Neurodegenerative diseases, including Alzheimer's disease (AD), Parkinson's disease (PD) and other neurological disorders, are emerging as a major concern in public health in Gulf Cooperation Council (GCC) countries. The number of cases has increased over the years, but research and development has not matched the pace of demographic and healthcare shifts. Population surveillance is limited in Saudi Arabia, Oman, Qatar and the United Arab Emirates (UAE), with weak hospital-academia links, inadequate funding of research, deficits in subspecialist training, a paucity of research output, weak biobanking infrastructure and a young innovation ecosystem. This policy perspective introduces a cross-cutting policy approach to modify the existing scattered infrastructure into a functioning neurodegeneration research and innovation ecosystem. This can be accomplished via a combination of interdisciplinary training and workforce development, enhanced research strength, strengthened clinician–academic partnerships, larger clinical databases and biobanks, increased research funding, faster translation of biotech developments, and digital-health innovation. Incubation centres and public-private partnerships are crucial for achieving these objectives. GCC Health Council’s coordination throughout the region can align research priorities, allow studies in multiple countries, share data and bolster engagement with neurodegeneration initiatives at an international level. The proposed framework positions research institutes, universities, hospitals, industry and government as interconnected components of a translational ecosystem rather than isolated entities. This approach can help the four GCC countries convert existing healthcare investments and expanding scientific capacity into locally relevant discoveries and strengthen the region’s contribution to global neurodegeneration research.

Emodin is a naturally occurring anthraquinone and has been of great interest as a multi-target anticancer agent with potential anti-metastatic effects. There is a growing body of evidence that emodin inhibits the progression of cancer by regulating essential events of epithelial–mesenchymal transition (EMT) and extracellular matrix remodeling. It suppresses matrix metalloproteinases and other associated proteolytic enzymes, thus hindering tumor invasion and metastatic spread. Emodin also suppresses key EMT-related transcription factors, such as Snail, Slug and Twist resulting in lower expression of mesenchymal markers, recovery of epithelial phenotype and lack of cellular motility. These effects are mechanistically mediated by disrupting central oncogenic pathways including transforming growth factor-β (TGF-β)/Smad, Akt/mTOR, MAPK and other signaling pathways that promote EMT plasticity. Recent research also indicates that emodin has a role in regulating cytoskeletal organization, ROS signal, and interactions with the tumor microenvironment that promote metastatic behavior. Although there is strong preclinical evidence, there are still a number of translational gaps. This limits its possible therapeutic use due to low bioavailability, low stability, and inconsistent tumor responsiveness. Possible resistance mechanisms, such as the compensatory activation of other pathways such as Wnt/ β-catenin and survival signaling cascades, are not sufficiently characterized. There is also lack of clinical validation with few controlled trials assessing safety and anti-metastatic efficacy across different types of cancer. The future directions are to focus on optimization of formulation and delivery, improvement of the pharmacokinetics, patient stratification, biomarker-based guided, and rigorous comparisons of combination regimens with chemotherapy, radiotherapy, and targeted agents. These approaches can be used to achieve the full potential of emodin as a therapeutic candidate, which is a metastasis-modulating agent.