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SRI Profiles

Photo of JoAnne McLaurin
JoAnne McLaurin

Senior scientist

Sunnybrook Health Sciences Centre
2075 Bayview Ave., Room S1 13
Toronto, ON
M4N 3M5

Phone: 416-480-6100, ext. 7720
Fax: 416-480-5737

Administrative Assistant: Melanie Suttar
Phone: 416-480-6100, ext 3536
Email: melanie.suttar@sri.utoronto.ca

Education:

  • B.Sc., 1983, chemistry, Queen’s University, Canada
  • M.Sc., 1988, clinical biochemistry, University of Toronto, Canada
  • PhD, 1992, clinical biochemistry, U of T, Canada

Appointments and Affiliations:

Research Foci:

  • Alzheimer’s disease
  • Small molecule therapies
  • Stroke and Alzheimer’s disease
  • Neurodegeneration
  • Vascular risk factors for Alzheimer’s disease
  • Neuropsychiatric symptoms in Alzheimer’s disease

Research Summary:

Dr. McLaurin’s research focuses on the development of potential therapeutics to target protein-misfolding disorders, in particular Alzheimer’s disease. Stemming from the basic research of protein-lipid interactions, her laboratory identified a family of naturally occurring compounds that inhibit the formation of toxic soluble aggregates in Alzheimer’s disease. These molecules underwent preclinical studies to demonstrate efficacy and are now being evaluated in Phase II clinical trials. This work is being expanded to examine other neurodegenerative disorders such as amyotrophic lateral sclerosis, Huntington’s disease and Parkinson’s disease to investigate the possibility of a universal anti-aggregant small molecule.

Because amyloid formation and disease progression cannot be monitored at present, her lab is attempting to develop a diagnostic based on compounds that bind amyloid but are not effective therapeutics. The latest endeavours include characterization of novel therapeutics that might be used in combination with small molecule therapies to recover full functioning in patients with Alzheimer’s disease. This work is based on the premise that strategies in clinical trials to date will have some beneficial effects in stabilizing disease progression, yet to achieve optimal cognitive functioning, combination therapies that address other targets will be necessary.

Selected Publications:

See current publications list at PubMed.

  1. Ma K, McLaurin J. a-Melanocyte stimulating hormone prevents GABAergic cell loss to improve cognition in Alzheimer’s disease. J Neuroscience. 2014;34(20):673–6745.
  2. Lai AY, Lan C, Hasan S, McLaurin J. scyllo-inositol-induced inhibition of inclusion body formation promotes robust mutant Huntington protein degradation. J Biol Chem. 2014;289:3666–3676.
  3. Dorr A, Sahota B, Chinta, LV, Lai, AY, Ma K, Brown ME, Hawkes CA, McLaurin J, Stefanovic B. Progressive β-amyloid dependent compromise of microvascular structure and function in Alzheimer’s disease. Brain. 2012;135:3039–3050.
  4. Hawkes CA, McLaurin J. Cerebral amyloid angiopathy is cleared by perivascular macrophages in the TgCRND8 mouse model of Alzheimer’s disease. Proc Natl Acad Sci USA. 2009:106:1261–1266.
  5. McLaurin J, Barakat ME, Brown ME, Hawkes CE, Lambermon MHL, Phinney AL, Darabie AA, Cousins JE, French JE, Lan MF, Chen F, Wong SFFN, Mount HTJ, Fraser PE, Westaway DE, St George-Hyslop P. Cyclohexanehexol-based inhibitors of Ab-aggregation prevent and reverse Alzheimer-like features in a transgenic model of Alzheimer disease. Nature Medicine. 2006;12:801–808.

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