Finula Irem Isik

Finula is a postgraduate researcher based at the BMC, University of Sydney. She started laboratory research into MSA in 2018.

Forefront Group: Halliday Lab


A/Professor Scott Woojin Kim, Professor Glenda Halliday

Affiliate Organisations

Brain and Mind Centre, University of Sydney


  • Oligodendrogliopathy
  • Proteins
  • Lipids

Neurodegeneration of interest:

MSA, PD, Lipidopathy

Specific Skills:

  • Mammalian and bacterial cell culture
  • Brain tissue extractions
  • PCR
  • Western blotting
  • Immunofluorescence
  • Lipid extraction
  • Data analysis

Project - Functional Study of the Cadherin-4 Gene in Multiple System Atrophy

Disease area:


Research Project Aims

  • To determine whether CDH4 protein expression is altered in MSA brain
  • To determine the impact of CDH4 on α-synuclein expression
  • To determine any alterations in CDH4 protein coding regions in genomic DNA
  • To determine variation in lipid expression between different disease affected regions, and investigate changes to lipid synthesis pathways
  • To determine how patterns of lipid expression alterations are related to CDH4 in vitro

Research Project Description


MSA is a rare neurodegenerative disease of the central and autonomic nervous system. The neuropathological hallmark of MSA are glial cytoplasmic inclusions (GCI) within oligodendrocytes, the myelinating neural support cells. The inclusions are predominantly formed by misfolded α-synuclein, a small presynaptic protein which additionally encompasses Lewy bodies and Lewy neurites in neurons affected by Parkinson’s disease and related syndromes. However, MSA is distinguishable from Parkinson’s disease as an oligodendrogliopathy resulting in subsequent neuron death, indicating a separate pathogenic mechanism. This distinction warrants researching MSA neuropathogenesis in its own right. Incidentally, a genome wide association study (Sailer et al., 2016) identified a number of novel gene variants in an MSA cohort. These were the subject of recent investigation at the Halliday laboratory, with preliminary findings indicating alterations in CDH4 expression in MSA disease-affected tissue, and an impact of this protein on downstream MSA neuropathic genes in a cell model. It is vital to replicate and investigate this further to determine the role CDH4 may play in MSA neuropathogenesis.

Objectives & Methods:

This research will measure CDH4 gene and protein expression in MSA cohorts using sanger sequencing, quantitative polymerase chain reaction, protein fractionation and western blotting. The involvement of lipids in MSA and their relationship to CDH4 will be considered via lipidomics. We will additionally conduct CDH4 transfection of oligodendrocyte cells to investigate the impact on downstream MSA neuropathic genes and processes. Following this, we will decipher structural and functional features of CDH4 to determine the role it may play in MSA, and thus, its suitability as a therapeutic target or diagnostic biomarker.