Brett Lidbury

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Brett A. Lidbury, B.Sc, B.Sc (Hons) (Newcastle), PhD (ANU), FFSc (RCPA), is an Associate Professor with the National Centre for Epidemiology and Population Health (Research School of Population Health), College of Health and Medicine at the Australian National University. His areas of expertise are medical virology, innate immunity, and biostatistics. Research interests include improving the efficacy of diagnostic pathology and biomarker pattern discovery, particularly in relation to ME/CFS and infectious diseases. Earlier research activity was interested in Ross River virus (RRV) pathogenesis, which as an Australian viral suspect in long-term fatigue, lead to current endeavors for chronic fatigue syndrome/myalgic encephalomyelitis. His work is entirely focused on human biology and pathology, without the requirement to develop an animal model.[1]

ME/CFS research[edit | edit source]

Dr Lidbury and his colleagues are conducting Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) studies that are ongoing with research participants recruited and assessed by CFS Discovery in Melbourne (Donvale, VIC 3111), in collaboration with the Hudson Research Institute, Paranta Biosciences, Bio21 Institute (University of Melbourne), La Trobe University and Universidad del Rosario, Bogota (School of Medicine and Health Sciences). Via these collaborations we are gathering data on potential immune serum markers (see Activin B), mitochondrial function and metabolomics, as well as genetics, with the ANU group applying computational methods, for example machine learning, to interrogate these results as a systems biology investigation. A strength at the ANU is also the assessment of pathology and clinical data to increase diagnostic prediction, while developing rules to simplify decision-making for patient assessment.

The ME/CFS project for the validation of Activin markers is funded by the Judith Jane Mason & Harold Stannett Williams Memorial Foundation, and projects concerning genetic analyses are funded by ME Research UK.[2]

Awards[edit | edit source]

  • Nominee for 2016 ACT Scientist of the Year[3]
  • Fellowship to the Faculty of Science, The Royal College of Pathologists of Australasia.

Notable studies[edit | edit source]

Talks and interviews[edit | edit source]

Online presence[edit | edit source]

See also[edit | edit source]

Learn more[edit | edit source]

References[edit | edit source]

  1. "Associate Professor Brett Lidbury". researchers.anu.edu.au. Retrieved September 25, 2019.
  2. "ME Research UK | Energising ME research". Retrieved September 25, 2019.
  3. Australia, ~ ME news (July 11, 2016). "ME microbiome scientist nominated as ACT Scientist of the Year". ME Australia. Retrieved September 25, 2019.
  4. Reynolds, G. K.; Lewis, D. P.; Richardson, A. M.; Lidbury, B. A. (April 2014). "Comorbidity of postural orthostatic tachycardia syndrome and chronic fatigue syndrome in an Australian cohort". Journal of Internal Medicine. 275 (4): 409–417. doi:10.1111/joim.12161.
  5. Lidbury, Brett; Badia, Kita; Lewis, Donald; Hayward, Susan; Ludlow, Helen; Hedger, Mark; de Kretser, David (2017), "Activin B is a novel biomarker for chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) diagnosis: a cross sectional study", Journal of Translational Medicine, doi:10.1186/s12967-017-1161-4
  6. Richardson, Alice M.; Lewis, Don P.; Kita, Badia; Ludlow, Helen; Groome, Nigel P.; Hedger, Mark P.; de Kretser, David M.; Lidbury, Brett A. (December 2018). "Weighting of orthostatic intolerance time measurements with standing difficulty score stratifies ME/CFS symptom severity and analyte detection". Journal of Translational Medicine. 16 (1): 97. doi:10.1186/s12967-018-1473-z. ISSN 1479-5876. PMC 5898049. PMID 29650052.
  7. Missailidis, Daniel; Annesley, Sarah; Allan, Claire; Sanislav, Oana; Lidbury, Brett; Lewis, Don; Fisher, Paul (September 4, 2019). "An Isolated Complex V Inefficiency and Dysregulated Mitochondrial Function in Immortalized Lymphocytes from ME/CFS Patients". Preprints. doi:10.20944/preprints201909.0043.v1.
  8. Lidbury, Brett A.; Fisher, Paul R. (February 8, 2020). "Biomedical Insights That Inform the Diagnosis of ME/CFS". Diagnostics. 10 (2): 92. doi:10.3390/diagnostics10020092. ISSN 2075-4418.

myalgic encephalomyelitis (M.E.) - A disease often marked by neurological symptoms, but fatigue is sometimes a symptom as well. Some diagnostic criteria distinguish it from chronic fatigue syndrome, while other diagnostic criteria consider it to be a synonym for chronic fatigue syndrome. A defining characteristic of ME is post-exertional malaise (PEM), or post-exertional neuroimmune exhaustion (PENE), which is a notable exacerbation of symptoms brought on by small exertions. PEM can last for days or weeks. Symptoms can include cognitive impairments, muscle pain (myalgia), trouble remaining upright (orthostatic intolerance), sleep abnormalities, and gastro-intestinal impairments, among others. An estimated 25% of those suffering from ME are housebound or bedbound. The World Health Organization (WHO) classifies ME as a neurological disease.

serum The clear yellowish fluid that remains from blood plasma after clotting factors have been removed by clot formation. (Blood plasma is simply blood that has had its blood cells removed.)

mitochondria Important parts of the biological cell, with each mitochondrion encased within a mitochondrial membrane. Mitochondria are best known for their role in energy production, earning them the nickname "the powerhouse of the cell". Mitochondria also participate in the detection of threats and the response to these threats. One of the responses to threats orchestrated by mitochondria is apoptosis, a cell suicide program used by cells when the threat can not be eliminated.

mitochondria Important parts of the biological cell, with each mitochondrion encased within a mitochondrial membrane. Mitochondria are best known for their role in energy production, earning them the nickname "the powerhouse of the cell". Mitochondria also participate in the detection of threats and the response to these threats. One of the responses to threats orchestrated by mitochondria is apoptosis, a cell suicide program used by cells when the threat can not be eliminated.

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