Nickname: Parul
Hometown: Chandigarh
Graduate School: Panjab University, Chandigarh
E-mail: parul28bali@gmail.com
LinkedIn Profile: https://www.linkedin.com/in/parul-bali-phd-8b6635107 Click Here
Current Organization: Miningeal Lymphatics and Neurological Disorders Lab, Mayo Clinic, 4500 San Pablo Road, Jacksonville, FL 32224.
Website: https://www.mayoclinic.org/

Tell briefly about yourself.

My name is Parul Bali, and I have spent 33 years living in Chandigarh, the city where I was born and raised. The experiences and opportunities I encountered here have profoundly shaped my development, leading me to become a well-rounded and evolved neuroscientist.

How was your experience in the Neuroscience Research Lab? How did it contribute to your academic or professional development?

My experience in the Neuroscience Research Lab has been transformative in both my academic and professional journey. Engaging in cutting-edge research allowed me to deepen my understanding of complex neural processes for learning & memory and develop a robust set of technical skills, such as developing animal models of AD, molecular analysis, data analysis, and neuroimaging.

Collaborating with a diverse team of researchers honed my ability to work in interdisciplinary settings, enhancing my communication and problem-solving skills. Additionally, presenting our findings at conferences and contributing to publications boosted my confidence and expanded my professional network within the neuroscience community.

This experience solidified my passion for neuroscience, providing me with the practical expertise and theoretical knowledge to pursue advanced research and further my career in this dynamic field.

What are your Research interests?

My research focuses on understanding the development of Alzheimer’s disease (AD) pathology in transgenic mouse models and its correlation with retinal changes. I am particularly interested in identifying common molecular pathways underlying neurodegeneration in both the brain and retina. Using molecular, histological, and imaging approaches, I aim to uncover shared mechanisms that drive pathology across these systems, with implications for broader understanding of neurodegenerative diseases.

What are your current affiliations?

Miningeal Lymphatics and Neurological Disorders Lab, Mayo Clinic, 4500 San Pablo Road, Jacksonville, FL

What was your PhD thesis in or research work? Timeline?

My doctoral work targeted Alzheimer’s disease symptoms using alternative pre-clinical platforms. My graduate work spanned six years. This allowed me to be organized, quality conscious, and competent in various animal surgeries utilizing stereotaxic, subretinal, intravitreal, and Pterygopalatine artery occlusion tools. I was also trained in the fundamental biology protocols, neurobehavioral, and electrophysiological techniques to address the research questions. During the initial phase of graduation, I was involved in developing a deeper understanding of the prior scientific work carried out in the field of stem cell transplantation in Alzheimer’s disease. This propelled me to publish a compilation of fast-evolving perspectives in this field.

Considering the failure of translational science in the field, my primary aim was to examine the efficacy of lineage-negative stem cells (Lin-ve SC) from human umbilical cord blood in the mouse model of amyloidβ-induced memory loss. For this, we first characterized the Lin-ve SC by quantifying the expression of CD117 and CD34-positive cells in the CD45-positive population and reported significantly higher expression in the Lin-ve cells in comparison to the Lin+ve and mononucleated cells (MNCs). Further, morphological characterization of this population by SEM revealed that Lin-ve cells were more homogeneous than the cells from Lin+ve and MNCs. The efficacy of intrahippocampal transplantation of Lin-ve SC, when tested with dose-dependent Aβ, induced memory loss, revealed superior amelioration at higher doses of Aβ, which was intriguing.

We remained curious to gain insights about the mechanism underlying the observed rescue of memory loss by the stem cells in the aforementioned model. The increased expression of neurotrophic factors, i.e., BDNF, GDNF, and CNTF, concomitant with a decline in Aβ deposition after stem cell transplantation, led us to use the ANA-12 (a TrkB inhibitor of BDNF) as an antagonist, so we could ask whether such reversal was mediated by BDNF or not. The results surprised us into believing that Lin-ve SC possibly rescues memory loss by exerting the paracrine effects, either by activation of astrocytes mediated Aβ clearance or by delaying cell death.