Study shows that young blood can slow Alzheimer’s disease in mice

The study was conducted by scientists from the Latin American Institute for Brain Health (BrainLat) at the Adolfo Ibáñez University, in collaboration with collaborators from the Melissa Institute, the University of Texas Health Science Center at Houston, and the University of Mayor.

How Alzheimer’s disease destroys the brain

Alzheimer’s disease is characterized by the accumulation of amyloid beta (Aβ) protein in the brain. These proteins clump together to form plaques that interfere with communication between nerve cells and trigger processes that gradually damage brain tissue. While beta-amyloid is produced in the brain, recent research has suggested that it can also be detected in the bloodstream. This discovery has raised new questions about whether blood-based factors may play a role in how the disease develops.

Small and large blood trace tests

To investigate this possibility, the researchers used transgenic Tg2576 mice (a model widely used in Alzheimer’s disease research). Over the course of 30 weeks, the mice received weekly blood infusions from young or aged donor mice. The goal was to determine whether blood components could influence amyloid buildup in the brain as well as memory and behavior.

According to Dr. Claudia Duran Añuetz of the Latin American Institute for Brain Health (BrainLat) at the Adolfo Ibáñez University, the findings highlight the importance of looking beyond the brain itself. She explained: “This collaborative work between various institutions reinforces the importance of understanding how systemic factors influence the brain environment and directly influence mechanisms that promote disease progression. By demonstrating that peripheral signals derived from old blood can modulate processes central to the pathophysiology of Alzheimer’s disease, these findings open new opportunities to study therapeutic targets targeting the blood-brain axis.”

Measuring memory and molecular changes

The research team assessed cognitive performance using the Barnes test and measured amyloid plaque accumulation through histological and biochemical methods. They also performed a detailed proteomic analysis of the brain tissue of the treated mice. This analysis identified more than 250 proteins whose activity levels changed. Many of these proteins are involved in synaptic function, endocannabinoid signaling, and regulation of calcium channels, offering potential explanations for observed differences in brain health and behavior.

The Melissa Institute has played a key role in analyzing complex protein data. Mauricio Hernandez, a proteomics specialist at the institute, pointed to the technical challenges involved. “Within this study, we performed a large-scale proteomic analysis that allowed us to generate data of excellent quality in such a complex matrix as plasma, which is a technical challenge for any proteomics laboratory. Thanks to our state-of-the-art instrumentation (timsTOF Pro2), we are proud of our contribution to the production of a robust, high-quality scientific article.”

What this means for future Alzheimer’s research

These findings add to growing evidence that factors circulating in the blood can directly influence the course of neurodegenerative diseases such as Alzheimer’s disease. By determining how these blood-based signals affect the brain, scientists may be able to uncover new therapeutic targets and develop strategies to slow or prevent disease progression. Future research will focus on identifying the specific factors involved and determining whether they can be safely targeted in humans.

“It is a pleasure to contribute our proteomic capabilities to support innovative research initiatives such as this study, which allows us to advance knowledge and develop new treatments for neurodegenerative diseases, which currently represent a global health problem,” said Dr. Ellard Koch, President of the Melissa Institute.

Funding and research support

very. was supported by ANID/FONDECYT Regular 1210622, ANID/PIA/ANILLOS ACT210096, the Alzheimer’s Association (AARGD-24-1310017), ANID/FOVI240065, ANID/Proyecto Exploracion 13240170, and the Multi-Partner Extension Consortium. Dementia Research in Latin America (ReDLat), supported by National Institutes of Health Research Grant R01AG057234 with funding from the National Institute on Aging (NIA), the Fogarty International Center (FIC), an Alzheimer’s Association grant (SG-20-725707-ReDLat), the Rainwater Charitable Foundation, and the Global Brain Health Institute with additional support from the Bluefield Project for Frontotemporal Therapy. Dementia, National Institutes of Health contract (75NS95022C00031), and NIA under Awards R01AG075775, R01AG082056, and R01AG083799. The content is solely the responsibility of the authors and does not represent the official views of the National Institutes of Health, the Alzheimer’s Association, Rainwater Charities, the Bluefield Frontotemporal Dementia Project, or the Global Brain Health Institute. The contribution of RM and the team to this work was supported by National Institutes of Health grants RF1AG072491 and RF1AG059321. UW was supported by ANID/FONDECYT Regular 1240176.