Lyndsey E. Collins-Praino, PhD
Post-doctoral Research Fellow
The Taub Institute
630 West 168th Street
New York, NY 10032
Phone: 212-305-2046
Fax: 212-342-1838
Email: lec2158@columbia.edu
Ongoing Research:
Neuroinflammation and cognition. Over the past decade, a growing body of literature has highlighted the critical role that inflammatory processes play in cognitive aging, linking markers of inflammation to poorer cognitive test performance and increased risk of dementia. In my research, I seek to understand the neural mechanisms that may mediate the relationship between markers of inflammation and the emergence of cognitive impairment, both in healthy aging and in neurodegenerative diseases, such as Alzheimer's and Parkinson's. The ultimate goal of this work is to identify novel targets that may lead to the development of more efficacious therapeutic strategies for the treatment of cognitive decline.
Genetic risk factors for cognitive impairment. In recent years, technological advances in gene mapping have made it possible to begin to identify genetic risk factors associated with the development of cognitive impairment. Carriers of the epsilon 4 allele of the APOE gene, for example, have been shown to exhibit more rapid declines in cognitive performance, particularly in the memory domain, over time, as well as an increased risk of developing Alzheimer's disease (Reitz and Mayeux, 2010). I am particularly interested in investigating the neural mechanisms via which a particular allele may lead to the development of cognitive impairment, as well as in understanding the neuromorphological changes that may occur over time in individuals who possess genetic risk factors. Furthermore, I am interested in how genetic risk factors may help us to predict the rate of progression of mild cognitive impairment to dementia.
Role of the basal ganglia in cognition.I am interested in the role of the basal ganglia, particularly the caudate and subthalamic nuclei, in cognition. The caudate nucleus is considered to play a critical role in the planning and execution of strategies needed for goal-directed behavior (Grahn et al. 2008), while the subthalamic nucleus, more recently, has been hypothesized to serve a “frontal cortex-like” function in attention, inhibition control, and motivation (Baunez and Lardeux, 2011). As part of my research, I am investigating the functional connectivity of the basal ganglia during the performance of several cognitive tasks, particularly those measuring executive control ability. I am also investigating declines in cognition that occur following deep brain stimulation of the subthalamic nucleus. The goal of this work is to gain a better understanding of the complex neural circuitry of cognition, in the hopes that this may lead to improvements in current strategies for the treatment of cognitive impairment.
Representative Publications
Collins, L.E., Sager, T.N., Sams, A.G., Pennarolla, A., Port, R.G., Shahriari, M. & Salamone, J.D. (2011). The novel adenosine antagonist Lu AA47070 reverses the motor and motivational effects produced by dopamine D2 receptor blockade. Pharmacology, Biochemistry, and Behavior, 100(3), 498-505.
Collins-Praino, L.E., Paul, N.E., Rychalsky, K.R., Hinman, J.R., Chrobak, J.J., Senatus, P.B. & Salamone, J.D. (2011). Pharmacological and physiological characterization of the tremulous jaw movement model: Potential insights into the pathophysiology of tremor. Review. Frontiers in Systems Neuroscience, 5, 49.
Collins, L.E., Paul, N.E., Abbas S.F., Leser C.E., Podurgiel, S.J., Galtieri, D.J., Chrobak, J.J., Baqi, Y., Muller, C.E. & Salamone J.D. (2011). Oral tremor induced by galantamine in rats: A model of the parkinsonian side effects of cholinomimetics used to treat Alzheimer's disease. Pharmacology, Biochemistry, and Behavior, 99(3), 414-422.
Collins, L.E., Galtieri, D.J., Collins, P., Jones, S.K., Collins, P., Port, R.G., Paul, N.E., Hockemeyer, J., Muller, C., & Salamone, J.D. (2010). Interactions between adenosine and dopamine receptor antagonists with different selectivity profiles: Effects on locomotor activity. Behavioural Brain Research, 211(2), 148-155.
Collins, L.E., Galtieri, D.J., Hockemeyer, J., Muller, C., & Salamone, J.D. (2010). Oral tremor induced by the muscarinic agonist pilocarpine is suppressed by the adenosine A2A antagonists MSX-3 and SCH58261, but not the adenosine A1 antagonist DPCPX. Pharmacology, Biochemistry, and Behavior, 94(4), 561-569.