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Full NameDr Yvonne Nolan

Department:Anatomy & Neuroscience

Organisation:University College Cork

Webpage:research.ucc.ie

Email Address:Email hidden; Javascript is required.

Research Fields

  • infectious disease and the immune system
  • neuroscience and mental health

Postgrad Medical Specialties

  • Medicine
  • Surgery
  • Psychiatry
  • Pathology
  • Sports and Exercise Medicine

Medical Subspecialties

  • Adolescent medicine
  • Child and Adolescent Psychiatry
  • Dementia
  • Immunology
  • Neurology
  • Neurophysiology
  • Neuropsychiatry

My Work

Research in Dr Nolan's laboratory focuses on the effects of inflammation, exercise, alpha-synuclein and stress on hippocampal neurogenesis (the birth of new neurons) during development and in the adult brain, and on associated learning and memory. She also investigates the contribution of inflammation to neuronal demise in models of Parkinson’s disease.

Her research is currently funded by Science Foundation Ireland, Marigot Ireland Ltd, Molecular Medicine Ireland and British Neuropathological Society, and previously by the Irish Research Council for Science Engineering and Technology, Health Research Board and Vasogen Inc., Canada. Her H index is 25 and her work has been cited >2000 times. She has supervised 10 PhD/MSc/postdoctoral researchers and currently supervise 8 researchers (2 postdocs, 5 PhD and 1 MD). To date she has secured almost €2.5M in research funding as Lead/Sole Investigator and is currently an SFI Investigator.

• Ryan SM, Nolan YM (2016) Neuroinflammation negatively affects adult hippocampal neurogenesis and cognition: can exercise compensate? Neurosci Biobehav Rev 61:121-131

Potential Projects

Parkinson’s disease (PD) is a common age-related neurodegenerative disorder. The main pathological hallmarks are the loss of dopaminergic (DA) neurons in the substantia nigra (SN) of the midbrain and the appearance of Lewy bodies which are composed of intracellular aggregates of α-synuclein. In addition to the characteristic motor symptoms seen in PD, cognitive dysfunction such as depression and dementia can manifest as the disease progresses, and these non-motor symptoms can cause considerable disturbance in patients’ quality of life. Adeno-associated viral vector-mediated overexpression of α-synuclein (AAV-α-synuclein) in the nigrostriatal pathway of rodent brains has been developed as an animal model of PD. Compared to many of the neurotoxic and genetic animal models of the disease, it more closely resembles the gradual loss of DA neurons and appearance of Lewy bodies that occurs in PD. In addition, our preliminary studies have demonstrated that late-stage cognitive decline occurs in AAV- α-synuclein rats.

A compelling body of evidence indicates that inflammation is a major contributor to the pathogenesis of PD. Specifically, it is proposed that inflammation may act as an environmental stressor to promote degeneration of DA neurons by inducing microglial activation and release of reactive oxygen species and cytokines. Under normal circumstances, microglia are involved in immune surveillance in order to maintain brain homeostasis. Under pathological conditions however, microglia undergo morphological and functional changes and become activated. Indeed excessive microglial activation is associated with the pathophysiology of PD, and α-synuclein-mediated neurotoxicity has previously been shown to be enhanced by microglial activation. Activated microglia have been implicated in the cognitive dysfunction associated with other neurodegenerative diseases such as Alzheimer’s disease, and with ageing itself.

We propose that microglia may precipitate development of PD pathology and symptomology in individuals with a predisposition to the disease such as those with α-synuclein aggregation. In this regard, a recent important development in the field is the concept of “model fusion” to study gene-environment interactions in PD. We hypothesise that challenging the α-synuclein rat model of PD with an environmental inflammatory stressor (lipopolysaccharide (LPS)) may precipitate an acceleration of disease symptoms.

The overall aim of this project is to investigate if peripheral challenge with LPS accelerates depression and cognitive dysfunction, microglial activation and associated neuronal pathology in the AAV- α-synuclein rat model of PD.