Hend Almunaidi

I received my MSc with the completion of a thesis project from the University of Michigan-Ann Arbor in the United States. In my thesis project, I worked in Prof. Gyorgyi Csankovszki’s Lab where I investigated how the dosage compensation complex (DCC) in nematode hermaphrodites affects aging by regulating age-linked genes on the X chromosome. My research primarily focused on gbb-1, which encodes GABA beta receptors in neurons. Through my work, I made fascinating discoveries where I have demonstrated that X chromosomes undergo decondensation in worms as they age. Additionally, I have uncovered that one of the DCC accessory proteins, dpy-21, downregulates the gbb-1 gene on the X chromosome. Interestingly, defects in dpy-21 lead to gbb-1 overexpression and decreased longevity. This experience was what first ignited my passion for aging and age-related diseases. Alzheimer's disease (AD) is one of the prominent age-related diseases and is the most common form of dementia. It is characterized by several cellular alterations, including the accumulation of Amyloid-beta plaques, mitochondrial dysfunction and energy metabolism alterations which serve as the hallmarks of AD progression. However, cognitive decline, a hallmark of AD symptoms is only observed in two-thirds of AD individuals while others remain cognitively intact “resilient”. This raises the question of how these cellular alterations contribute to the progression of cognitive decline in AD. In my research in the Carlyle Group, I aim to study the correlation between these cellular changes and the progression of cognitive decline in AD by utilizing cortical neuronal cells derived from human stem cells and cerebrospinal fluid samples from AD patients.