Maryka Quik, Director, Neurodegenerative Diseases, Center for Health Sciences | SRI International

Toggle Menu

Maryka Quik

Director, Neurodegenerative Diseases, Center for Health Sciences

Maryka Quik, Ph.D., focuses on research about the relationship between the nicotinic cholinergic system and the dopaminergic system in addiction and neurodegenerative disorders. Tobacco addiction is associated with major health problems worldwide. Therefore strategies to reduce or stop smoking are needed urgently. Her lab investigates the effects of nicotine, an important addictive component in tobacco. They are investigating the role of novel nicotinic receptor subtypes using electrophysiological, molecular biology and behavioral techniques. These studies represent a new direction for understanding the changes in the brain that may be responsible for addiction. Such knowledge may lead to more effective treatment strategies for smoking cessation, which are critical in view of the detrimental health-related affects associated with tobacco use.

Quik’s group is also investigating the potential usefulness of nicotine and nicotinic receptor drugs for Parkinson’s disease. This neurological movement disorder is characterized by a loss of dopaminergic neurons in the nigrostriatal pathway. Accumulating studies now show that nicotine protects against nigrostriatal damage. The mechanisms responsible for nicotine’s protective effects against degeneration of dopamine neurons are currently being investigated. Other work in progress shows that nicotine may be useful for treating movement problems associated with L-dopa therapy in Parkinson's disease, as nicotine reduces L-dopa-induced abnormal involuntary movements in different Parkinsonian animal models. Studies are underway to determine the optimal nicotine treatment regimen and nicotine’s mechanisms of action, including the use of knockout mouse models.  

Overall, this work has the potential to lead to the development of improved therapeutic approaches for addiction and neurodegenerative disorders such as Parkinson’s disease.

Quik received her Ph.D. in biochemistry from McGill University in Montreal, Canada. After a Medical Research Council postdoctoral fellowship at Cambridge University in England, she joined the faculty in the Department of Pharmacology at the university. She continued research and teaching there and subsequently became a full professor of pharmacology. Quik then joined the Parkinson's Institute as Professor and Senior Research Scientist, after which she joined SRI. Quik has published more than 125 research articles and reviews.

Selected publications

Huang LZ, Parameswaran N, Bordia T, Michael McIntosh J, Quik M (2009) Nicotine is neuroprotective when administered before but not after nigrostriatal damage in rats and monkeys. J Neurochem 109:826-837.

Perez XA, O'Leary KT, Parameswaran N, McIntosh JM, Quik M (2009) Prominent role of alpha3/alpha6beta2* nAChRs in regulating evoked dopamine release in primate putamen: effect of long-term nicotine treatment. Mol Pharmacol 75:938-946.

Quik M, Campos C, Parameswaran N, Langston JW, McIntosh JM, Yeluashvili M (2009a) Chronic Nicotine Treatment Increases nAChRs and Microglial Expression in Monkey Substantia Nigra After Nigrostriatal Damage. J Mol Neurosci.

Quik M, Huang LZ, Parameswaran N, Bordia T, Campos C, Perez XA (2009b) Multiple roles for nicotine in Parkinson's disease. Biochem Pharmacol 78:677-685.

Bordia T, Campos C, Huang L, Quik M (2008) Continuous and intermittent nicotine treatment reduces L-3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesias in a rat model of Parkinson's disease. J Pharmacol Exp Ther 327:239-247.

O'Leary K, Parameswaran N, McIntosh JM, Quik M (2008a) Cotinine selectively activates a subpopulation of alpha3/alpha6beta2 nicotinic receptors in monkey striatum. J Pharmacol Exp Ther 325:646-654.

O'Leary KT, Parameswaran N, Johnston LC, McIntosh JM, Di Monte DA, Quik M (2008b) Paraquat exposure reduces nicotinic receptor-evoked dopamine release in monkey striatum. J Pharmacol Exp Ther 327:124-129.

Olivera BM, Quik M, Vincler M, McIntosh JM (2008) Subtype-selective conopeptides targeted to nicotinic receptors: Concerted discovery and biomedical applications. Channels (Austin) 2.

Perez XA, Bordia T, McIntosh JM, Grady SR, Quik M (2008a) Long-term nicotine treatment differentially regulates striatal alpha6alpha4beta2* and alpha6(nonalpha4)beta2* nAChR expression and function. Mol Pharmacol 74:844-853.

Perez XA, Parameswaran N, Huang LZ, O'Leary KT, Quik M (2008b) Pre-synaptic dopaminergic compensation after moderate nigrostriatal damage in non-human primates. J Neurochem 105:1861-1872.

Quik M, O'Leary K, Tanner CM (2008) Nicotine and Parkinson's disease: implications for therapy. Mov Disord 23:1641-1652.

Quik M, O'Neill M, Perez XA (2007b) Nicotine neuroprotection against nigrostriatal damage: importance of the animal model. Trends Pharmacol Sci 28:229-235.

Riveles K, Huang LZ, Quik M (2008) Cigarette smoke, nicotine and cotinine protect against 6-hydroxydopamine-induced toxicity in SH-SY5Y cells. Neurotoxicology 29:421-427.

Bordia T, Grady SR, McIntosh JM, Quik M (2007) Nigrostriatal damage preferentially decreases a subpopulation of alpha6beta2* nAChRs in mouse, monkey, and Parkinson's disease striatum. Mol Pharmacol 72:52-61.

Cox H, Togasaki DM, Chen L, Langston JW, Di Monte DA, Quik M (2007) The selective kappa-opioid receptor agonist U50,488 reduces L-dopa-induced dyskinesias but worsens parkinsonism in MPTP-treated primates. Exp Neurol 205:101-107.

Khwaja M, McCormack A, McIntosh JM, Di Monte DA, Quik M (2007) Nicotine partially protects against paraquat-induced nigrostriatal damage in mice; link to alpha6beta2* nAChRs. J Neurochem 100:180-190.

Quik M, Bordia T, O'Leary K (2007a) Nicotinic receptors as CNS targets for Parkinson's disease. Biochem Pharmacol 74:1224-1234.

Quik M, Cox H, Parameswaran N, O'Leary K, Langston JW, Di Monte D (2007c) Nicotine reduces levodopa-induced dyskinesias in lesioned monkeys. Ann Neurol 62:588-596.

Maryka Quik of SRI International