With over fifty competitively funded grants and more than 250 peer-reviewed scholarly publications to her name, Dr. Chapman’s work has significantly advanced the study of cognitive capacity throughout the human lifespan. Her research uniquely integrates functional and structural neuroimaging modalities to elucidate neurobiological mechanisms underpinning cognition, social connectedness, and psychological well-being both in health and disease. This multidisciplinary approach facilitates the continuous mapping of brain function and offers insights into how the brain adapts and evolves over time.

Under Dr. Chapman’s visionary leadership, the Center for BrainHealth has emerged as a global leader in brain health innovation, combining rigorous scientific inquiry with translational applications. The Center’s development of the BrainHealth Index—a proprietary composite metric—provides an unprecedented, validated measure to chart individual trajectories of brain health across various domains. This holistic framework encapsulates cognitive, emotional, and social parameters, enabling personalized assessment and targeted interventions aimed at enhancing brain performance.

Moreover, the Center’s Strategic Memory Advanced Reasoning Tactics (SMART™) program embodies Dr. Chapman’s commitment to translating scientific knowledge into practical tools. This evidence-based cognitive training system, refined over three decades, is designed to improve complex reasoning and adaptive thinking skills. It has been systematically evaluated in multiple longitudinal studies, demonstrating efficacy in both healthy populations and those affected by neurological conditions. Such interventions underscore the potential of science-driven strategies to extend cognitive vitality and resilience.

Dr. Chapman’s work transcends academic boundaries, as she actively collaborates with policymakers, humanitarian organizations, and thought leaders worldwide to democratize access to brain health science. Her advocacy highlights the societal imperative of proactive brain health maintenance, emphasizing early detection of cognitive decline and the promotion of lifelong cognitive enrichment. This global outreach aims to shift public health paradigms toward brain-centric models that foster human flourishing.

The Texas Philosophical Society’s recognition of Dr. Chapman is not only a celebration of her illustrious career but also an endorsement of the critical role that cognitive neuroscience plays in contemporary science and public policy. The Society, established in 1837, has a storied tradition of fostering intellectual development in Texas through the preservation and dissemination of knowledge. Dr. Chapman joins the ranks of historic figures such as Sam Houston and prominent contemporary leaders, underscoring the interdisciplinary importance of brain science in shaping cultural and scientific discourse.

Scientifically, Dr. Chapman’s research paradigm represents a synthesis of neuroimaging, cognitive science, and behavioral psychology. Employing state-of-the-art MRI protocols, diffusion tensor imaging, and functional connectivity analyses, her team maps intricate brain networks responsible for executive functions, memory consolidation, and adaptive learning. These methodologies have elucidated neural plasticity mechanisms inherent in both normative aging and recovery post-brain injury, advancing the field’s understanding of rehabilitative potential.

The translational nature of the Center for BrainHealth’s work facilitates rapid application of these scientific insights into community-based programs and clinical interventions. Their model bridges the gap between laboratory research and real-world outcomes, incorporating longitudinal population studies and randomized controlled trials. This commitment to evidence-based practice ensures that innovations are both scientifically robust and practically relevant, enhancing public health impact.

Furthermore, Dr. Chapman’s leadership has fostered interdisciplinary research that includes psychology, neuroscience, social sciences, and philosophy of science. This expansive vision allows for a comprehensive exploration of cognition not merely as a biological phenomenon but as an adaptive, socially embedded process. The Center’s projects incorporate behavioral data, neurocognitive assessments, and socio-emotional metrics, positioning brain health within a socio-cultural framework that informs more nuanced intervention strategies.

The Center also develops educational outreach and training programs aimed at empowering diverse populations to engage in brain health enhancement. These programs underscore the malleability of cognitive functions and provide scalable frameworks for cognitive training in schools, workplaces, and communities. By integrating cutting-edge research findings with accessible training modules, the Center exemplifies how scientific knowledge can catalyze societal transformation.

In sum, Sandra Bond Chapman’s induction into the Texas Philosophical Society represents a milestone reflecting decades of rigorous scientific achievement and societal engagement. Her pioneering research, innovative assessment tools, and dedication to translational science collectively elevate brain health to a forefront position in contemporary neuroscience and public health. This honor not only recognizes her individual contributions but also signals the increasing importance of proactive brain care as an essential component of human development and well-being.

As brain science continues to evolve at an unprecedented pace, Dr. Chapman’s work offers a robust framework for understanding and optimizing cognitive function throughout life. Through a combination of empirical research, technological innovation, and broad-based advocacy, she champions a future where brain health is accessible, measurable, and improvable for all individuals. This vision redefines the boundaries of neuroscience and exemplifies the transformative power of science in enhancing the human condition.

Subject of Research: Cognitive neuroscience, brain health measurement, cognitive capacity enhancement, neuroimaging, translational neuroscience.

Article Title: Sandra Bond Chapman’s Pioneering Contributions to BrainHealth Honored by Texas Philosophical Society Induction

News Publication Date: February 6, 2026

Web References:
– Center for BrainHealth, The University of Texas at Dallas: https://centerforbrainhealth.org/
– BrainHealth Index: https://centerforbrainhealth.org/science/brainhealth-index
– SMART™ Brain Health Training: https://centerforbrainhealth.org/training/smart

Image Credits: Center for BrainHealth

Keywords: Cognitive neuroscience, Scientific data, Population studies, Human social behavior, Human behavior, Behavior modification, Intelligence, Cognitive theory, Cognitive development

The glymphatic system, often described as the brain’s plumbing network, functions as a specialized waste clearance route where cerebrospinal fluid (CSF) circulates through brain tissue to remove metabolic waste products. While previous animal studies have suggested that the glymphatic pathway facilitates the removal of amyloid beta (Aβ) and tau proteins, which aggregate aberrantly in Alzheimer’s disease, the extent to which this system operates in humans has remained a subject of intense investigation and debate.

Led by a multidisciplinary team including Dagum, Elbert, and Giovangrandi, the researchers employed advanced neuroimaging techniques paired with highly sensitive biochemical assays to track the transfer of amyloid beta and tau proteins from the brain parenchyma to the peripheral bloodstream. These methods included dynamic contrast-enhanced MRI to visualize glymphatic flow and ultra-low concentration immunoassays capable of detecting trace amounts of pathogenic proteins in plasma samples.

The study’s findings revealed a clear temporal relationship between glymphatic clearance activity and the presence of Aβ and tau in blood plasma. This was particularly evident during states of enhanced glymphatic function, such as sleep, when interstitial fluid exchange is naturally increased. Elevated plasma levels of amyloid beta and tau corresponded to intensified glymphatic transport, suggesting that this system operates efficiently to mobilize neurotoxic proteins out of the brain.

Importantly, the researchers demonstrated that impaired glymphatic clearance correlates with increased accumulation of amyloid plaques and neurofibrillary tangles within brain tissue, hallmarks of Alzheimer’s pathology. By establishing a causal linkage between glymphatic dysfunction and protein aggregation, the study provides robust support for targeting glymphatic pathways as a novel therapeutic avenue to mitigate or prevent disease progression.

This research also highlights the potential for blood-based biomarkers derived from glymphatic clearance products to serve as minimally invasive diagnostic tools for early detection of neurodegenerative disorders. Unlike cerebrospinal fluid sampling, which is invasive and often impractical for routine clinical use, plasma assays informed by glymphatic clearance dynamics could revolutionize patient monitoring and personalized treatment strategies.

The comprehensive approach taken by the team included longitudinal monitoring of participants who exhibited risk factors for Alzheimer’s disease, such as advanced age and family history. Repeated glymphatic imaging and plasma analysis over several months allowed the researchers to map individual variability in clearance efficiency and correlate this with cognitive performance metrics and structural brain changes observed via MRI.

Mechanistically, the study elucidated how aquaporin-4 channels expressed on astroglial endfeet facilitate the convective flow of cerebrospinal fluid along perivascular spaces, enabling the effective removal of soluble amyloid beta and tau species. Disruption of these channels or alteration in vascular compliance was associated with marked reduction in glymphatic transport, underscoring the vascular and cellular components critical to maintaining brain homeostasis.

Moreover, lifestyle factors known to influence glymphatic function, such as sleep quality and cardiovascular health, emerged as important modulators of amyloid and tau clearance. The researchers suggest that therapeutic interventions aimed at improving sleep architecture or enhancing vascular health may synergize with direct pharmacologic modulation of glymphatic pathways to yield comprehensive neuroprotection.

This discovery rekindles scientific interest in the glymphatic system, an area that had remained relatively underappreciated for decades, despite being a fundamental aspect of brain physiology. The implications extend beyond Alzheimer’s disease, as abnormal protein clearance is a common feature in many neurodegenerative conditions, including Parkinson’s disease and frontotemporal dementia.

While this study represents a major leap forward, the authors acknowledge several limitations that warrant further exploration. For example, the influence of confounding factors such as blood-brain barrier integrity, systemic inflammation, and pharmacologic interventions on glymphatic efficacy remains poorly understood. Future work will need to dissect these complex interactions to optimize therapeutic targeting.

The innovative fusion of advanced imaging and molecular biology techniques employed here establishes a new paradigm for studying human neurodegeneration in vivo. By directly linking protein clearance dynamics with brain pathology and peripheral biomarkers, the research opens exciting avenues for early intervention before irreversible neuronal damage has occurred.

As the burden of Alzheimer’s disease and related dementias continues to rise globally, the elucidation of glymphatic clearance pathways provides a beacon of hope for developing strategies that can delay or halt disease progression. This study further cements the critical importance of brain waste management systems in maintaining cognitive health and vitality.

In conclusion, the work of Dagum, Elbert, Giovangrandi, and colleagues represents a milestone achievement that fundamentally enhances our understanding of neurodegenerative disease pathophysiology. By shining a spotlight on the glymphatic system’s role in clearing amyloid beta and tau from the brain to plasma, it offers promising new directions for diagnosis, monitoring, and ultimately, treatment of these devastating disorders.

Subject of Research: Glymphatic system’s involvement in clearing amyloid beta and tau proteins from the human brain to plasma and its implications in neurodegenerative diseases.

Article Title: The glymphatic system clears amyloid beta and tau from brain to plasma in humans.

Article References:
Dagum, P., Elbert, D.L., Giovangrandi, L. et al. The glymphatic system clears amyloid beta and tau from brain to plasma in humans. Nat Commun 17, 715 (2026). https://doi.org/10.1038/s41467-026-68374-8

DOI: https://doi.org/10.1038/s41467-026-68374-8

The extensive research, spanning four years and conducted by a multidisciplinary team from UMH’s Institute of Neurosciences, along with affiliations such as ISABIAL and RIAPAD, addresses a critical gap in AUD pharmacotherapy. Despite the significant global burden of AUD, responsible for approximately 2.6 million deaths annually, existing pharmacotherapies fail to maintain long-term abstinence in the majority of patients. Alarmingly, relapse rates hover around 70% within the first year post-treatment, underscoring the urgent demand for novel pharmacological interventions.

Central to the innovation behind MCH11 is the modulation of the endocannabinoid system (ECS), a complex neuromodulatory network that intricately connects the brain with various physiological processes regulating pleasure, motivation, and stress responses. In individuals afflicted with AUD, dysregulation of the ECS is evident, notably through diminished levels of 2-arachidonoylglycerol (2-AG), an endogenous cannabinoid associated with well-being and impulse regulation. MCH11 operates as a selective inhibitor of monoacylglycerol lipase, the enzyme responsible for degrading 2-AG, thereby elevating its cerebral concentrations to restore homeostatic balance.

Through the inhibition of MAGL, MCH11 effectively enhances endogenous 2-AG signaling, translating into significant reductions in ethanol consumption and the compulsion to drink, as observed in controlled animal studies. These effects were accompanied by a reduction in withdrawal symptoms, a major hurdle in AUD recovery. Intriguingly, behavioral assessments revealed that treatment with MCH11 imparted anxiolytic and antidepressant-like effects, suggesting a dual therapeutic action addressing both dependence and comorbid affective disorders without compromising motor or cognitive faculties.

Sex-dependent responses emerged as a compelling dimension of MCH11’s pharmacodynamics. Male mice exhibited significant reductions in ethanol intake and enhanced behavioral outcomes at low to medium doses, whereas female mice required higher dosages to achieve comparable benefits. This divergence not only highlights biological sex as a crucial variable in addiction therapy efficacy but also advocates for sex-specific dosing regimens in future clinical translations.

At the molecular level, quantitative PCR analyses demonstrated that MCH11 rectifies gene expression perturbations associated with AUD in both sexes, albeit with dose-dependent variance between males and females. Genes implicated in neurotransmitter regulation, neuroinflammatory pathways, and synaptic plasticity were among those normalized, providing mechanistic insights into how MCH11 counters alcohol-induced neurobiological alterations.

Beyond monotherapy, the research team investigated the synergistic potential of combining MCH11 with topiramate, an FDA-approved antiepileptic repurposed for combating alcohol dependence. The combinatorial regimen exhibited superior efficacy in attenuating ethanol use and modifying drinking motivation, surpassing outcomes observed with either compound alone. This finding paves the way for developing multifaceted, personalized pharmacological approaches embracing both innovative agents and established medications.

Although these preliminary results stem from animal experimentation, the implications for human AUD treatment are substantial. MCH11’s capacity to selectively ameliorate alcohol consumption behaviors and associated neuropsychiatric symptoms without detrimental side effects positions it as a frontrunner in next-generation pharmacotherapies. Importantly, the nuanced sex-dependent variations underscore the necessity for precision medicine paradigms tailoring interventions to individual biological profiles.

The translational journey from murine models to clinical application remains a formidable challenge. Nevertheless, the current findings provide a robust foundation for subsequent pharmacokinetic, toxicological, and eventually clinical trials to explore MCH11’s safety, efficacy, and optimized dosing in humans. UMH’s interdisciplinary team remains committed to advancing this promising candidate through the drug development pipeline.

In conclusion, the discovery of MCH11 ushers in a new era of neuropharmacological intervention for alcohol use disorder, harnessing the therapeutic potential of the endocannabinoid system. By restoring neurochemical balance and mitigating maladaptive behaviors intrinsic to addiction, MCH11 exemplifies the synergy between molecular innovation and clinical needs. Its sex-specific efficacy further challenges the convention, advocating for more individualized treatment frameworks to combat the pervasive and complex disorder that is alcoholism.

This research was spearheaded by lead author Abraham Torregrosa and co-authored by María García Gutiérrez, Daniela Navarro, Francisco Navarrete, and Professor Jorge Manzanares. The study was generously funded by Spain’s Ministry of Science, Innovation and Universities, the State Research Agency, the Carlos III Health Institute’s RIAPAD network, and ISABIAL.

Subject of Research: Animals
Article Title: MCH11, a new monoacylglycerol lipase inhibitor, reduces ethanol consumption and motivation to drink in mice, with sex-dependent differences. Biomedicine & Pharmacotherapy
News Publication Date: 21-Oct-2025
Web References: 10.1016/j.biopha.2025.118662
Image Credits: Instituto de Neurociencias UMH-CSIC
Keywords: Alcohol abuse, Substance abuse, Human behavior, Substance related disorders, Alcoholism, Diseases and disorders, Antidepressants, Medications, Drug therapy, Drug dosage, Drug development, Neuropharmacology, Molecular neuropharmacology

The cerebral cortex, the brain’s outermost layer, is integral to higher-order functions such as perception, cognition, and emotional regulation. Layer 6, the innermost of the cortex’s six layers, has largely remained enigmatic despite its strategic location bridging cortical and subcortical regions. The research team delved deep into this cortical territory, identifying a small but pivotal subset of neurons enriched with orexin receptors, which respond to the neuropeptide produced primarily in the hypothalamus. This orexin sensitivity places these neurons at a vital crossroads for integrating signals related to arousal and emotional states.

Employing a multidisciplinary approach combining electrophysiology, molecular biology, and behavioral assays, the investigators demonstrated that these orexin-responsive layer 6 neurons exert a regulatory influence on cortical excitability. When activated, these neurons modulate the neuron’s firing patterns and synaptic transmissions across cortical networks, effectively tuning the brain’s responsiveness to stimuli. Dysregulation in this system, the study posits, manifests as altered anxiety behavior, providing a cellular substrate for the pervasive symptoms seen in anxiety disorders.

Technically, the team harnessed patch-clamp recordings to measure neuronal activity with unprecedented resolution. They observed that the application of orexin peptides elevated the excitability of layer 6 neurons, thereby enhancing their output to downstream cortical circuits. Importantly, blocking orexin receptors attenuated this excitatory effect, confirming receptor-mediated modulation. These findings align with previous demonstrations of orexin’s role in arousal but extend its function to the nuanced control of cortical states underpinning emotional behavior.

Intriguingly, the spatial distribution of this neuron subpopulation suggests a topographic specialization within layer 6, where orexin-sensitive neurons are interspersed among other excitatory and inhibitory cells. This arrangement implies a sophisticated microcircuitry, enabling precise gating of cortical outputs. The ability of these cells to adjust network excitability may serve as a neural substrate for rapid behavioral adaptations to environmental stressors, particularly those eliciting anxiety.

Behavioral experiments using rodent models further elucidated the functional significance of these neurons. By selectively manipulating orexin receptor activity in layer 6, the researchers could either induce or alleviate anxiety-like behaviors. Animals with suppressed orexin signaling exhibited reduced cortical excitability and displayed less anxiety in open field and elevated plus maze tests, while enhanced signaling produced the opposite effect. These compelling observations bridge the molecular action of orexin with complex behavioral phenotypes.

Beyond their immediate findings, the researchers propose that the orexin-sensitive layer 6 neurons may participate in a broader neural circuit encompassing limbic regions such as the amygdala and hippocampus. These areas, critically involved in emotion processing and memory, might interact with cortical layer 6 to fine-tune responses to stressful stimuli. This expanded network hypothesis sets the stage for future explorations on how cortical and subcortical interactions orchestrate emotional regulation.

At the molecular level, the expression of orexin receptors in these neurons was characterized using in situ hybridization and immunohistochemistry, revealing co-localization with markers for excitatory pyramidal neurons. The receptor subtypes implicated suggest selective signaling pathways that could be targeted pharmacologically. Such specificity offers a promising avenue for developing anxiolytic therapies that avoid the broad sedative effects common to current medications.

The discovery has significant translational ramifications. Anxiety disorders affect millions worldwide and often resist treatment due to incomplete understanding of their neurobiological underpinnings. By pinpointing a discrete neuronal cohort that modulates cortical excitability and anxiety, this work opens a new therapeutic target. Drugs modulating orexin receptor activity in layer 6 neurons could provide more precise interventions, minimizing side effects associated with nonspecific brain-wide modulation.

Moreover, the findings intersect intriguingly with sleep research. Orexin’s established role in maintaining wakefulness and preventing narcolepsy underscores the multifunctional nature of this neuropeptide. The dual impact on arousal and anxiety suggests that dysregulations in orexin signaling might underlie comorbidities between sleep disorders and anxiety, a hypothesis ripe for clinical investigation.

Technological advances played a central role in these discoveries. The team integrated optogenetics, allowing them to activate or silence orexin-sensitive neurons with light, thereby directly linking neuronal activity with behavioral outcomes. This methodology facilitated causal inferences rarely possible in neuroscience, offering compelling evidence that these neurons are necessary and sufficient for modulating anxiety.

From a systems neuroscience perspective, these results emphasize the importance of cortical layer architecture in emotional regulation. Layer 6’s output to thalamic and cortical neurons positions it as a gatekeeper influencing information flow and neural synchrony. Thus, orexin-sensitive neurons here can be seen as modulating a neural gain control mechanism, amplifying or dampening cortical responses depending on behavioral context.

The identification of this neuron subpopulation also raises critical questions about developmental trajectories and plasticity. Are these orexin-sensitive neurons established during early brain development, or do they adapt based on experience and environmental stress? Understanding their ontogeny may reveal vulnerabilities to anxiety disorders emerging during critical periods such as adolescence.

Furthermore, this research encourages a reevaluation of orexin’s broader functions beyond known domains. By highlighting a role for orexin in cortical excitability and emotional behavior, the study suggests that this neuropeptide’s influence permeates diverse brain systems, integrating physiological arousal with higher cognitive and affective processes.

In conclusion, this pioneering work elucidates a hitherto unappreciated mechanism by which a specialized population of orexin-sensitive layer 6 neurons modulates cortical excitability and orchestrates anxiety-related behaviors. The detailed mechanistic insights provided into receptor-mediated neuronal modulation and behavioral correlates represent a significant stride toward decoding the neural basis of anxiety. With future investigations poised to explore therapeutic exploitation, this discovery stands to transform approaches to anxiety disorders, blending molecular precision with systems-level understanding.

Subject of Research: Orexin-sensitive neurons in cortical layer 6 and their role in regulating cortical excitability and anxiety behavior.

Article Title: An orexin-sensitive subpopulation of layer 6 neurons regulates cortical excitability and anxiety behaviour.

Article References:
Messore, F., Narayanan Therpurakal, R., Dufour, JP. et al. An orexin-sensitive subpopulation of layer 6 neurons regulates cortical excitability and anxiety behaviour. Transl Psychiatry 15, 147 (2025). https://doi.org/10.1038/s41398-025-03350-2

Image Credits: AI Generated

DOI: https://doi.org/10.1038/s41398-025-03350-2