A NEW animal study suggests that Alzheimer’s progression can be significantly influenced by circulating blood factors, with transfusions from older donors accelerating brain pathology and memory decline while blood from younger donors appears to exert protective neurological effects.
Blood Age and Alzheimer’s Progression
Alzheimer’s disease is defined by progressive cognitive impairment and the accumulation of amyloid beta in the brain. Traditionally, these pathological processes were believed to be confined largely to neural tissue. Growing evidence now indicates that peripheral blood components play a measurable role in shaping Alzheimer’s progression by influencing amyloid clearance, inflammation, and synaptic integrity. Blood based strategies such as plasma exchange have already demonstrated potential benefits in reducing amyloid burden in human studies, raising interest in how the biological age of circulating blood may modify disease trajectories.
Long-Term Infusion Study in Transgenic Mice
Researchers infused transgenic Tg2576 mice with weekly blood transfusions from either young or old wild type donors over a prolonged period. Mice receiving old donor blood displayed significantly impaired short- and long-term spatial memory and increased cortical amyloid deposition compared with animals receiving young blood. Proteomic profiling identified more than 250 differentially expressed proteins affecting synaptogenesis, calcium channel regulation, and endocannabinoid signalling. Among these, the α2δ2 calcium channel subunit emerged as a potential mediator of Alzheimer’s progression, showing higher expression in mice treated with old blood. In contrast, young donor blood was associated with protein changes consistent with improved synaptic and neuronal function, suggesting a biologically protective influence on neurodegenerative pathways.
Clinical Implications and Future Directions
Although conducted in animal models, these findings reinforce the concept that Alzheimer’s progression is not solely driven by intrinsic brain pathology but is also shaped by systemic biological factors. Understanding how circulating proteins and inflammatory mediators influence amyloid deposition and synaptic health could open new avenues for blood-based diagnostics and therapies. Future translational research may focus on identifying harmful and protective blood-borne factors, developing targeted plasma modification strategies, and refining patient selection for emerging blood-based interventions.
Reference
Pizarro M et al. Infusion of blood from young and old mice modulates amyloid pathology. Aging (Albany NY). 2025;17(11):2664.
