Neuroinflammation Group

Neurodegenerative diseases cause neurons to deteriorate and die. A result of this is the abnormal build-up of proteins such as tau or TPD-43. Evidence from our group suggests that inflammation is dysregulated in these diseases, playing a detrimental role in the disease progression. It is our goal to identify disease-causing inflammation and treat these diseases as early as possible.

Research interests

  • Neuroinflammation
  • Neurodegenerative diseases
  • Motor neurone disease
  • Frontotemporal dementia
  • Tauopathies

  • Human iPSC technology
  • CRISPR/Cas9
  • Spatial transcriptomics
  • Western blot, qPCR
  • Preclinical mouse models

About our research

Emerging evidence from our group has shown that inflammation is dysregulated and escalates from the earliest stages of neurodegeneration; indicating that inflammation actively modulates disease development.

Our group seeks to elucidate the molecular events underlying disease causing inflammatory responses in neurodegenerative disease. This involves investigating immune-mediated cellular and molecular changes which arise as result of the abnormal build-up of protein (i.e. tau or TDP-43).

We bring together expertise in immunology, neuroscience and computational biology, using techniques such as molecular biology, advanced imaging, preclinical mouse models, human induced pluripotent stem cell technology and translational research.

Identifying the disease-causing inflammatory pathways will enable us to better understand the causes of neurodegenerative disease and allow us to work towards earlier diagnosis and targeted therapies.

Watch Alan talk about the research in the video Attacking the causes of MND.

“We aspire to map the cause(s) of neurodegeneration through the lens of immunology towards novel therapeutic strategies for ALS-FTD. Our work is dynamic, collaborative and inspiring. We love to explore the truth behind the microscope.”


Research project

Research team

Research team head

Headshot_Alan Yu

Dr Alan Yu

Group Head

Team members

Research fellows

  • Dr Samaneh Mirzaei

Research and technical staff

  • Emily Hart

PhD students

  • Pawat Laohamonthonkul

Honours students

  • Pippa Priguer
  • Aggie Hansen

Selected publications

  • Yu C-H, Davidson S, Harapas CR, Hilton JB, Mlodzianoski MJ, Laohamonthonkul P, Louis C, Low RRJ, Moecking J, De Nardo D, Balka KR, Calleja DJ, Moghaddas F, Ni E, McLean CA, Samson AL, Tyebji S, Tonkin CJ, Bye CR and Turner BJ (2020), ‘TDP-43 triggers mitochondrial DNA release via mPTP to activate cGAS/STING in ALS’, Cell, 183(3):636-649.e18, doi:10.1016/j.cell.2020.09.020
  • ‌McDonald BK, Pawat Laohamonthonkul and Yu C-H (2023), ‘Stray self-nucleic acids: the emerging drivers of neurodegeneration’, Trends in Cell Biology, 33(6):451-454, doi:10.1016/j.tcb.2023.02.006
  • Davidson S, Yu C-H, Steiner A, Ebstein F, Baker PJ, Jarur-Chamy V, Hrovat Schaale K, Laohamonthonkul P, Kong K, Calleja DJ, Harapas CR, Balka KR, Mitchell J, Jackson JT, Geoghegan ND, Moghaddas F, Rogers KL, Mayer-Barber KD, De Jesus AA and De Nardo D (2022), ‘Protein kinase R is an innate immune sensor of proteotoxic stress via accumulation of cytoplasmic IL-24’, Science Immunology, 7(68): eabi6763, doi:10.1126/sciimmunol.abi6763
  • Eitan C, Siany A, Barkan E, Olender T, van Eijk KR, Moisse M, Farhan SMK, Danino YM, Yanowski E, Marmor-Kollet H, Rivkin N, Yacovzada NS, Hung S-T, Cooper-Knock J, Yu C-H, Louis C, Masters SL, Kenna KP, van der Spek RAA and Sproviero W (2022), ‘Whole-genome sequencing reveals that variants in the interleukin 18 receptor accessory protein 3’UTR protect against ALS’ Nature Neuroscience, 25(4):433–445, doi:10.1038/s41593-022-01040-6
  • Tye H, Yu CH, Simms LA, de Zoete MR, Kim ML, Zakrzewski M, Penington JS, Harapas CR, Souza-Fonseca-Guimaraes F, Wockner LF, Preaudet A, Mielke LA, Wilcox SA, Ogura Y, Corr SC, Kanojia K, Kouremenos KA, De Souza DP, McConville MJ, Flavell RA, Gerlic M, Kile BT, Papenfuss AT, Putoczki TL, Radford-Smith GL, Masters SL (2018), ‘NLRP1 restricts butyrate producing commensals to exacerbate inflammatory bowel disease’, Nature Communications, 9(1): 3728, doi:10.1038/s41467-018-06125-0

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