32 Brain tumours develop within an organ that changes substantially with age, and a new review suggests these changes may influence tumour progression, treatment resistance, and cognitive outcomes. The study published in Ageing and Cancer Research and Treatment, the article, “Navigating the ageing brain: The interplay between brain malignancy and the ageing microenvironment,” brings together emerging evidence from ageing biology, cancer neuroscience, and neuro-oncology. Rather than treating ageing as a background clinical variable, the review proposes that the ageing brain may actively shape the biology of tumours that develop within it. The review identifies several interconnected processes associated with brain ageing, including the accumulation of senescent cells, chronic low grade inflammation, metabolic dysfunction, altered neurotransmitter signalling, ion channel dysregulation, and changes to the blood brain barrier. Together, these changes can reshape the neural microenvironment in which tumours arise and progress. Chronic low grade inflammation, often described as inflammaging, may also alter immune surveillance within the central nervous system, while changes to the blood brain barrier can affect tumour invasion and drug delivery. A central focus of the review is the two-way relationship between tumours and the nervous system. Evidence examined by the authors indicates that glioma cells can interact functionally with neurons through mechanisms including neuron-to-tumour synapses and neurotransmitter signalling. At the same time, brain tumours and their treatment may promote senescence in nearby neurons and glial cells. Metabolic changes, altered ion channels, and neurotransmitter systems may contribute to the functional interactions between glioma cells and neurons. The review highlights the dual role of cellular senescence. Senescence can prevent damaged or abnormal cells from continuing to proliferate. However, senescent cells can also release inflammatory and tissue remodelling factors collectively known as the senescence-associated secretory phenotype, or SASP. In an ageing brain, the accumulation of senescent neurons, astrocytes, microglia, and endothelial cells may therefore create a microenvironment that supports tumour progression. This can contribute to a feedback loop in which tumours exploit neuronal signals for growth, while tumour-related damage and treatment effects accelerate senescence in surrounding cells. The authors suggest that this interaction could have implications for both treatment resistance and cognitive decline. It also raises questions about the longer-term neurological effects of current therapies. Rather than proposing an immediate clinical treatment strategy, the authors outline several research directions for age-aware neuro-oncology. These include investigating senescence-modulating approaches, neuroinflammation, blood brain barrier biology, ion channels, neurotransmitter systems, and advanced patient-derived organoid models. Future research could include patient-derived organoids that better reproduce features of the aged brain, including models incorporating aged cells. Senolytic and senomorphic approaches that target cellular senescence are also being explored, although these remain at the preclinical stage. Similarly, strategies targeting neuroinflammation or restoring blood brain barrier integrity require rigorous evaluation before they can be translated into clinical care. The review stresses that interventions specifically targeting ageing-related mechanisms in brain tumours remain largely preclinical and require direct clinical evaluation. The authors also emphasise that chronological age alone should not determine treatment decisions for older people with brain tumours. Tumour molecular features, physiological fitness, frailty, cognitive reserve, neurological function, comorbidities, treatment tolerance, and quality of life should all be considered when planning care. Brain tumours remain among the most challenging cancers to treat, particularly in older adults, where incidence is higher and outcomes are often poorer. The review argues that chronological age should not be used as a simple prognostic marker or as a substitute for assessing an individual’s overall condition. By framing the ageing brain as an active participant in tumour biology rather than a passive backdrop, the review calls for tumour control and brain health to be considered interconnected outcomes. Understanding how an ageing neural microenvironment influences tumour behaviour, and how tumours in turn reshape that environment, may reveal previously overlooked mechanisms of treatment resistance and neurological decline. The authors suggest that integrating ageing biology with cancer neuroscience could ultimately identify new therapeutic targets aimed at both the tumour and the surrounding aged neural tissue, with the potential to improve survival while helping to preserve cognitive function.