Study shows young blood can slow Alzheimer’s in mice

The study was conducted by scientists from the Instituto Latinoamericano de Salud Cerebral (BrainLat) at Universidad Adolfo Ibáñez, working alongside collaborators from MELISA Institute, the University of Texas Health Science Center at Houston, and Universidad Mayor.

How Alzheimer's Damages the Brain

Alzheimer's disease is marked by the buildup of beta-amyloid protein (Aβ) in the brain. These proteins clump together to form plaques that interfere with communication between neurons 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 might play a role in how the disease progresses.

Testing the Effects of Young and Old Blood

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

According to Dr. Claudia Durán-Aniotz of the Instituto Latinoamericano de Salud Cerebral (BrainLat) at Universidad Adolfo Ibáñez, the results highlight the importance of looking beyond the brain itself. "This collaborative work between various institutions reinforces the importance of understanding how systemic factors condition the brain environment and directly impact mechanisms that promote disease progression. By demonstrating that peripheral signals derived from aged blood can modulate central processes in the pathophysiology of Alzheimer's, these findings open new opportunities to study therapeutic targets aimed at the blood-brain axis," she explained.

Measuring Memory and Molecular Changes

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

MELISA Institute played a key role in analyzing the complex protein data. Mauricio Hernández, a proteomics specialist at the institute, noted the technical challenges involved. "Within this study, we conducted a large-scale proteomic analysis that allowed us to generate excellent quality data in this complex matrix like plasma, a technical challenge for any proteomics laboratory. Thanks to our state-of-the-art equipment (timsTOF Pro2), we are proud to have contributed to the production of a robust and high-quality scientific article."

What This Means for Future Alzheimer's Research

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

"It is a pleasure to contribute our proteomic capabilities to support innovative research initiatives like this study, which allow us to advance the knowledge and development of new therapies for neurodegenerative diseases, which are currently a global health problem," said Dr. Elard Koch, Chairman of MELISA Institute.

Funding and Research Support

C.DA. was supported by ANID/FONDECYT Regular 1210622, ANID/PIA/ANILLOS ACT210096, the Alzheimer's Association (AARGD-24-1310017), ANID/FOVI240065 and ANID/Proyecto Exploracion 13240170 and MULTI-PARTNER CONSORTIUM TO EXPAND DEMENTIA RESEARCH IN LATIN AMERICA (ReDLat), supported by NIH research grant R01AG057234 funded by the National Institute of Aging (NIA) and 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 to Cure Frontotemporal Dementia, an NIH 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 Charitable Foundation, Bluefield Project to Cure Frontotemporal Dementia, or the Global Brain Health Institute. The contribution of RM and team in this work was supported by NIH grants RF1AG072491 and RF1AG059321. UW was supported by ANID/FONDECYT Regular 1240176.