Research Showcase – Wearable Technology in Depression and Dementia
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.
Neuroimmune Mechanisms of Depression
Scott J. Russo examines how chronic psychosocial stress alters communication between the immune system and the brain in depression and anxiety. Human observations and mouse experiments connect persistent increases in circulating monocytes and inflammatory signals with stress-related illness. The talk describes stress-responsive neurons that project to bone marrow and regulate monocyte production, release and trafficking. It also considers how stress disrupts the blood–brain barrier, allowing peripheral inflammatory proteins to affect reward regions such as the nucleus accumbens. Together, these findings examine how peripheral immune cells act at the neurovascular interface to change brain circuits and behaviour, providing potential mechanisms relevant to treatment-resistant mood disorders. Online via Rutgers Brain Health Institute Zoom. Thursday 1 October 2026, 12:00–13:00 EDT (America/New_York; UTC−4). Open the organizer’s event page and follow its Zoom link; the meeting ID and passcode are supplied there. Hosted by Yong Kim as part of the BHI Plenary Seminar Series. This listing advertises the verified remote option.
SSFN Webinar - Depression and antidepressants
Decoding ketamine: Neurobiological mechanisms underlying its rapid antidepressant efficacy
Unlike traditional monoamine-based antidepressants that require weeks to exert effects, ketamine alleviates depression within hours, though its clinical use is limited by side effects. While ketamine was initially thought to work primarily through NMDA receptor (NMDAR) inhibition, our research reveals a more complex mechanism. We demonstrate that NMDAR inhibition alone cannot explain ketamine's sustained antidepressant effects, as other NMDAR antagonists like MK-801 lack similar efficacy. Instead, the (2R,6R)-hydroxynorketamine (HNK) metabolite appears critical, exhibiting antidepressant effects without ketamine's side effects. Paradoxically, our findings suggest an inverted U-shaped dose-response relationship where excessive NMDAR inhibition may actually impede antidepressant efficacy, while some level of NMDAR activation is necessary. The antidepressant actions of ketamine and (2R,6R)-HNK require AMPA receptor activation, leading to synaptic potentiation and upregulation of AMPA receptor subunits GluA1 and GluA2. Furthermore, NMDAR subunit GluN2A appears necessary and possibly sufficient for these effects. This research establishes NMDAR-GluN2A activation as a common downstream effector for rapid-acting antidepressants, regardless of their initial targets, offering promising directions for developing next-generation antidepressants with improved efficacy and reduced side effects.
Brain Connectivity Workshop
Founded in 2002, the Brain Connectivity Workshop (BCW) is an annual international meeting for in-depth discussions of all aspects of brain connectivity research. By bringing together experts in computational neuroscience, neuroscience methodology and experimental neuroscience, it aims to improve the understanding of the relationship between anatomical connectivity, brain dynamics and cognitive function. These workshops have a unique format, featuring only short presentations followed by intense discussion. This year’s workshop is co-organised by Wellcome, putting the spotlight on brain connectivity in mental health disorders. We look forward to having you join us for this exciting, thought-provoking and inclusive event.
From pecking order to ketamine - neural mechanism of social and emotional behavior
Emotions and social interactions color our lives and shape our behaviors. Using animal models and engineered manipulations, we aim to understand how social and emotional behaviors are encoded in the brain, focusing on the neural circuits underlying dominance hierarchy and depression. This lecture will highlight our recent discoveries on how downward social mobility leads to depression; how ketamine tames depression by blocking burst firing in the brain’s antireward center; and, how glia-neuron interaction plays a surprising role in this process. I will also present our recent work on the mechanism underlying the sustained antidepressant activity of ketamine and its brain region specificity. With these results, we hope to illuminate on a more unified theory on ketamine’s mode of action and inspire new treatment strategies for depression.
From pecking order to ketamine - neural mechanism of social and emotional behavior
Emotions and social interactions color our lives and shape our behaviors. Using animal models and engineered manipulations, we aim to understand how social and emotional behaviors are encoded in the brain, focusing on the neural circuits underlying dominance hierarchy and depression. This lecture will highlight our recent discoveries on how downward social mobility leads to depression; how ketamine tames depression by blocking burst firing in the brain’s antireward center; and, how glia-neuron interaction plays a surprising role in this process. I will also present our recent work on the mechanism underlying the sustained antidepressant activity of ketamine and its brain region specificity. With these results, we hope to illuminate on a more unified theory on ketamine’s mode of action and inspire new treatment strategies for depression.
Causal Symptom Network Mapping Based on Lesions and Brain Stimulation; Converging Evidence about a Depression Circuit Using Causal Sources of Information
It’s our pleasure to announce that we will host Shan Siddiqi and Michael D. Fox on Thursday, March 30th at noon ET / 6PM CET. Shan Siddiqi, MD, is an Assistant Professor of Psychiatry at Harvard Medical School and the director of Psychiatric Neuromodulation Research at the Brigham and Women’s Hospital. Michael D. Fox, MD, PhD, is an Associate Professor of Neurology at Harvard Medical School and the founding director of the Center for Brain Circuit Therapeutics at the Brigham and Women’s Hospital. The talks will be followed by a shared discussion. You can register via talks.stimulatingbrains.org to receive the (free) Zoom link!
Targeting thalamic circuits rescues motor and mood deficits in PD mice
Although bradykinesia, tremor, and rigidity are hallmark motor defects in Parkinson’s disease (PD) patients, they also experience motor learning impairments and non-motor symptoms such as depression. The neural basis for these different PD symptoms are not well understood. While current treatments are effective for locomotion deficits in PD, therapeutic strategies targeting motor learning deficits and non-motor symptoms are lacking. We found that distinct parafascicular (PF) thalamic subpopulations project to caudate putamen (CPu), subthalamic nucleus (STN), and nucleus accumbens (NAc). While PF-->CPu and PF-->STN circuits are critical for locomotion and motor learning respectively, inhibition of the PF-->NAc circuit induced a depression-like state. While chemogenetically manipulating CPu-projecting PF neurons led to a long-term restoration of locomotion, optogenetic long-term potentiation at PF-->STN synapses restored motor learning behavior in PD model mice. Furthermore, activation of NAc-projecting PF neurons rescued depression-like PD phenotypes. Importantly, we identified nicotinic acetylcholine receptors capable of modulating PF circuits to rescue different PD phenotypes. Thus, targeting PF thalamic circuits may be an effective strategy for treating motor and non-motor deficits in PD.
Early life adversity, inflammation, and depression-onset: Results from the Teen Resilience Project
My research focuses broadly on the lifelong health disparities associated with experiences of adversity early in life. In this talk I will present the results of our recently completed Teen Resilience Project, a prospective and longitudinal study of first onset depression during adolescence. First, I will present the results on whether and how inflammatory processes may be shaped by early life adversity. Second, I will present data on the role of stress-induced inflammation in reward-related psychological processes. Finally, I will discuss the biobehavioral predictors of first-onset depression in this sample.
Brain and behavioural impacts of early life adversity
Abuse, neglect, and other forms of uncontrollable stress during childhood and early adolescence can lead to adverse outcomes later in life, including especially perturbations in the regulation of mood and emotional states, and specifically anxiety disorders and depression. However, stress experiences vary from one individual to the next, meaning that causal relationships and mechanistic accounts are often difficult to establish in humans. This interdisciplinary talk considers the value of research in experimental animals where stressor experiences can be tightly controlled and detailed investigations of molecular, cellular, and circuit-level mechanisms can be carried out. The talk will focus on the widely used repeated maternal separation procedure in rats where rat offspring are repeatedly separated from maternal care during early postnatal life. This early life stress has remarkably persistent effects on behaviour with a general recognition that maternally-deprived animals are susceptible to depressive-like phenotypes. The validity of this conclusion will be critically appraised with convergent insights from a recent longitudinal study in maternally separated rats involving translational brain imaging, transcriptomics, and behavioural assessment.
Emerging Treatment Options in Psychiatry
The World Health Organization (WHO) estimates that untreated mental disorders accountfor 13% of the total global burden of disease, and by 2030, depression alone will be the leadingcause of disability around the world – outpacing heart disease, cancer, and HIV. This grim pictureis further compounded by the mental health burden delivered by the coronavirus pandemic.The lack of novel treatment options in psychiatry is restricted by a limited understanding in theneuroscience basis of mental disorders, availability of relevant biomarkers, poor predictability inanimal models, and high failure rates in psychiatric drug development. However, theannouncement in 2019 from the Federal Drug Administration (FDA) for approvals of newinterventions for treatment-resistant depression (intranasal esketamine) and postpartumdepression (i.v. brexanolone), demand critical attention. Novel public-private partnerships indrug discovery, new translational data on co-morbid biology, in particular the ascendance ofpsycho-immunology, have highlighted the arrival of a new frontier in biological psychiatryresearch for depressive disorders.
Dissecting the neural circuits underlying prefrontal regulation of reward and threat responsivity in a primate
Gaining insight into the overlapping neural circuits that regulate positive and negative emotion is an important step towards understanding the heterogeneity in the aetiology of anxiety and depression and developing new treatment targets. Determining the core contributions of the functionally heterogenous prefrontal cortex to these circuits is especially illuminating given its marked dysregulation in affective disorders. This presentation will review a series of studies in a new world monkey, the common marmoset, employing pathway-specific chemogenetics, neuroimaging, neuropharmacology and behavioural and cardiovascular analysis to dissect out prefrontal involvement in the regulation of both positive and negative emotion. Highlights will include the profound shift of sensitivity away from reward and towards threat induced by localised activations within distinct regions of vmPFC, namely areas 25 and 14 as well as the opposing contributions of this region, compared to orbitofrontal and dorsolateral prefrontal cortex, in the overall responsivity to threat. Ongoing follow-up studies are identifying the distinct downstream pathways that mediate some of these effects as well as their differential sensitivity to rapidly acting anti-depressants.
Neural stem cells as biomarkers of cognitive aging and dementia
Adult hippocampal neurogenesis is implicated in memory formation and mood regulation. The Thuret lab investigates environmental and molecular mechanisms controlling the production of these adult-born neurons and how they impact mental health. We study neurogenesis in healthy ageing as well as in the context of diseases such as Alzheimer’s and depression. By approaching neurogenesis in health and disease, the strategy is two folds: (i) Validating the neurogenic process as a target for prevention and pharmacological interventions. (ii) Developing neurogenesis as a biomarker of disease prediction and progression. In this talk, I will focus on presenting some recent human studies demonstrating how hippocampal neural stem cells fate can be used as biomarkers of cognitive aging and dementia.
Unpacking Nature from Nurture: Understanding how Family Processes Affect Child and Adolescent Mental Health
Mental Health problems among youth constitutes an area of significant social, educational, clinical, policy and public health concern. Understanding processes and mechanisms that underlie the development of mental health problems during childhood and adolescence requires theoretical and methodological integration across multiple scientific domains, including developmental science, neuroscience, genetics, education and prevention science. The primary focus of this presentation is to examine the relative role of genetic and family environmental influences on children’s emotional and behavioural development. Specifically, a complementary array of genetically sensitive and longitudinal research designs will be employed to examine the role of early environmental adversity (e.g. inter-parental conflict, negative parenting practices) relative to inherited factors in accounting for individual differences in children’s symptoms of psychopathology (e.g. depression, aggression, ADHD ). Examples of recent applications of this research to the development of evidence-based intervention programmes aimed at reducing psychopathology in the context of high-risk family settings will also be presented.
Modelling affective biases in rodents: behavioural and computational approaches
My research focuses, broadly speaking, on how emotions impact decision making. Specifically, I am interested in affective biases, a phenomenon known to be important in depression. Using a rodent decision-making task, combined with computational modelling I have investigated how different antidepressant and pro-depressant manipulations that are known to alter mood in humans alter judgement bias, and provided insight into the decision processes that underlie these behaviours. I will also highlight how the combination of behaviour and modelling can provide a truly translation approach, enabling comparison and interpretation of the same cognitive processes between animal and human research.
Blurring the boundaries between neuroscience and organismal physiology
Work in my laboratory is based on the assumptions that we do not know yet how all physiological functions are regulated and that mouse genetics by allowing to identify novel inter-organ communications is the most efficient ways to identify novel regulation of physiological functions. We test these two contention through the study of bone which is the organ my lab has studied since its inception. Based on precise cell biological and clinical reasons that will be presented during the seminar we hypothesized that bone should be a regulator of energy metabolism and reproduction and identified a bone-derived hormone termed osteocalcin that is responsible of these regulatory events. The study of this hormone revealed that in addition to its predicted functions it also regulates brain size, hippocampus development, prevents anxiety and depression and favors spatial learning and memory by signaling through a specific receptor we characterized. As will be presented, we elucidated some of the molecular events accounting for the influence of osteocalcin on brain and showed that maternal osteocalcin is the pool of this hormone that affects brain development. Subsequently and looking at all the physiological functions regulated by osteocalcin, i.e., memory, the ability to exercise, glucose metabolism, the regulation of testosterone biosynthesis, we realized that are all need or regulated in the case of danger. In other words it suggested that osteocalcin is an hormone needed to sense and overcome acute danger. Consonant with this hypothesis we next showed this led us to demonstrate that bone via osteocalcin is needed to mount an acute stress response through molecular and cellular mechanisms that will be presented during the seminar. overall, an evolutionary appraisal of bone biology, this body of work and experiments ongoing in the lab concur to suggest 1] the appearance of bone during evolution has changed how physiological functions as diverse as memory, the acute stress response but also exercise and glucose metabolism are regulated and 2] identified bone and osteocalcin as its molecular vector, as an organ needed to sense and response to danger.
Fluoxetine and vortioxetine reverse depressive-like phenotype and memory deficits induced by amyloid-β (1-42) oligomers in mice: implication of transforming growth factor-β1 and oxidative stress
A long-term treatment with antidepressants reduces the risk to develop AD and different second-generation antidepressants such as selective serotonin reuptake inhibitors (SSRIs) are currently studied for their neuroprotective properties in AD. An impairment of neurotrophic factors signaling seems to be a common pathophysiological event in depression and AD. In particular a deficit of transforming growth factor-β1 (TGF-β1) and increased oxidative stress have been found both in depression and AD. In the present work the SSRI fluoxetine and the new multimodal antidepressant vortioxetine were tested for their ability to prevent memory deficits and depressive-like phenotype in a non-transgenic mouse model of AD (i.c.v. Aβ1-42 injection) by rescue of TGF-β1 signaling. The same drugs were also tested for their ability to modulate the expression of pro-oxidant genes as well as of genes related to the antioxidant machinery.