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Professor Shane O'Mara

Professor Shane O'Mara

Position & Discipline

Director Trinity College Institute of Neuroscience


I summarise my research interests as the attempt to answer the following question: How does the brain make memories? This is a difficult question, which speaks to the heart of what it is to be human: What would a life without our enduring personal record of our hopes, experiences, desires, wishes, needs, loves and hatreds be like? Without memory, we would live in a continual present; the experience of memory gives meaning and continuity to our lives. This central research question can be rephrased in other, more technical, ways: How are memories encoded by neurons in the brain? How is this encoding affected by psychiatric or other conditions? An important and general hypothesis within the field is that memories are encoded as a result of changes in the strengths of connections between brain cells. This is known generally recognised as Hebb’s hypothesis:  that connections (synapses) between brain cells (neurons) are plastic and change as a result of learning, disease or other conditions.

In technical terms, therefore, the central theme of my research has been the investigation of the relations between synaptic plasticity (the mechanisms by which the brain changes as a result of experience), cognition (the abstract psychological processes by which we know, represent and understand the external world), and changes in learned behaviour. Within this broad domain I have concentrated my research on two particular and inter-related areas: (1) the neurobiology and neuropsychology of learning and memory, and (2) the neurobiology and neuropsychology of stress and depression. At present we know that these two seemingly diverse areas overlap to a very considerable degree. The synaptic plasticity that allows for memories to be encoded is disordered to a very considerable degree in depression, and treatments reducing the effects of depression (exercise, drugs, social interaction) enhance synaptic plasticity and hence memory function. In turn, these treatments also form the basis of therapy for age-related decline in memory and cognitive function.

Key Publications

Wang, B, Hok, V, Della-Chiesa, A, Callaghan, C, Tsanov, M, Barlow, S, Bechara, R, Irving, E, Virley, DJ, Upton, N. & O'Mara, SM. (2011). Rosiglitazone enhances learning, place cell activity and synaptic plasticity in middle-aged rats. Neurobiology of Aging, in press

Irish M, Lawlor BA, Coen RF, O'Mara SM. Everyday episodic memory in amnestic Mild Cognitive Impairment: A preliminary investigation. BMC Neurosci. 2011 Aug 4;12(1):80.

Irish, M, Lawlor, BA, O'Mara, SM & Coen, RF. (2011). Impaired capacity for autonoetic reliving during autobiographical event recall in mild Alzheimer's disease. Cortex, 47, 236-249.

Kelly, L, Grehan, B, Della Chiesa, A, O'Mara SM, Downer, E, Sahyoun, G, Massey, KA, Nicolaou, A, & Lynch, MA (2010). The polyunsaturated fatty acids, EPA and DPA exert a protective effect in the hippocampus of the aged rat. Neurobiology of Aging, in press.

Irish, M, Lawlor, BA, O'Mara, SM & Coen, RF. (2010). Exploring the recollective experience during autobiographical memory retrieval in amnestic Mild Cognitive Impairment. Journal of the International Neuropsychological Society, 16, 546-555.

Roche, RAP, Mullally, SL, McNulty, JP, Hayden, J, Brennan, P, Doherty, CP, Fitzsimons, M, McMackin, D, Prendergast, J, Sukumaran, S, Mangaoang, M, Robertson IH & O'Mara, SM. Prolonged rote learning produces delayed memory facilitation and metabolic changes in the hippocampus of the ageing human brain. BMC Neuroscience, 10,136-153.

Last updated 14 June 2012

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