Salk scientists explore long-standing mystery of why iron that builds up in neuronal cells becomes harmful over time in neurodegenerative diseases like Alzheimer’s and Parkinson’s, finding a new cellular process, named chronoferroptosis, wherein chronic iron dysregulation in neurons makes them more vulnerable to stressors. The study complements other ongoing research at Salk to design compounds that inhibit this pathway, and could be a promising future avenue for creating therapies that boost resilience in aging brains.

Markers of a new mechanism for cell death, called karyoptosis, have been found in brains of patients with Alzheimer’s disease and frontotemporal dementia (FTD).

With the increasing clinical use of anti-amyloid-β monoclonal antibodies in Alzheimer’s disease in China, some patients have completed or are approaching the predefined treatment period, leading to emerging clinical questions regarding post-treatment maintenance, discontinuation, monitoring, and retreatment. However, no consensus has yet been established on long-term management or sequential-like treatment strategies after anti-amyloid-β monoclonal antibody therapy. Based on current clinical evidence and the practical experience of Renji Cognitive Center, this article proposes an experience-based protocol for sequential-like management of anti-amyloid-β monoclonal antibody therapy. The protocol uses amyloid PET-derived Centiloid values as the core objective reference and recommends stratified management according to clinical clearance status and prior amyloid clearance rate. This protocol is intended to provide a clinical reference and requires further validation and optimization through real-world studies and long-term follow-up.

Often-overlooked costs, including diminished quality of life and informal care provided by loved ones, account for most of dementia's staggering economic toll.