Scientists have made a significant discovery, finding that components in young blood can effectively slow Alzheimer’s-related brain damage in mice, while conversely, older blood appears to accelerate it. This groundbreaking research, detailed on ScienceDaily.com in January 2026, points to the profound influence of blood factors on brain health and offers promising new therapeutic targets to combat neurodegenerative diseases.
Alzheimer’s disease remains the leading cause of dementia globally, presenting a formidable challenge to public health systems worldwide. For years, research has primarily focused on brain-specific mechanisms. However, these new findings shift the focus, suggesting that systemic factors circulating in the bloodstream play a critical role in how quickly the disease progresses.
This paradigm shift highlights the potential of exploring the complex interplay between the circulatory system and brain health. Understanding these peripheral signals could unlock novel approaches to prevent or slow the devastating effects of Alzheimer’s, moving beyond traditional brain-centric interventions.
The blood-brain axis and amyloid buildup
How Alzheimer’s damages the brain centers on the accumulation of beta-amyloid protein (Aβ), forming plaques that disrupt neuronal communication and degrade brain tissue. While Aβ is produced in the brain, its detection in the bloodstream has prompted new questions about the influence of blood-based factors on disease progression.
To investigate this, researchers utilized Tg2576 transgenic mice, a standard model in Alzheimer’s studies. Over 30 weeks, these mice received weekly blood infusions from either young or aged donor mice. The objective was to determine if blood components could impact amyloid buildup, memory, and behavior.
Dr. Claudia Durán-Aniotz of BrainLat at Universidad Adolfo Ibáñez emphasized the broader implications of these findings. “This collaborative work reinforces the importance of understanding how systemic factors condition the brain environment and directly impact mechanisms that promote disease progression,” she stated, highlighting new opportunities for therapeutic targets along the blood-brain axis.
Unpacking the molecular mechanisms
The research team rigorously evaluated cognitive performance using the Barnes test and quantified amyloid plaque accumulation through histological and biochemical methods. Crucially, they conducted an in-depth proteomic analysis of brain tissue, identifying over 250 proteins with altered activity levels.
These proteins are intricately involved in vital brain functions, including synaptic function, endocannabinoid signaling, and calcium channel regulation. Such changes offer plausible explanations for the observed differences in brain health and behavior between the groups receiving young versus old blood.
Mauricio Hernández, a proteomics specialist at MELISA Institute, underscored the technical complexity. “We conducted a large-scale proteomic analysis that allowed us to generate excellent quality data in this complex matrix like plasma,” he noted, acknowledging the institute’s role in producing a robust scientific article with state-of-the-art equipment.
These findings significantly contribute to the growing body of evidence indicating that circulating factors in the blood directly influence the course of neurodegenerative diseases like Alzheimer’s. By pinpointing how these blood-based signals affect the brain, scientists are better positioned to uncover specific treatment targets. Future research will focus on identifying these precise factors and assessing their safety and efficacy in human trials, potentially paving the way for revolutionary therapies to slow or even prevent the disease.
