On 24–25 February 2026, Alzheimer’s Research UK held its annual research conference at Manchester Central Convention Complex and online. The meeting brought together over 700 researchers spanning molecular biology, data science, clinical trials, prevention, and patient engagement. Over 2 days of plenaries, parallel sessions, and discussions, a clear message emerged: the field of dementia research is entering a new, more hopeful era. This report summarises a meeting that highlighted how dementia research is moving beyond the search for a single solution and instead embracing a multidimensional, collaborative framework for precision care.
Background & Objectives Atypical parkinsonism syndromes (multiple system atrophy (MSA), progressive supranuclear palsy (PSP), and corticobasal syndrome (CBS)) are life-limiting neurodegenerative disorders with complex motor and nonmotor symptoms. A person-centered, coordinated, multidisciplinary approach may provide optimal care. Interdisciplinary care models in complex neurologic diseases are shown to improve disease outcomes. It is unknown whether specialized interdisciplinary care benefits people with atypical parkinsonism. Our study sought to determine patient satisfaction with a specialized atypical parkinsonism interdisciplinary clinic. Methods A retrospective, cross-sectional analysis was conducted of anonymous satisfaction surveys from patients who attended the UNC atypical parkinsonism interdisciplinary clinic from 10/2017-3/2024. The survey was divided into four subcategories – Services, Results, Clinicians, and Overall Experience. Responses were converted to numerical values for statistical analysis. Linear regression was used to determine predictors of overall experience scores. Qualitative data was analyzed and categorized into themes. Results 51.4% of all clinic attendees were diagnosed with PSP, 36.5% with MSA, and 9.5% with CBS. 39 of 74 (52.7%) satisfaction surveys were completed. Survey responses indicated high levels of satisfaction across all categories. Responses in the services category were the strongest predictor of variability in overall experience scores. Common themes from qualitative data were expressions of gratitude and constructive feedback. Discussion We report high patient satisfaction ratings in this first investigation of patient-centered outcomes in specialized interdisciplinary clinics for atypical parkinsonism. Future investigations focused on quality of life and care partner burden will provide additional insights for best care practices for people living with atypical parkinsonisms.
The BNA ’s winter research meeting took place high above the City of London at Canary Wharf, an inspiring setting to consider new perspectives. The central theme was ‘delivery’ , focusing on translation of fundamental neuroscience into effective therapies. The event targeted three main questions: How can therapies be effectively delivered to the brain? How might ‘meaningful intervention’ be realised for patients? How might hope be maintained for people with neurological and psychiatric disorders? Several interlocking ideas and debates emerged, circling around a central concern of how to move from molecular promise to effective and equitable real-world change for patients.
Late-onset alzheimer’s disease is the most common form of dementia, and it arises from complex genetic and environmental interactions. Preclinical models that replicate the slow progression and long prodromal phase of late-onset alzheimer’s disease are critical for identifying early therapeutic targets. The LOAD2 mouse model, developed on the C57BL/6J genetic background, integrates key late-onset alzheimer’s disease genetic risk factors: APOE4 , Trem2 *R47H, and an App allele encoding humanised amyloid beta. This study aimed to characterise key disease-relevant phenotypes of LOAD2 mice during ageing. Behavioural assays were conducted on 18- and 24-month-old LOAD2 and age-matched C57BL/6J wild-type control mice. At 18 months, LOAD2 mice exhibited significantly reduced locomotor activity compared to wild-type controls. However, this difference was diminished at 24 months as wild-type mice displayed an age-related decline in total distance travelled. Similarly, anxiety-like behaviour was elevated in 18-month-old LOAD2 mice relative to wild-type controls, but this difference was no longer evident at 24 months due to increased anxiety levels in aged wild-type mice. In contrast, spatial working memory and associative fear learning were intact in both LOAD2 and wild-type mice at 18 and 24 months of age, indicating no age- or genotype-dependent deficits in these forms of memory. Both groups of mice performed equally poorly in novel object and novel location recognition tasks at both ages. Thus, compared to age-matched wild-type mice, LOAD2 mice exhibit early locomotor deficits and heightened anxiety, but not overt cognitive impairment beyond that of normal ageing. These phenotypes are reminiscent of prodromal symptoms of late-onset alzheimer’s disease in humans.
The term 'cognitive reserve' broadly refers to better-than-expected cognitive abilities in old age, presumed to reflect environmental/lifestyle factors earlier in life. This commentary addresses the question of what determines 'better than expected' cognition; specifically, whether cognitive reserve can be 'explained away' by considering multiple brain measurements. Using simulations, I show that, once one allows for multiple brain properties related to cognition, differential maintenance of those properties can reproduce the clinical picture associated with cognitive reserve. Using real data, I then show that white-matter microstructure and functional connectivity explain significant additional variance in fluid intelligence beyond grey-matter volume (at least cross-sectionally), supporting the importance of measuring multiple brain properties. Using multimodal, longitudinal data to identify changes in those brain properties that are especially important for changes in cognition will help decide which interventions are most likely to be effective at maintaining cognition in old age.
Neuronal activity can modulate myelination throughout life, influencing circuit function and behaviour. Pathological changes in neuronal activity have been associated with myelin remodelling in a rat model of idiopathic absence seizures, raising the question of whether this represents a common mechanism underlying absence epilepsy. Here we examined oligodendrocyte populations and myelin architecture in a rat model of GRIN2B neurodevelopmental disorder, a rare and severe condition that is frequently accompanied by absence seizures. Using histology and 3D imaging, we report that despite robust seizure-like activity in this model, there was no evidence of changes in oligodendrocyte lineage cell populations, overall myelin content, or node of Ranvier organization. These results contrast with prior reports of seizure-associated myelin modulation, indicating that seizure-induced myelin plasticity may not be a uniform feature across all models of absence seizures. Our findings indicate that such adaptations may depend on additional factors including seizure burden and timing, highlighting the need for further analysis to determine when and how myelin plasticity contributes to absence epilepsy.
On 10–11 September 2025, the Cambridge Neuroscience Interdisciplinary Research Centre held its eighth biennial symposium on the topic of Interventions and Recovery . The meeting saw basic and clinical neuroscientists come together from Cambridge and beyond to discuss the latest advancements in cell and gene therapies, pharmaceutical innovations and cutting-edge neurotechnology aimed at addressing neurological diseases. Here, we provide a summary of the meeting, which shined a light on reasons to be optimistic for the future of treating conditions of the nervous system.
This year’s British Neuroscience Association (BNA) International Festival of Neuroscience, held from 27 to 30 April 2025 at the iconic ACC Liverpool, offered a remarkable convergence of scientific enthusiasm and professional networking. With over 1000 delegates from across the world, BNA2025 was not simply a scientific meeting – it was a vibrant, living reflection of the state of neuroscience in the UK and beyond. Across 4 days, the festival integrated cutting-edge research, collaborative initiatives, career development, and wide-reaching public engagement.
On 28 April 2025, the Epilepsy Research Institute Symposium at BNA2025 brought together four early career researchers to present on their findings in different areas of fundamental epilepsy research. Here, we provide a snapshot of the Symposium and highlights from the researchers' talks.
Understanding the specific barriers and possible solutions to credible research for early career researchers is key to enabling the next generation of scientists to implement these practices. Here we describe the outcomes of a workshop that tackled these issues, held at the BNA Festival of Neuroscience 2025. Workshop attendees highlighted various challenges to credible research that are highly relevant for early career researchers. In particular, time constraints were highlighted as a universal barrier across multiple credible research practices, and attitudes of more senior researchers/supervisors were perceived as an important challenge. Participants also highlighted solutions to help implement credible research that can be pursued by individual researchers, but, importantly, also emphasised the importance of "structural" solutions, requiring initiative by stakeholders, including academic institutions, journals and funders. We hope the summary of the workshop will foster active debate on the topic within the neuroscience community.
Understanding the neurocognitive impact of digital integration in education is essential, particularly in sub-Saharan Africa, where socio-economic and geographical disparities amplify the need for effective learning strategies. This study investigated how visuospatial working memory performance is affected by the modality of task presentation (screen versus print) and geographical context (urban, economically advantaged region versus rural, economically disadvantaged region) in Ivorian primary school students. We employed a behavioural approach with 222 students (aged 4–13). Students from urban (Abidjan) and rural (Man) schools were assigned to perform a visuospatial working memory task presented either on a computer screen or using printed physical materials. An analysis of covariance, with age as a covariate, revealed that students performing the task on-screen showed significantly better performance (fewer errors) compared to those using printed materials (p < 0.001). A significant interaction between presentation modality and geographical context was also found (p = 0.009). Specifically, the performance difference between screen and print modalities was larger in the urban setting, primarily due to urban students performing more poorly with printed materials compared to rural students in that same condition; rural students using printed materials outperformed urban students using printed materials (post hoc, p = 0.002). No significant difference in performance on screen-based tasks was found between urban and rural students. The main effect of geographical context was not significant. These findings suggest potential cognitive benefits of screen-based presentation but highlight a complex interplay with geographical context, which itself is intertwined with socio-economic factors and initial age differences that were statistically controlled. Future research should further incorporate direct socio-economic status controls and explore factors like motivation and task engagement, alongside neuroimaging approaches, to elucidate the underlying mechanisms.
Win-paired cues drive maladaptive decision-making in laboratory-based gambling tasks. However, humans prefer these cued games that facilitate gambling addiction. Whether rats prefer tasks that employ win-paired cues is unknown, yet this has consequences for the validity of using rodent models to investigate problem gambling. Here, we allowed rats to choose on a trial-by-trial basis whether to work for cued or uncued rewards on the rat gambling task. We also performed computational modelling to investigate individual differences in decision-making strategies. Rats could be grouped based on preference for task type, which became more pronounced across training, or preference for risky options, as is standard for the rat gambling task. Risk-preferring rats increasingly preferred the cued task over time. Decision-making was marginally riskier on cued trials, particularly in risk-preferring rats, but this was independent of task preference. Pairing of rewards with audiovisual cues accelerated response times and enhanced impulsivity in both cue- and risk-preferring rats. Cued wins also resulted in greater post-reinforcement pauses in risk-preferring animals only. Diffusion model analyses revealed optimal decision-makers have longer non-decision times before risky or impulsive choices, yet this is absent in risk-preferring animals. As such, lapses in cognitive control could be responsible for maladaptive trial outcomes in optimal, but not risk-preferring, rats. Collectively, these data support the use of high-risk preference at baseline as a proxy for vulnerability to problem gambling. Furthermore, diverse computational mechanisms could be responsible for the negative impact of win-paired cues on gambling-like behaviour in at-risk versus resilient individuals.
Protease-activated receptor 2 is proposed to be a novel target for several inflammation-related diseases but its role in the central nervous system remains unclear. Protease-activated receptor 2 activation is protective in cell death and excitotoxicity assays whereas examination into the role of protease-activated receptor 2 in vivo has been hindered due to the lack of suitable pharmacological tools. Recently, a small molecule protease-activated receptor 2 activator, AC264613 (AC), was reported to be a potent and selective protease-activated receptor 2 activator that crosses the blood-brain barrier. Furthermore, peptide mimetic molecules, for example GB88, were developed that were reported to act as protease-activated receptor 2 biased antagonists. Here, we examine their signalling pathways and neuroprotective properties in central nervous system preparations. AC induced significant increases in intracellular Ca 2+ in both neurons and astrocytes of primary hippocampal cultures, whereas in contrast, GB88 induced a small but significant reduction in intracellular Ca 2+ in both cell types. However, both AC and GB88 induced receptor internalisation when examined using fluorescently tagged protease-activated receptor 2. Both AC and GB88 did not induce neurotoxicity in organotypic hippocampal slice cultures when applied alone but reduced neurotoxicity when co-applied with kainate in excitotoxicity assays. Furthermore, both AC and GB88 reduced neurotoxicity when applied post kainate insult indicating they exhibit neuroprotective properties even after excitotoxicity is induced. These data indicate that protease-activated receptor 2 activation is neuroprotective but this is independent of Gq-induced Ca 2+ activation. Given that AC crosses the blood–brain barrier, this highlights its use as a novel tool to examine the protective properties of protease-activated receptor 2 in in vivo models of central nervous system disorders.
