Dr. Jacob M Levenstein
MRI Scientist, Thompson Institute
Member, Healthy Ageing Research Cluster
Email: jlevenstein@usc.edu.au
Telephone: +61 4 5456 5140
As a neuroscientist specialising in neuroimaging, I am passionate about exploring brain structure, function, and neurochemistry to deepen our understanding of the human brain in both health and disease. Since 2012, I have been involved in neuroimaging research, working across several world-leading neuroimaging institutes, including the Martinos Center (Harvard), FMRIB (Oxford) and SFIM (NIH).
Research
Publications
Journal article
Correction to “The Myokine Irisin Represents an Indirect Pathway Linking Exercise to Hippocampal Subfields Relevant to Alzheimer's Disease and Neurogenesis” ↗
by Thomas Pace, Jacob M. Levenstein, Bonnie L. Quigley, Sophie C. Andrews, Rhys Houston and Ana P. Bouças
2026
Aging Cell
In the published article, the commercial ELISA kit used to measure circulating irisin was reported incorrectly. The kit used in the present study was Phoenix Pharmaceuticals catalogue number EK-067-29, not EK-067-52. The Methods section reported the quantifiable range associated with EK-067-52, and the Discussion section named EK-067-52 as the kit used in the validation passages. The corrections below identify each affected passage and provide the corrected text. All 74 samples were assayed using a single lot of EK-067-29 under identical conditions, and all irisin values were natural log-transformed and z-scored prior to analysis. Every measurement, analysis, and reported result was derived from the EK-067-29 assay throughout, so correcting the catalogue label in the text does not alter any raw value, statistical model, or finding. The results, statistical analyses, figures, and conclusions of the article remain as published.....
Journal article | Peer reviewed
Age-related inhibitory decline: Examining inhibition subcomponents and their impact on sustained attention in healthy aging ↗
by Ciara Treacy, Sophie C Andrews and Jacob M Levenstein
2026
Neuropsychology
Objective: The inhibition deficit hypothesis postulates that inhibitory functioning declines with age, which negatively impacts other cognitive abilities. Yet still, the impact of healthy aging on inhibitory functioning remains unclear, with the multifaceted nature of inhibition often an overlooked factor. Moreover, no prior study has empirically tested whether inhibitory subcomponents explain differential age effects in sustained attention—an open question that this work aimed to address. Method: We cross-sectionally investigated the inhibition deficit hypothesis in 80 healthy older adults (Mage = 67.78 years, 44 female). We utilized the PsyToolkit platform to administer three inhibition tasks (i.e., flanker, Stroop, and go/no-go), each targeting a distinct subcomponent process, along with the Sustained Attention to Response Task. Results: The flanker task had low internal consistency and was deemed unreliable. Semipartial correlations of the remaining inhibition measures with age resulted in significant positive relationships with task performance on the Stroop (errors: ρ = 0.337, p = .014; reaction time: ρ = 0.313, p = .028) and a negative association with the go/no-go (balanced integrated score: ρ = −0.471, p < .001), such that older individuals had more pronounced Stroop effects and worse overall go/no-go performance. Finally, go/no-go performance completely mediated the relationship between aging and sustained attention performance (t = −2.30, 95% CI [−0.05, −0.01]), while Stroop effects partially mediated this association (t = −2.16, 95% CI [−0.03, −0.002]). Conclusions: Age-related declines were observed across reliable inhibition tasks, lending support for the inhibition deficit hypothesis. The mediation findings demonstrate that inhibitory subcomponents account for age-related declines in sustained attention, over and beyond aging itself via an indirect path, representing an important cognitive domain to maintain throughout aging.
Journal article | Peer reviewed
The Myokine Irisin Represents an Indirect Pathway Linking Exercise to Hippocampal Subfields Relevant to Alzheimer's Disease and Neurogenesis ↗
by Sophie C. Andrews, Thomas Pace, Jacob M. Levenstein, Bonnie L. Quigley, Rhys Houston and Ana P. Bouças
2026
Aging Cell
While exercise is shown to reduce hippocampal atrophy, the underlying molecular mechanisms remain to be fully elucidated. Animal studies suggest the myokine irisin underlies exercise‐related hippocampal benefits, though human evidence is lacking. We cross‐sectionally examined 74 healthy older adults (age 65.47 ± 8.56 years). Participants completed Godin Leisure‐Time exercise questionnaires, provided fasting blood for irisin measurement and underwent structural MRI with hippocampal subfield segmentation. Hierarchical regression and mediation analyses tested irisin‐mediated exercise‐hippocampus relationships, controlling for age, sex and education. Exercise positively associated with circulating irisin (β = 0.365, p = 0.003). Irisin positively associated with bilateral hippocampal volumes (right: β = 0.353, p = 0.001; left: β = 0.275, p = 0.012), strongest in right‐CA3 (β = 0.530), right‐CA4/dentate gyrus (β = 0.471), and bilateral CA1 (β = 0.336–0.373) subfields. Mediation analysis revealed all exercise‐hippocampus relationships operated indirectly through irisin. This study provides first human evidence that irisin is a molecular mechanism linking exercise to hippocampal volume, particularly in subfields critical for memory, neurogenesis and Alzheimer's pathology. Trial Registration: Australian New Zealand Clinical Trials Registry: ACTRN12620000054910 We provide the first human evidence that the exercise‐induced myokine irisin mediates the relationship between physical activity and hippocampal volume in older adults, with strongest effects in CA1, CA3 and CA4 subfields. These regions are critical for memory and particularly vulnerable to Alzheimer's disease.
Journal article | Peer reviewed
Resting-state EEG aperiodic exponent moderates the association between age and memory performance in older adults ↗
by Sophie C. Andrews, Thomas Pace, Alicia J. Campbell, Jim Lagopoulos, Daniel F. Hermens, Jacob M. Levenstein, Toomas Erik Anijärv and Mikael Johansson
2026
Neurobiology of Aging
Memory functions are susceptible to age-related cognitive decline, making it essential to explore the underlying neurophysiological mechanisms that contribute to memory function during healthy ageing. Resting-state EEG (rsEEG) parameters, particularly the aperiodic exponent, a marker of cortical excitation-inhibition balance, and individual alpha peak frequency, a correlate of neural processing efficiency, have demonstrated associations with ageing and cognitive functions. This study investigated associations between these rsEEG markers and performance across multiple memory systems in healthy older adults (n = 99) aged 50–84 years, specifically the direct associations of these markers on memory across episodic, working, and visual short-term memory systems, assessed via computerised tasks, as well as their moderating effects on age-memory relationships. While no direct associations were seen between rsEEG markers and memory performance across tasks beyond the contribution of age, gender and education, results revealed significant moderating effects of the aperiodic exponent on age-related performance in episodic and visual short-term memory. Notably, for individuals with a higher exponent, age was not significantly associated with episodic or visual short-term memory performance, whereas those with average and lower exponent values showed poorer performance with older age. These findings suggest that average and lower aperiodic exponents may reflect a marker of decrement in age-related memory performance and higher exponents may index an underlying protective mechanism against age-related memory decline. This investigation extends the current understanding of cognitive ageing mechanisms by identifying the aperiodic exponent as a potential biomarker explaining individual differences in cognitive ageing trajectories in older adult populations, particularly in episodic and visual short-term memory systems, and establishes a framework for studying neuroprotective mechanisms and developing interventions to preserve cognitive function in older adults.
Journal article | Peer reviewed
Diet quality, nutrient adequacy, and symptom associations in ADHD: A case-control study of Australian adolescents ↗
by Naomi Lewis, Jacob M. Levenstein and Anthony Villani
2026
Nutritional Psychiatry
Introduction
Nutrition may influence attention-deficit/hyperactivity disorder (ADHD) symptom severity however evidence is limited. This study examined adherence to a healthy dietary pattern, nutrient intakes, and associations with symptoms and cognitive performance in Australian adolescents with ADHD.
Methods
This case-control study included 39 adolescents (18 ADHD; 21 healthy controls) aged 13-18 years. Groups were compared on dietary variables including Mediterranean diet (MedDiet) adherence (KIDMED) and energy-adjusted nutrient intakes, and on nutrient adequacy against nutrient reference values (NRVs). Associations between dietary variables and self-reported ADHD symptoms (Adult ADHD Self-Report Scale) and cognitive performance (Test of Variables of Attention) were examined. Combined (ADHD-C) and inattentive (ADHD-I) subtypes were also analysed.
Results
Dietary variables and nutritional adequacy did not significantly differ between groups, however sweets consumption was greater in ADHD (p = .002). Group × age interactions were observed for KIDMED (p = .022, η2p = .15), magnesium (p = .011, η2p = .20), and iron (p = .010, η2p = .20), and a group × gender interaction for beta-carotene (p = .032, η2p = .14). The strongest correlations involved cognitive outcomes with KIDMED and vitamin B12 (positive), and omega-6:omega-3 (negative), and KIDMED with symptoms (negative). Among subtypes, ADHD-C met more NRVs than ADHD-I (69.2% vs. 38.5%, p = .014).
Conclusion
Although few dietary differences were observed between ADHD and controls, symptom and cognitive performance associations highlight the clinical relevance of dietary factors. Larger studies are needed to further examine nutrition in ADHD, particularly the potential moderating effects of age, gender, and subtype.
Showing the five most recent publications. Explore all Dr. Jacob M Levenstein's publications in UniSC Research Bank
Grants
1 January 2024 - 10 April 2026
Study of Brain Imaging & Gut Microbiome in Anorexia Nervosa & Exposure to Trauma (SIGNET)
University of the Sunshine Coast (Australia, Sunshine Coast) - UniSC
Grant no. 0980028704.
Kathina Ali, Catherine Houlihan, Kate Mulgrew, Jacob Levenstein and Daniel Hermens
1 November 2024 - 31 March 2026
Acquisition of MRI-Compatible EEG Nets for a Simultaneous EEG-fMRI Platform
University of the Sunshine Coast (Australia, Sunshine Coast) - UniSC
Grant no. 0980029647.
Amanda Boyes, Mathew Summers, Varghese Peter, Jacob Levenstein, Sophie Andrews, Michael Carey, Daniel Hermens and Thomas Pace
15 June 2023 - 27 July 2024
Naturalistic-fMRI Functional Connectivity Biomarkers Define Subtypes of Healthy Brain Aging and Cognitive Profiles
University of the Sunshine Coast (Australia, Sunshine Coast) - UniSC
Grant no. 0980028321.
Jacob Levenstein
Teaching and supervision
Supervision
Doctoral Thesis Supervision - Completed
Low Dose Oral Ketamine as a Treatment for Post-Traumatic Stress Disorder
Students: Grace Forsyth
Principal Supervisor: Robert Harvey
Co-Supervisor: Dr. Jacob M Levenstein
2020 - 2026
Doctoral Thesis Supervision - Completed
Dietary intake, gut microbiome, and neurometabolite profiles in adolescents with attention-deficit/hyperactivity disorder
Students: Naomi Lewis
Principal Supervisors: Dr. Jacob M Levenstein and Anthony Villani
2021 - 2026
Doctoral Thesis Supervision - Completed
Executive Functioning and Brain Ageing: Investigating the MRI-assessed Neurobiology Subserving Sustained Attention and Inhibitory Sub-components in Healthy Older Adults
Students: Ciara Treacy
Principal Supervisor: Dr. Jacob M Levenstein
Co-Supervisor: Sophie Andrews
1 January 2022 - 4 June 2025
Doctoral Thesis Supervision - Current
Investigating the Impact of MTHFR Genetic Variations on Brain Electrical Activity: A qEEG Study
Students: Research student (name withheld)
Principal Supervisor: Florin Oprescu
Co-Supervisors: Barnaby J W Dixson, Varghese Peter and Dr. Jacob M Levenstein
2025
Doctoral Thesis Supervision - Completed
Conditioning on the Brain: Electroencephalography Derived Non-Linear Indices of Brain Dynamics and the Association with Oral Ketamine Treatment Response
Students: Jules Mitchell
Principal Supervisor: Daniel Hermens
Co-Supervisor: Dr. Jacob M Levenstein
2022 - 2025
Showing the five most recent supervisions. Explore all Dr. Jacob M Levenstein's supervisions in UniSC Research Bank
Professional
Awards and memberships
2016-2021
NIH Oxford-Cambridge Scholars Program
National Institutes of Health (United States, Bethesda) - NIH
Education
October 2016 - 22 February 2021
Doctor of Philosophy
Neuroscience, Neuroimaging
University of Oxford (United Kingdom, Oxford)
October 2014 - October 2015
Master of Science (MSc, MSc, MSci, MSi, ScM, MS, MSHS, MS, Mag, Mg, Mgr, SM, or SM)
Experimental Psychology
University of Oxford (United Kingdom, Oxford)
September 2008 - June 2012
Bachelor of Arts (BA, AB, BS, BSc, SB, ScB)
Cognitive Studies
Endicott College (United States, Beverly Cove)