Dr. Paul R. Albert obtained his Ph.D. in Pharmacology from Harvard (1985) and did post-doctoral studies with Drs. Herbert and Civelli (Vollum Institute, Portland OR), where he cloned several dopamine and serotonin receptor genes. His first academic position was as Assistant then Associate Professor, Dept. of Pharmacology and Therapeutics, McGill University. In 1995, he was awarded the CIHR/Novartis Michael Smith Chair in Neuroscience at University of Ottawa, and is currently Full Professor and Senior Scientist at the Ottawa Hospital Research Institute. He is also Associate Director of Neuroscience, and has served as Director of the Neuroscience Graduate Program. He has served on several editorial boards (Neuroreport, Endocrinology, J. Biol. Chem., Int. J. Neuropsychopharmacol.), grants panels (CIHR, HSFC, etc.) and organized international meetings (ISAD, ISSR, CCNP, GPCR Retreat). He is currently Editor-in-Chief of the Journal of Psychiatry and Neuroscience, in which he has the most cited paper and is 4th most cited author. He is also a founding member of the HSFO Centre for Stroke Recovery and HSFC Canadian Partnership for Stroke Recovery. He has published 157 research papers with 10,600 citations and H-index of 52 (Scopus 2024).
Dr. Albert’s research is at the interface between molecular biology and psychiatry and focuses on the mechanistic link between the transcriptional regulation of genes of the serotonin and dopamine systems and mental illness. Since cloning the 5-HT1A and dopamine-D2 receptor genes, his laboratory has identified signaling mechanisms and novel transcription factors involved in their regulation. In collaboration with psychiatrists, his laboratory has identified novel functional polymorphisms in the 5-HT1A and dopamine-D2 receptor genes and their association with depression, suicide and treatment response. More recently, his laboratory has begun to use animal models to evaluate the roles of these transcription factors in vivo. For example, in probing the molecular mechanisms that regulate the 5-HT1A gene his lab identified human 5-HT1A variant (rs6295) that increases 5-HT1A autoreceptor expression and is associated with SSRI-resistant depression. To test whether these transcription changes really affect depression they have knocked them out in serotonin neurons of adult mice. This results in SSRI-resistant anxiety and depression-like behaviors. The lab is now testing whether other types of antidepressants or direct stimulation of serotonin neurons will reverse the depression in these mice.
In addition to genetic studies, Dr. Albert has also established a new mouse model of post-stroke depression and currently examine pharmacological, exercise and optogenetic approaches to enhance recovery. This mouse model responds to SSRI but not to exercise and chronic SSRI induces a regrowth of serotonin projections to the injured brain that correlates with recovery. The Albert lab is currently addressing the mechanisms of this regrowth and its importance in behavioral recovery.