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AD is characterised by progressive neurodegeneration and cognitive decline, whereas GBM is characterised by aggressive cellular proliferation and a poor prognosis. Despite these differences, converging evidence indicates that both conditions share molecular pathways and network\u2010level dysfunction that emerge during brain ageing. Central to this convergence are G protein\u2010coupled receptors (GPCRs), which act as integrative signalling hubs that regulate inflammation, metabolism, calcium (CA\n                    <jats:sup>2+<\/jats:sup>\n                    ) homeostasis, and cell survival. In AD, GPCR signalling modulates amyloid\u2010\u03b2 production and clearance, Tau phosphorylation, intracellular CA\n                    <jats:sup>2+<\/jats:sup>\n                    dynamics, and glial\u2010driven neuroinflammation. In contrast, the same receptor families promote tumour growth, angiogenesis, immune evasion, and therapeutic resistance in patients with GBM. Core intracellular cascades, such as PI3K\u2010AKT\u2013mTOR and MAPK\u2013ERK, are dysregulated in both diseases and function as shared signalling backbones, with outcomes dictated by cellular context rather than receptor identity. CXCR4, LPA\u2081, and FPR1 exemplify this duality, driving either oncogenic proliferation or neuronal dysfunction, depending on the biological environment. Recent advances in integrative multiomics, computational modelling, artificial intelligence, and organoid systems have revealed GPCR\u2010centred regulatory nodes and accelerated the identification of druggable targets. Collectively, these findings suggest that AD and GBM, although pathologically antithetical, share a molecular fingerprint shaped by ageing\u2010associated inflammation, metabolic disruption, cellular senescence and dysregulated GPCR networks. Deciphering this context\u2010dependent duality may enable precision therapeutic strategies to either restore neuronal integrity in AD or suppress malignant programmes in GBM while fostering cross\u2010fertilisation between neurodegeneration and neuro\u2010oncology research.\n                  <\/jats:p>","DOI":"10.1111\/jcmm.71131","type":"journal-article","created":{"date-parts":[[2026,4,10]],"date-time":"2026-04-10T05:53:44Z","timestamp":1775800424000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["The\n                    <scp>GPCR<\/scp>\n                    Connection: Linking Alzheimer's Disease and Glioblastoma"],"prefix":"10.1111","volume":"30","author":[{"given":"Ana B.","family":"Caniceiro","sequence":"first","affiliation":[{"name":"CNC\u2010UC \u2010 Center for Neuroscience and Cell Biology University of Coimbra  Coimbra Portugal"},{"name":"CiBB \u2010 Centre for Innovative Biomedicine and Biotechnology University of Coimbra  Coimbra Portugal"},{"name":"PhD in Biosciences, Department of Life Sciences University of Coimbra  Coimbra Portugal"},{"name":"Department of Life Sciences University of Coimbra  Coimbra Portugal"},{"name":"PURR.AI, Rua Pedro Nunes, IPN Incubadora, Ed C  Coimbra Portugal"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sofia P.","family":"Agostinho","sequence":"additional","affiliation":[{"name":"PURR.AI, Rua Pedro Nunes, IPN Incubadora, Ed C  Coimbra Portugal"},{"name":"Department of Bioengineering, Instituto Superior T\u00e9cnico Universidade de Lisboa  Lisbon Portugal"},{"name":"Instituto de Telecomunica\u00e7\u00f5es (IT)  Lisbon Portugal"},{"name":"iBB \u2013 Institute for Bioengineering and Biosciences, Instituto Superior T\u00e9cnico Universidade de Lisboa  Lisbon Portugal"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Luiz F.","family":"Piochi","sequence":"additional","affiliation":[{"name":"CNC\u2010UC 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