NeuroTrax Science Team and Glen M. Doniger, PhD

Advances in genetic testing have made it possible to identify individuals at increased risk for neurological conditions long before symptoms appear. However, understanding how genetic risk translates into measurable changes in brain function remains a critical challenge. NeuroTrax, a digital neuromarker, helps bridge this gap by providing objective cognitive assessments that can detect subtle changes in brain performance and support the longitudinal monitoring of at-risk populations [1].

Research has demonstrated the value of NeuroTrax in studying individuals who carry genetic mutations associated with Parkinson's disease. In healthy carriers of the LRRK2 mutation, NeuroTrax executive function performance was lower compared with non-carriers, despite both groups appearing cognitively normal on conventional screening measures [2]. These findings suggest that with precision neurometrics, cognitive differences may be detectable years before clinical symptoms emerge.

Similarly, NeuroTrax has been used to evaluate individuals carrying GBA1 variants, which are associated with an increased risk of Parkinson's disease and Gaucher disease. Studies have identified differences in executive and visual spatial functioning among carriers, helping researchers better understand the earliest stages of disease-related cognitive change [1,3]. By capturing these subtle patterns, NeuroTrax provides an objective way to monitor brain wellness and track potential changes over time.

NeuroTrax has contributed to research involving inherited metabolic and lysosomal storage disorders, including the aforementioned Gaucher disease and Tay-Sachs disease. In late-onset Tay-Sachs disease, NeuroTrax assessments revealed significant impact on verbal and executive function, helping define disease-specific cognitive profiles that may support earlier detection and monitoring [4].

Genetic influences can also contribute to resilience rather than risk. Research involving carriers of the CCR5-Δ32 polymorphism found improved cognitive recovery following stroke and traumatic brain injury, highlighting how NeuroTrax can be used to measure both vulnerability and recovery across diverse patient populations [5].

As precision medicine continues to advance, NeuroTrax is helping researchers and clinicians better understand the relationship between genetics, cognition, and brain health. As a digital neuromarker, it provides objective, repeatable insights into cognitive performance, enabling earlier detection of change, more informed risk stratification, and a deeper understanding of brain wellness across genetically at-risk populations.

References:

[1] Becker-Cohen, M., Zimran, A., Dinur, T., Tiomkin, M., Rolfs, A., Arkadir, D., Bauer, P., Shulman, E., Yahalom, G., Cohen, M.E., Manor, O., Paltiel, O., and Revel-Vilk, S. (2025). Prodromal Parkinsonian features in carriers of Gaucher disease compared to controls. Life, 15:952. DOI: 10.3390/life15060952

[2] Thaler, A., Mirelman, A., Simon, E., Orr-Urtreger, A., Gurevich, T., and Giladi, N. (2012). Lower cognitive performance in healthy G2019S LRRK2 mutation carriers. Neurology, 79(10), 1027–1032. DOI: 10.1212/WNL.0b013e3182684646

[3] Thaler, A., Kliper, E., Maidan, I., Herman, T., Rosenberg-Katz, K., Bregman, N., Gurevich, T., Shiner, T., Hausdorff, J.M., Orr-Urtreger, A., Giladi, N., and Mirelman, A. (2018). Cerebral imaging markers of GBA and LRRK2 related Parkinson’s disease and their first-degree unaffected relatives. Brain Topography, 31(6), 1029–1036. DOI: 10.1007/s10548-018-0653-8

[4] Elstein, D., Doniger, G.M., Simon, E., Korn-Lubetzki, I., Navon, R., and Zimran, A. (2008). Neurocognitive testing in Late-onset Tay-Sachs disease: A pilot study. Journal of Inherited Metabolic Disease, 31(4), 518–523. DOI: 10.1007/s10545-008-0884-z

[5] Joy, M.T., Ben Assayag, E., Shabashov-Stone, D., Liraz-Zaltsman, S., Mazzitelli, J., Arenas, M., Abduljawad, N., Kliper, E., Korczyn, A.D., Thareja, N.S., Kesner, E.L., Zhou, M., Huang, S., Silva, T.K., Katz, N., Bornstein, N.M., Silva, A.J., Shohami, E., and Carmichael, S.T. (2019). CCR5 is a therapeutic target for recovery after stroke and traumatic brain injury. Cell, 176(5), 1143–1157. DOI: 10.1016/j.cell.2019.01.044

NeuroTrax Science Team and Glen M. Doniger, PhD

The linkage between brain health and cellular processes is becoming increasingly clear. While cognitive performance has traditionally been assessed with behavioral testing, emerging research shows how underlying cellular processes like telomere dynamics play a critical role in shaping brain function over time. This body of research points to a more integrated view of cognitive health. Brain function is not only influenced by neurological or psychological factors, but also by the underlying biological systems that support cellular integrity and resilience.

Telomeres, the protective caps at the ends of chromosomes, are widely recognized as markers of biological aging. As cells divide, telomeres naturally shorten, and accelerated shortening has been linked to a range of age-related conditions. It is becoming apparent that these cellular processes may be specifically tied to cognitive health.

A longitudinal study by Cohen-Manheim and colleagues provides one of the clearest links between telomere dynamics and cognition. The researchers tracked leukocyte telomere length in nearly 500 healthy individuals over more than a decade, measuring changes in early adulthood and then assessing cognitive performance in midlife using NeuroTrax as a standardized digital neuromarker (1). Their findings showed that individuals with faster telomere attrition in young adulthood performed significantly poorer in global cognition and multiple cognitive domains later in life, including memory, information processing speed, and visual-spatial function.

These findings represent a shift in our understanding of cognitive aging. Rather than viewing cognitive decline as emerging later in life, the study suggests that its cellular foundations may be laid decades earlier. Telomere attrition, in this context, may represent one of the earliest measurable markers of future cognitive health (1).

In addition to telomeres, other biological markers are tied to cognitive outcomes. For example, related research has shown that increased systemic inflammation, measured by biomarkers like GlycA, are associated with poorer cognitive performance and slower processing speed in midlife (2). Similarly, lipid profiles and apolipoprotein levels in early adulthood have been shown to predict cognitive decline on NeuroTrax neurometrics nearly two decades later (3). Taken together, these findings reinforce the idea that cognitive health is closely tied to physiological processes.

Critically, interventions targeting biological markers may improve cognitive function. A recent hyperbaric oxygen therapy (HBOT) case report demonstrated that changes in cellular health, including increased telomere length, were accompanied by gains in multiple cognitive domains captured by NeuroTrax (4). Further research is needed, but these findings suggest that targeting biological aging processes may have a direct and measurable impact on brain efficiency.

Insights into biological processes become actionable when paired with objective neurometrics. NeuroTrax serves as a digital neuromarker, providing standardized, high-resolution data that quantifies brain efficiency. This allows researchers and clinicians to translate cellular-level changes into measurable cognitive outcomes, bridging the gap between laboratory biomarkers and real-world brain performance. By combining biological markers like telomere dynamics with NeuroTrax, brain health can be monitored proactively across the lifespan. Rather than waiting for symptoms to emerge, early changes in cellular aging may offer a window into cognitive risk and facilitate earlier intervention.

References:

[1] Cohen-Manheim, I., Doniger, G.M., Sinnreich, R., Simon, E.S., Pinchas, R., Aviv, A., and Kark, J.D. (2016). Increased attrition of leukocyte telomere length in young adults is associated with poorer cognitive function in midlife. European Journal of Epidemiology, 31, 147–157. DOI: 10.1007/s10654-015-0051-4

[2] Cohen-Manheim, I., Doniger, G.M., Sinnreich, R., Simon, E.S., Pinchas-Mizrach, R., Otvos, J.D., and Kark, J.D. (2015). Increase in the inflammatory marker GlycA over 13 years in young adults is associated with poorer cognitive function in midlife. PLoS ONE, 10(9):e0138036. DOI: 10.1371/journal.pone.0138036

[3] Lutski, M., Weinstein, G., Goldbourt, U., and Tanne, D. (2019). Plasma lipids, apolipoproteins, and subsequent cognitive decline in men with coronary heart disease. Journal of Alzheimer's Disease, 67(3), 827–837. DOI:  10.3233/JAD-180849

[4] Maroon, J C. (2022). The effect of hyperbaric oxygen therapy on cognition, performance, proteomics, and telomere length—The difference between zero and one: A case report. Frontiers in Neurology, 13:949536. DOI: 10.3389/fneur.2022.949536