Ramesh Vijay, PhD, had intensive training from the National Institute of Mental Health and Neurosciences, India and received his PhD from the Interdisciplinary Brain Research Center, JN Medical College and All India Institute of Medical Sciences, India. He worked on narcoleptic dogs as a post-doctoral fellow at the Stanford University School of Medicine. He later moved to Harvard Medical School, where he was promoted to junior faculty. Then he joined the University of Louisville School of Medicine as Assistant Professor. Recently, Dr. Vijay joined the pediatric sleep program in the Department of Pediatrics at the University of Chicago as an Assistant Professor. His passion is the neurophysiology of sleep and sleep disorders.

Dr. Vijay’s laboratory is interested in studying whether intermittent hypoxia (IH) and sleep fragmentation (SF), two distinct but separate pathological manifestations of obstructive sleep apnea (OSA) trigger early onset of disease condition, accelerate tauopathies, and modify gene and protein expression.

Neurodegenerative diseases like AD, Parkinson’s and ALS gradually destroy groups of neurons, severely disrupting learning and memory, reasoning, judgment and communication.  This leads to a stage where it becomes impossible to carry out daily activities and ultimately leads to death. Significant disruption in sleep/wake patterns is observed in these patients. Loss of slow wave sleep (SWS) is compounded by increased amount and frequency of nighttime wakefulness. During later stages of the disease, there is a significant loss of rapid eye movement (REM) sleep and a breakdown of sleep/wake circadian rhythm. Obstructive sleep apnea, wherein patients undergo cyclic intermittent hypoxia and sleep fragmentation throughout their sleep time, is thought to accelerate the progression of these diseases, by disrupting sleep, thermoregulation, and accelerated aging through early deposition of b-amyloid peptides, neurofbrillary tangles and hyperphosporylation of tau proteins. Chronic exposure to IH leads to severe cognitive impairments. Cognitive impairments can occur due to inadequate generation of cortical high frequency gamma activity. The mechanism of how OSA accelerates the progression of sleep disruption in these neurodegenerative diseases is still unknown. Given that OSA is a major risk factor in accelerating these conditions, it is imperative to identify the underlying factors that contribute to morbidities associated with these diseases. Studies will be carried out in adult mice and transgenic models using sleep recordings, SF, sleep deprivation (SD), Morris water maze, forced swim test (FST), sucrose consumption test (SCT), markers of oxidative stress and apoptosis, ROS production and mitochondrial injury.  

Book Chapters:

Ramesh V and Kumar VM. Monoanimergic mechanisms in the regulation of Sleep-wakefulness: special emphasis on preoptic noradrenergic system. Sleep and sleep disorders: A neuropsychopharmacological approach, eds. Lader et al. Landes Bioscience and Springer.

Ramesh V, Kaushal N and Kumar VM. Sleep inducing substances in the regulation of sleep. Neuroendocrine correlates of sleep/wakefulness Eds. Cardinalli et al., Kluwer Academic/Plenum Publishers.

Awards:

C.L. Malhotra Research Prize in Pharmacology

Late Prof. Kandula Pampapathi Rao Memorial Gold Medal

Trainee Research Excellence Award 

Young Investigator Honorable Mention Award