Postdoctoral Research Assistant in Synaptic Signalling
- MSc Neuroscience
- BSc Physics with specialisation in biophysics
My research focuses on how two major cell types of the brain interact, and how this interaction might be perturbed in a neurodegenerative disorder like Alzheimer’s disease.
To develop new treatments for Alzheimer’s disease (AD), scientists need to understand which aspects of normal cell function are altered in a human brain with AD. However, human brain tissue is normally inaccessible to cellular studies, but by taking advantage of induced pluripotent stem cell technology, my project aims to generate an in vitro co-culture system of human brain cells.
In particular, I derive human neurons and astrocytes from healthy individuals or from patients diagnosed with AD and grow them together in order to study their interactions. Neurons communicate via synaptic connections with each other and astrocytes help maintain and strengthen these connections. Unsurprisingly, dysfunction of this crucial interaction between neurons and astrocytes is thought to be implicated in AD where malfunctioning of synapses is followed by a huge loss of neurons.
My aim is to explore neuron-astrocyte interactions at both normal and disease-relevant synapses, in particular in cells with the genetic risk variant for sporadic Alzheimer’s disease, APOE4.
Pro-maturational Effects of Human iPSC-Derived Cortical Astrocytes upon iPSC-Derived Cortical Neurons.
Hedegaard A. et al, (2020), Stem Cell Reports
The Sub-Primary Range of firing is present in both cat and mouse spinal motoneurones and its relationship to force development is similar for the two species.
Bo Jensen D. et al, (2018), J Neurosci
Potassium channel abnormalities are consistent with early axon degeneration of motor axons in the G127X SOD1 mouse model of amyotrophic lateral sclerosis.
Maglemose R. et al, (2017), Exp Neurol, 292, 154 - 167
Activity-Dependent Exocytosis of Lysosomes Regulates the Structural Plasticity of Dendritic Spines.
Padamsey Z. et al, (2017), Neuron, 93, 132 - 146
Postactivation depression of the Ia EPSP in motoneurons is reduced in both the G127X SOD1 model of amyotrophic lateral sclerosis and in aged mice.
Hedegaard A. et al, (2015), J Neurophysiol, 114, 1196 - 1210