Gerontology seminars

Ta-Wei Guu examines whether continuous data from wearable devices can reveal aspects of older adults’ depression and dementia that conventional clinical assessments miss. The session covers behavioural patterns, sleep disruption and treatment responses measured outside clinical settings, and considers how repeated observations can track changes in health over time. Guu also presents plans for a technology-enabled longitudinal cohort to study ageing populations over months and years, discussing how the resulting patterns could inform research and clinical practice. The session includes questions and discussion. Guu is an assistant professor and consultant psychiatrist at CMUBH in Taiwan, with an affiliation to King’s College London. Online via Dementia Researcher Communities livestream. Wednesday 21 October 2026, 12:00–12:45 BST (Europe/London; UTC+1). This free event requires a Dementia Researcher Communities account: open the event page, sign in or create an account, and RSVP to access the livestream. Organized by Dementia Researcher, delivered by University College London.

Celina Valencia examines how social and environmental conditions may alter susceptibility to Alzheimer’s disease and related dementias through neuroendocrine and immune adaptation. The talk presents a contextual-stress framework connecting cumulative exposures across the lifespan with neurodegenerative vulnerability. Evidence from the NIH All of Us Research Program, the Precision Aging Network, and longitudinal studies of menopausal aging links neighborhood deprivation, depression, inflammatory signaling, and biomarkers of vulnerability. These findings motivate an integrated account of how contextual stress contributes to differences in neuroimmune regulation and dementia risk.

Brain metabolism supplies the energy underlying brain injury, recovery and aging. This webinar brings together three complementary approaches to understanding how repetitive mild traumatic brain injury affects these processes. Sakthivel Ravi examines repetitive mild TBI and aging through multimodal imaging and molecular profiling. Adam Khalifa presents wireless brain glucose sensing for TBI research, and Joe Abisambra discusses disruption of bioenergetic pathways following repetitive mild TBI. The talks are followed by a moderated question-and-answer discussion.

This public discussion examines the factors that help preserve brain health during aging. Researchers working on neuroscience, brain stimulation, the microbiome and brain health consider how stress, everyday behavior and social and environmental conditions can affect resilience over a lifetime. The panel discusses emerging evidence about early vulnerability, possible interventions through lifestyle changes and stress management, and more targeted approaches. It also addresses the limits of current knowledge and the uncertainties that remain when translating these findings into ways to protect cognitive health.

Navigation and memory require coordination between map-like allocentric representations and body-centered egocentric actions. Aaron Wilber examines how the parietal–retrosplenial–anterior thalamic–hippocampal network performs these transformations, and how disrupted coordination contributes to spatial deficits in aging and Alzheimer’s disease. Rat sequence-task experiments reveal bidirectional hippocampal–parietal interactions across route-centered, place and egocentric representations. Because that task does not isolate reference-frame use, the laboratory developed a freely available task separating egocentric, allocentric and transformation conditions. Validation indicates that parietal cortex and anterior thalamus are required for transformation; ongoing work examines population states associated with each condition. The talk then connects impaired hippocampal–cortical communication during sleep to navigation deficits in 3xTg-AD mice, reporting recovery of circuit function and cognition after early, circuit-targeted 40 Hz entrainment. Related investigations examine this network during waking navigation. In TgF344-AD rats, egocentric impairments appear before transformation deficits, addressing the shortage of rodent studies of reference-frame coordination in Alzheimer’s disease.

Meagan McManus examines mitochondrial dysfunction as an early driver of brain ageing and neurodegeneration. Reactive oxygen species and other mitochondrial stress signals connect impaired energy metabolism with glial activation. The talk presents preclinical evidence for [18F]ROStrace PET, a redox-sensitive tracer that crosses the blood–brain barrier, as a non-invasive way to detect mitochondrial and immune distress before overt pathology in models relevant to late-onset Alzheimer’s and Parkinson’s diseases. Online via the University of Arizona Zoom meeting. Use the Zoom link published on the organizer’s event page. Tuesday 22 September 2026, 16:00–17:00 MST (America/Phoenix; UTC−7). Organized by the Graduate Interdisciplinary Program in Neuroscience and the Department of Neuroscience. This listing advertises the verified remote attendance option.

Emmanuelle Passegué examines why mechanisms that maintain blood-forming stem cells in early life can contribute to their deterioration with age. The lecture connects cell-cycle control, marrow support, inflammation, metabolic regulation and cellular memory to altered self-renewal and blood-cell production. It also considers genomic instability, clonal hematopoiesis and progression toward leukemia.

Efficient cognition requires flexible interactions between distributed neural networks in the human brain. These networks adapt to challenges by flexibly recruiting different regions and connections. In this talk, I will discuss how we study functional network plasticity and reorganization with combined neurostimulation and neuroimaging across the adult life span. I will argue that short-term plasticity enables flexible adaptation to challenges, via functional reorganization. My key hypothesis is that disruption of higher-level cognitive functions such as language can be compensated for by the recruitment of domain-general networks in our brain. Examples from healthy young brains illustrate how neurostimulation can be used to temporarily interfere with efficient processing, probing short-term network plasticity at the systems level. Examples from people with dyslexia help to better understand network disorders in the language domain and outline the potential of facilitatory neurostimulation for treatment. I will also discuss examples from aging brains where plasticity helps to compensate for loss of function. Finally, examples from lesioned brains after stroke provide insight into the brain’s potential for long-term reorganization and recovery of function. Collectively, these results challenge the view of a modular organization of the human brain and argue for a flexible redistribution of function via systems plasticity.

Sleep supports learning both by preparing the brain to encode information and by stabilizing memories afterward. This seminar examines the brain activity involved in sleep-dependent consolidation and how those mechanisms change across the lifespan, from childhood into older age.

My laboratory has made an intriguing discovery that mitochondrial stress in one tissue can be communicated to distal tissues. We find that mitochondrial stress in the nervous system triggers the production of entities known as mitokines. These mitokines are discharged from the nervous system, orchestrating a response in peripheral tissues that extends the lifespan of C. elegans. The revelation came as a surprise, given the prevalent belief that cell autonomous mechanisms would underlie the relationship between mitochondrial function and aging. It was also surprising given the prevailing dogma that mitochondrial function must be increased, not decreased, to improve health and longevity. Our work also underscores the fact that mitochondria, which originated as a microbial entity and later evolved into an intracellular symbiont, have retained their capacity for intercommunication, now facilitated by signals from the nervous system. We hypothesize that this communication has evolved as a mechanism to reduce infection from pathogens.

2024 BACN Early-Career Prize Lecture Many of our decisions affect other people. Our choices can decelerate climate change, stop the spread of infectious diseases, and directly help or harm others. Prosocial behaviours – decisions that help others – could contribute to reducing the impact of these challenges, yet their computational and neural mechanisms remain poorly understood. I will present recent work that examines prosocial motivation, how willing we are to incur costs to help others, prosocial learning, how we learn from the outcomes of our choices when they affect other people, and prosocial preferences, our self-reports of helping others. Throughout the talk, I will outline the possible computational and neural bases of these behaviours, and how they may differ from young adulthood to old age.

Understanding and potentially reversing memory decline necessitates a comprehensive examination of memory's evolution throughout life. Traditional memory assessments, however, suffer from a lack of comparability across different age groups due to the diverse nature of the tests employed. Addressing this gap, our study introduces a novel, ACT-R model-based memory assessment designed to provide a consistent metric for evaluating memory function across a lifespan, from 5 to 85-year-olds. This approach allows for direct comparison across various tasks and materials tailored to specific age groups. Our findings reveal a pronounced U-shaped trajectory of long-term memory function, with performance at age 5 mirroring those observed in elderly individuals with impairments, highlighting critical periods of memory development and decline. Leveraging this unified assessment method, we further investigate the therapeutic potential of rs-fMRI-guided TBS targeting area 8AV in individuals with early-onset Alzheimer’s Disease—a region implicated in memory deterioration and mood disturbances in this population. This research not only advances our understanding of memory's lifespan dynamics but also opens new avenues for targeted interventions in Alzheimer’s Disease, marking a significant step forward in the quest to mitigate memory decay.

Qualitative coding is the process of categorizing and labeling raw data to identify themes, patterns, and concepts within qualitative research. This process requires significant time, reflection, and discussion, often characterized by inherent subjectivity and uncertainty. Here, we explore the possibility to leverage large language models (LLM) to enhance the process and assist researchers with qualitative coding. LLMs, trained on extensive human-generated text, possess an architecture that renders them capable of understanding the broader context of a conversation or text. This allows them to extract patterns and meaning effectively, making them particularly useful for the accurate extraction and coding of relevant themes. In our current approach, we employed the chatGPT 3.5 Turbo API, integrating it into the qualitative coding process for data from the SWISS100 study, specifically focusing on data derived from centenarians' experiences during the Covid-19 pandemic, as well as a systematic centenarian literature review. We provide several instances illustrating how our approach can assist researchers with extracting and coding relevant themes. With data from human coders on hand, we highlight points of convergence and divergence between AI and human thematic coding in the context of these data. Moving forward, our goal is to enhance the prototype and integrate it within an LLM designed for local storage and operation (LLaMa). Our initial findings highlight the potential of AI-enhanced qualitative coding, yet they also pinpoint areas requiring attention. Based on these observations, we formulate tentative recommendations for the optimal integration of LLMs in qualitative coding research. Further evaluations using varied datasets and comparisons among different LLMs will shed more light on the question of whether and how to integrate these models into this domain.

Humans and other animals evolved in habitats fraught with a range of environmental challenges to their bodies and brains. Accordingly, cells and organ systems possess adaptive stress-responsive signaling pathways that enable them to not only withstand environmental challenges, but also to prepare for future challenges and function more efficiently. These phylogenetically conserved processes are the foundation of the hormesis principle in which repeated exposures to low to moderate amounts of an environmental challenge improve cellular and organismal fitness. Here I describe cellular and molecular mechanisms by which cells in the brain and body respond to intermittent fasting and exercise in ways that enhance performance and counteract aging and disease processes. Switching back and forth between adaptive stress response (during fasting and exercise) and growth and plasticity (eating, resting, sleeping) modes enhances the performance and resilience of various organ systems. While pharmacological interventions that engage a particular hormetic mechanism are being developed, it seems unlikely that any will prove superior to fasting and exercise.

Web-based self-help interventions for coping with prolonged grief have established their efficacy. However, few programs address recent losses and investigate the effect of self-tailoring of the content. In an international project, the text-based self-help program LIVIA was adapted and complemented with an Embodied Conversational Agent, an initial risk assessment and a monitoring tool. The new program SOLENA was evaluated in three trials in Switzerland, the Netherlands and Portugal. The aim of the trials was to evaluate the clinical efficacy for reducing grief, depression and loneliness and to examine client satisfaction and technology acceptance. The talk will present the SOLENA program and report results of the Portuguese and Dutch trial as well as preliminary results of the Swiss RCT. The ongoing Swiss trial compares a standardised to a self-tailored delivery format and analyses clinical outcomes, the helpfulness of specific content and the working alliance. Finally, lessons learned in the development and evaluation of a web-based self-help intervention for older adults will be discusses.

The hippocampus is a brain region with key roles in memory formation, cognitive flexibility and emotional control. Yet hippocampal function is impaired severely during aging and in neurodegenerative diseases, and impairments in hippocampal function underlie age-related cognitive decline. Accumulating evidence suggests that the deterioration of the neuron-specific epigenetic landscape during aging contributes to their progressive, age-related dysfunction. For instance, we have recently shown that aging is associated with pronounced alterations of neuronal DNA methylation patterns in the hippocampus. Because neurons are generated mostly during development with limited replacement in the adult brain, they are particularly long-lived cells and have to maintain their cell-type specific gene expression programs life-long in order to preserve brain function. Understanding the epigenetic mechanisms that underlie the establishment and long-term maintenance of neuron-specific gene expression programs, will help us to comprehend the sources and consequences of their age-related deterioration. In this talk, I will present our recent work that investigated the role of DNA methylation in the establishment of neuronal gene expression programs and neuronal function, using adult neurogenesis in the hippocampus as a model. I will then describe the effects of aging on the DNA methylation landscape in the hippocampus and discuss the malleability of the aging neuronal methylome to lifestyle and environmental stimulation.