ADpheresis-Ace
What if part of the key to slowing Alzheimer’s disease were found not only in the brain, but also in the blood? This study aims to explore precisely that idea: understanding how therapeutic apheresis, a procedure that “renews” a patient’s plasma, could influence the progression of cognitive decline.
The main objective of the ADpheresis project is to understand the impact of peripheral changes induced by therapeutic plasma exchange (TPE) treatment in patients with Alzheimer’s disease and to analyze their relationship with cognitive decline progression. The study is based on the peripheral hypothesis of Alzheimer’s disease, which suggests that systemic processes such as inflammation, vascular dysfunction, peripheral immunity, and metabolic status can significantly influence brain pathophysiology and clinical progression of the disease.
Alzheimer’s Disease-Associated Autoantibodies
Specifically, the study aims to identify and characterize autoantibodies associated with Alzheimer’s disease and to evaluate longitudinally how TPE treatment modifies plasma levels of these autoantibodies. This objective is based on evidence that certain autoantibodies may participate in relevant pathogenic mechanisms, such as neuroinflammation, altered microglial response, and immune dysfunction observed in Alzheimer’s disease.
Plasma Proteomic Changes Induced by TPE
Another central objective is to perform a longitudinal characterization of plasma proteomic changes induced by TPE to identify peripheral biomarkers associated with treatment response and clinical progression.
Alterations in Peripheral Blood Mononuclear Cells (PBMCs)
The study also aims to analyze alterations in peripheral blood mononuclear cell populations in detail, including the frequency of cell subpopulations and their basal and ex vivo stimulated intracellular signaling patterns, to better understand the role of the peripheral immune system in the disease.
Nutritional Status and Metabolism
The project also evaluates the longitudinal macro- and micronutritional status of patients undergoing TPE treatment under fasting conditions, considering that nutritional deficits and metabolic alterations may contribute to neuronal dysfunction and cognitive decline.
Data Integration and Personalized Therapeutic Strategies
Finally, all these data, immunological, proteomic, metabolic, and clinical, are integrated through a multidimensional analysis to identify biological profiles associated with slower cognitive decline progression and to advance toward more personalized therapeutic strategies in Alzheimer’s disease.
