Genane Loheswaran, Msc, PhD
Research Manager Vielight
- Toronto ON
Dr. Loheswaran has 10 years of experience in research including, protocol design, trial management, and statistics/data analysis
Social
Areas of Expertise
Accomplishments
School of Graduate Studies Research Travel Grant
2014
Pharmacology Book Fund Travel Award
2014
University of Toronto Graduate Fellowship
2012 - 2013
Ontario Graduate Scholarship
2011 - 2012
Canadian Institute of Health Research Strategic Training Grant in Public Health Policy
2010 - 2011
Education
University of Toronto
Ph.D.
Pharmacology
2016
McMaster University
M.Sc.
Neuroscience
2010
University of Toronto
B.Sc.
Neuroscience
2008
Articles
Alcohol Impairs N100 Response to Dorsolateral Prefrontal Cortex Stimulation.
Scientific ReportsLoheswaran, G., Barr, M.S., Rajji, T.K., Zomorrodi, R., Le Foll, B., Daskalakis, Z.J.
2017
Impairment of Neuroplasticity in the Dorsolateral Prefrontal Cortex by Alcohol
Scientific ReportsLoheswaran, G., Barr, M.S., Rajji, T.K., Zomorrodi, R., Le Foll, B., Daskalakis, Z.J.
2017
Previous studies have demonstrated that alcohol consumption impairs neuroplasticity in the motor cortex. However, it is unknown whether alcohol produces a similar impairment of neuroplasticity in the dorsolateral prefrontal cortex (DLPFC), a brain region that plays an important role in cognitive functioning. The aim of the current study was to evaluate the effect of alcohol intoxication on neuroplasticity in the DLPFC. Paired associative stimulation (PAS) combined with electroencephalography (EEG) was used for the induction and measurement of associative LTP-like neuroplasticity in the DLPFC. Fifteen healthy subjects were administered PAS to the DLPFC following consumption of an alcohol (1.5 g/l of body water) or placebo beverage in a within-subject cross-over design. PAS induced neuroplasticity was indexed up to 60 minutes following PAS. Additionally, the effect of alcohol on PAS-induced potentiation of theta-gamma coupling (an index associated with learning and memory) was examined prior to and following PAS. Alcohol consumption resulted in a significant impairment of mean (t = 2.456, df = 13, p = 0.029) and maximum potentiation (t = -2.945, df = 13, p = 0.011) compared to the placebo beverage in the DLPFC and globally. Alcohol also suppressed the potentiation of theta-gamma coupling by PAS. Findings from the present study provide a potential neurophysiological mechanism for impairment of cognitive functioning by alcohol.
Brain Stimulation in Alcohol Use Disorders: Investigational and Therapeutic Tools.
Biological Psychiatry: Cognitive Neuroscience and NeuroimagingLoheswaran, G., Barr, M.S., Rajji, T.K., Zomorrodi, R., Le Foll, B., Daskalakis, Z.J.
2016
Alcohol use disorders (AUDs) are a major health and social problem worldwide. Brain stimulation holds great promise as an investigational tool to help us understand the pathophysiology of alcohol dependence and as a therapeutic tool to treat AUDs. Numerous studies suggest that glutamatergic, gamma-aminobutyric acidergic, and dopaminergic neurotransmission are altered by alcohol consumption and among patients with AUDs. Alcohol’s disruption of neurotransmission is likely to play an important role in its detrimental effects on neuroplasticity, which, in turn, may contribute to the pathophysiology of alcohol dependence. Specifically, aberrant neuroplasticity in the brain reward circuitry is a potential mechanism underlying the pathophysiology of alcohol dependence. The dorsolateral prefrontal cortex (DLPFC), a part of the brain’s reward circuitry, is directly accessible to noninvasive brain stimulation and may represent a potential target for the treatment of AUDs. While the literature suggests that impairments in neuroplasticity are likely to be present in the DLPFC and brain reward circuitry in alcohol-dependent patients, this is yet to be directly evaluated in humans. Findings from numerous neuromodulatory brain stimulation studies demonstrate that altering neuroplasticity in the DLPFC in alcohol-dependent patients holds promise as a treatment for alcohol dependence, but the optimal neuromodulatory parameters are yet to be identified. Gaining a better understanding of alcohol dependence vis à vis neuroplasticity in the DLPFC and brain reward circuitry can help us optimize the treatment of alcohol dependence using neuromodulatory brain stimulation in the DLPFC.
Alcohol Intoxication by Binge Drinking Impairs Neuroplasticity
Brain StimulationLoheswaran, G., Barr, M.S., Rajji, T.K., Blumberger, B., Le Foll, B., Daskalakis, Z.J.
2016
Binge drinking, resulting in acute alcohol intoxication, is considered an initial step in developing alcohol use disorders (AUDs). It has been suggested that alcohol intoxication may act on mechanisms of neuroplasticity to produce brain changes that contribute to the pathophysiology of AUDs. However, the effect of binge drinking on neuroplasticity has not been evaluated in humans.
(2014). Screening and Treatment for Alcohol, Tobacco and Opioid Use Disorders: A Survey of Family Physicians across Ontario
PLoS OneLoheswaran, G., Soklaridis, S., Selby, P., Le Foll, B.
2014
An online survey consisting of a series of 38 primarily close-ended questions was circulated to family physicians in Ontario. Rates of screening for alcohol, opioid and tobacco dependence, use of validated tools for screening, providing treatment for dependent individuals and the current barriers to the prescription of pharmacotherapies for these drug dependences were assessed.
