Yutong Zhang L&S Biological Sciences
Interneuron Restoration and Transcriptional Change via Optogenetics
Alzheimer’s disease (AD) is the most common cause of dementia, constituting close to two-thirds of all dementia diagnoses; the urgency and importance of AD research thus needs no further explanation. While much of AD research is focused on hallmark pathologies, namely Aβ plaques and tau tangles, there are less focus on new potential molecular targets.
Previous research has shown the dysfunction of inhibitory network, and specifically the interneurons within it, as a key pathology in many AD mouse models, yet the underlying cause of their selective vulnerability remains unknown. Inhibitory interneurons may critically contribute to early brain network alterations, including hyperactivity and deactivation deficits, amyloid deposition, and cognitive alterations. To further elucidate the mechanisms of interneuron dysfunction and its downstream effects, in this project I propose to 1) perform optogenetics stimulation treatment on interneurons in J20 Familial Alzheimer’s Disease (FAD) mouse model, and 2) examine changes in differentially expressed genes (DEG) expression in dysfunctional cell types in AD via quantification of RNA sequencing.
I hypothesize that after optogenetics stimulation treatment, dysfunctional interneurons in AD mouse models will have distinguishable DEG compared to untreated ones, leading to functional differences in brain network activity and potentially rescue of functions.
Message To Sponsor
Thank you so much for sponsoring my project. Conducting my independent research has always been a dream of mine and I am so thankful that it is made a reality through your generous help. I am so honored to receive this fellowship and am excited to contribute to the field of neurodegenerative disease however I can.