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A/Prof. Ryu Takechi

Associate Director and Associate Professor
(Research & Commercialisation)

Neurovascular and Metabolic Research

The human brain is an extraordinary and intricate organ that shapes who we are, how we think, and how we experience the world. From early in my career, I have been fascinated by its complexity and by how even subtle biological changes can profoundly affect memory, behaviour, and cognition. Dementia and other neurodegenerative diseases are devastating, taking away a person’s sense of self and independence. My research is driven by the belief that a deeper understanding of the brain’s biology can lead to new ways to prevent, delay, or treat these conditions, ultimately improving the lives of those affected and their families.    

About

Associate Professor Ryu Takechi is an accomplished neuroscientist and vascular biologist with membership in leading professional bodies, including the Australasian Neuroscience Society, ISCBFM, Australian Vascular Biology Society, and the International Alzheimer’s Association.

With over $12 million in competitive research funding, A/Prof Ryu Takechi has led major projects supported by the NHMRC, MRFF, ARC, and the Bryant Stokes Neurological Research Foundation, focusing on neurodegeneration, vascular health, and metabolic disease.

His work has been recognised through multiple honours, including the Curtinnovation Award (2022), Mid-Career Researcher Award (2023), and the NHMRC Marshall and Warren Award (2014).

He also holds several patents in therapeutic innovations for neurological and neurodegenerative disorders, including cannabinoid encapsulation and bile acid conjugate technologies.

 
  • ISCBFM
  • ANZ Microcirculation Society
  • Australian Vascular Biology Society
  • Society of Neuroscience WA (SWAN)
  • Australasian Neuroscience Society
  • Nutrition Society Australia
  • Australian Society of Medical Research
  • Australian Vascular Biology Society
  • Dementia Australia Research Foundation
  • International Alzheimers Association
  • 2025-2026 Bryant Stokes Neurological Research Foundation Project Grant $75,000 (CIA)
  • 2024-2025 ARC LIEF $754,000 (CI)
  • 2023-2024 Department of Health FHRIF Innovation Fellowship $150,000
  • 2021-2024 NHMRC Ideas Grant $637,000
  • 2021 Neurotrauma Research Program Project Grant $100,000 (CIA)
  • 2020-2023 MRFF Neurological Disorders Grant $1,720,000 (CI)
  • 2020 NHMRC Equipment Grant $25,000 (CI)
  • 2020 MHRIF, WA Department of Health $20,384 (CIA)
  • 2019 MSWA Project Grant $150,000 (CI)
  • 2019 MHRIF, WA Department of Health $23,467 (CIA)
  • 2019 Curtin Grant Success Panel Near-miss Funding $10,000 (CIA)
  • 2018-2020 Zelda Therapeutics Ltd $75,000 (CIA)
  • 2018-2019 Hunter Medical Foundation Diabetes Project Grant $20,000 (CIB)
  • 2018 NHMRC Euipment Grant $39,000 (CIA)
  • 2018 Dementia Australia Research Foundation Project Grant $50,000 (CIA)
  • 2018-2021 NHMRC Boosting Dementia Research Leadership Fellowship $719,000 (CIA)
  • 2017-2018 NHMRC Career Development Fellowship $425,048 (CIA)
  • 2018 MHRIF, WA Department of Health $17,375 (CIA)
  • 2017 Australian Synchrotron $2,860 (CIB)
  • 2017 Australian Synchrotron $2,860 (CID)
  • 2017 Australian Synchrotron $2,860 (CIC)
  • 2016-2019 NHMRC Project Grant $261,250 (CIA)
  • 2016- Curtin Senior Research Fellowship (CIA)
  • 2014-2018 NHMRC Project Grant $445,206 (CIB)
  • 2014-2015 New Independent Researcher Infrastructure Fund, Department of Health $10,000
  • 2013 Public Health Strategic Seed Funding $10,000 (CIA)
  • 2012-2015 NHMRC ECR Fellowship $294,892 (CIA)
  • 2010-2011 Curtin Health Innovation Research Institute Postdoctoral Fellowship $76,377 (CIA)
  • 2009-2011 NHMRC Project Grant $564,839 (CIC)
  • 2023 Mid-Career Researcher Award (Curtin University)
  • 2022 Curtinnovation Award
  • 2021 Best Research Mentor of the Year
  • 2021 Best Publication Award
  • 2014 NHMRC Marshall and Warren Award
  • 2014 Highest Resarch Performance Indext Prize, Curtin University
  • 2013 Early Career Resarcher of the Year, Curtin University
  • 2010 Best Graduate Award, 2nd International Symposium on Chylomicrons in disease
  • 2009 Best Student Award, Annual Scientific Meeting of Australian Atherosclerosis Society
  • 2009 International Graduate Student Award, 41st Annual Scientific Meeting of Japan Atherosclerosis Society
  • 2007 Young Scholar Travel Support Award, International Symposium on Chylomicrons in Disease
  • 2006-2009 Curtin International Research Tuition Scholarship
  • 2004 Research Traineeship, University of Alberta, Canada
  • 2003 Ochi Foundation Young Scholar Award, 3rd International Conference on Food Factors
  • 2002-2003 Hyogo University Mobility in Asia and Pacific Scholarship
  • Clinical Randomised Controlled Trial: Cerebrovascular-focussed drug intervention study to stabilize cognitive perfomance in subjects with mild cognitive impairment
  • The effects of medicinal cannabinoid on cerebrovascular integrity and cognitive decline in DiAD: Diabetes-induced Alzheimer's Disease
  • The role of lipoprotein-associated amyloid-beta in subjects with type-2 diabetes
  • The effects of repeated sub-concussive impacts on blood-brain barrier and cognitive performance
  • The acute effects of dietary fat ingestion on plasma levels of lipoprotein-associated amyloid-beta

EMAIL: r.takechi@curtin.edu.au
TEL: +61 (08) 9266 1715
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Curtin Staff Profile

Cannabinoid encapsulation technology AU2021376539A1
Bile Acid Conjugate WO2022094671A1
Provisional: agent for neurological disorders WO2023102613A1
Provisional: probucol for neurodegenerative disorders

Research Focus

Associate Professor Ryu Takechi is  a translational neuroscience researcher specialising in the study of neurodegenerative disorders. His research investigates how metabolic, vascular, and inflammatory factors contribute to cognitive decline and Alzheimer’s disease, particularly in the context of type 2 diabetes and brain injury.

His work combines biodiscovery science with clinical translation, identifying disease mechanisms and potential therapeutic agents through laboratory research, followed by clinical trials and cohort studies to validate preclinical findings. Current projects include:

 

Research Team

Dr Virginie Lam

EMCR Chair

Dr Arazu Shariff

Research Assistant

Harry Speed

Research Assistant

Michael Nesbit

Technical Specialist

Emily Brook

PhD Student

Publications

ABSTRACT

Natural aging is associated with mild memory loss and cognitive decline, and age is the greatest risk factor for neurodegenerative diseases, such as Alzheimer’s disease. There is substantial evidence that oxidative stress is a major contributor to both natural aging and neurodegenerative disease, and coincidently, levels of redox active metals such as Fe and Cu are known to be elevated later in life. Recently, a pronounced age-related increase in Cu content has been reported to occur in mice and rats around a vital regulatory brain region, the subventricular zone of lateral ventricles. In our study herein, we have characterized lateral ventricle Cu content in a unique murine model of accelerated aging, senescence accelerated mouse-prone 8 (SAMP8) mice. Our results confirm an age-related increase in ventricle Cu content, consistent with the studies by others in wild-type mice and rats. Specifically, we observed Cu content to increase over the time frame 1 to 5 months and 5 to 9 months, but interestingly, no significant increase occurred between 9 and 12 months (although brain Cu content at 12 months was significantly elevated relative to 1 and 5 month-old animals). Despite the magnitude of Cu increase observed within the cells that comprise the subventricular zone of lateral ventricles (average 3 mM Cu, with isolated subcellular concentrations of 17 mM), we did not detect spectroscopic markers of thiol oxidation, protein aggregation, or lipid oxidation. The lack of evidence for oxidative stress in ex vivo animal tissue is in contrast to in vitro studies demonstrating that thiol, protein, and lipid oxidation is pronounced at these Cu concentrations. We suggest that our findings most likely indicate that the Cu ions in this brain region are sequestered in an unreactive form, possibly extended chains of Cu-thiolate complexes, which do not readily redox cycle in the aqueous cytosol. These results also appear to partially challenge the long-held view that age-related increases in brain metal content drive oxidative stress as we did not observe a concomitant association between age-related Cu increase and markers of oxidative stress, nor did we observe a net increase in Cu content between mice aged 9 and 12 months.

Hollings, A. L., G. C. Ellison, M. Willans, V. Lam, T. Munyard, A. R. Remy, R. Takechi, J. C. L. Mamo, S. Webb, E. J. New, and 6 more contributors. 2025.Subventricular Accumulation of Cu in the Aging Mouse Brain Does Not Associate with Anticipated Increases in Markers of Oxidative Stress.ACS Chemical Neuroscience 16 (3): 292-302.
ABSTRACT

Peripheral amyloid-beta (Aβ), including those in bloodstream and intestine, is implicated in the pathogenesis of Alzheimer’s disease (AD). Additionally, diabetes and insulin resistance are associated with the impairment of Aβ metabolism and an increased risk of developing cognitive decline and AD. Previous research has demonstrated the neuroprotective effects of cannabidiol (CBD) and S-allyl-cysteine (SAC); however, their impact on Aβ levels in the context of diabetes remains unexplored. 5-week-old diabetic db/db mice underwent 23 weeks of dietary interventions with SAC, CBD, or a combination of SAC and CBD. Immunofluorescent imaging quantified enterocytic Aβ abundance and plasma concentrations of Aβ42, Aβ40, and Aβ oligomers were measured using ELISA. Our results reveal a progressive increase in enterocytic Aβ expression in db/db mice, which was mitigated by SAC administration. In contrast, CBD treatment alone and in combination with SAC, increased enterocytic Aβ abundance and elevated plasma Aβ42 concentrations. The combination therapy reduced Aβ oligomers. These findings suggest that the neuroprotective effects of SAC are partially mediated by its impact on peripheral Aβ levels. CBD could potentially exacerbate Aβ accumulation in diabetes.

Sharif, A., M. Majimbi, J. Mamo, V. Lam, M. Nesbit, and R. Takechi. 2025.Differential effects of S-allyl cysteine and cannabidiol on enterocytic and plasma amyloid-β in db/db diabetic mice.Scientific Reports 15 (1)

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