New Review Integrates Human, Animal, and Cellular Evidence to Reframe AD as a Triad-Centered Disorder

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder marked by memory loss, cognitive impairment, and widespread neuronal dysfunction. Although amyloid and tau pathologies have dominated the field for decades, growing evidence suggests that AD arises from broader homeostatic failures rather than a single molecular trigger.

Developed by a consortium of 30 public and private partners, ACCESS-AD (“Advancing Clinical Care and Equity through Scalable Solutions in Alzheimer’s Disease diagnosis and treatment”) is focused on bringing innovations to routine clinical practice for Alzheimer’s disease, supporting timely diagnosis, treatment and monitoring across diverse healthcare settings. Launching on 13 January 2026, ACCESS-AD is funded for a period of 5 years by the Innovative Health Initiative (IHI), an EU Public-Private Partnership supporting health research and innovation. 

Alzheimer’s disease (AD) is a serious neurodegenerative disease largely affecting older adults. Apart from age, it also shows sex-based differences, with women being more at risk. However, the origin of these differences remains unknown. While bone morphogenetic proteins (BMPs) play an important role in adult neurogenesis, their role in AD remains elusive. To address this, researchers have investigated sex-based differences and role of BMP signaling in neurogenesis in AD mice models, uncovering novel therapeutic targets

When the cell’s recycling stations, the lysosomes, start leaking, it can become dangerous. Toxic waste risks spreading and damaging the cell. Now, researchers at Umeå University have revealed the molecular sensors that detect tiny holes in lysosomal membranes so they can be quickly repaired – a process crucial for preventing inflammation, cell death, and diseases such as Alzheimer’s.