consequences for offspring development. With a growing interest in the gut microbiome within the field of neuroscience, we are seeking to identify microbe-dependent mechanisms by which stress alters immune function and neurodevelopment.
As an SRF Summer Scholar, I have been virtually working under the direction of Dr. Julie Andersen and Dr. Chaska Walton to better understand the capacity for neurons and glial cells, non-neuronal cell types residing in the nervous system, to undergo cellular senescence. Senescence is an irreversible state of cell cycle arrest, induced by a variety of cellular stressors that often result in DNA damage. A universal biomarker for detecting senescence has yet to be identified due to the varied nature of the senescent phenotype, being both dependent upon the cell type and form of stress exposure. Additionally, identification of biomarkers that are strictly specific to cellular senescence has been a challenge, with many markers overlapping with biological processes that can exist independently of senescence. Increasing research has documented higher incidence of biomarkers associated with cellular senescence in different central nervous system (CNS) cell types of patients with neurodegenerative diseases, such as Alzheimer’s. This has led researchers to speculate that senescence could play a role in pathogenesis of these diseases—making senescence in the CNS a potential therapeutic target. In particular, the Andersen lab is investigating whether accumulation of amyloid-beta—a peptide that forms aggregates in Alzheimer’s diseases—can induce senescence in cell culture of neurons and glial cells. With emerging interest in the potential role of cellular senescence in age-related neurodegenerative diseases, unique challenges have been presented for studying senescence in cell types inhabiting the CNS.
Establishing distinct biomarker profiles for cellular senescence in different cell types of the CNS as well as identifying triggers that induce senescence in these cells will be crucial to future investigations of senescence in neurons and glia. The Andersen lab has employed a microscopy technique called spectral scanning confocal microscopy with linear unmixing as a method to identify senescence. This technique allows them to simultaneously detect multiple markers of senescence within an individual cell to more accurately identify populations of senescent cells. Already using this technique to investigate the possibility of senescent-like phenotypes in neurons, I helped organize a protocol to induce and detect senescence in astrocytes—a type of glial cell residing in the CNS. This project will help to establish relevant biomarkers for detecting senescence in astrocytes and identify types of cellular stress that could induce senescence in these cells. Establishment of reliable methods for detecting senescence in the CNS will allow for robust, dependable identification of senescence in age-related neurodegenerative diseases—crucial to identifying a potential role of senescence in mediating neurodegenerative pathologies.
