Summary: New research shows that blood from older animals can speed up Alzheimer’s-related changes in the brain, while young blood can slow them down. In a long-term experiment, mice engineered to develop Alzheimer’s symptoms received weekly blood infusions from young or older donors.
Older blood increased amyloid accumulation and worsened cognitive performance, while young blood appeared to have protective effects. Proteomic analysis revealed more than 250 altered proteins related to synaptic signaling, calcium channels, and other pathways related to neurodegeneration. The findings highlight circulating blood factors as potential targets for future Alzheimer’s therapies.
Key facts
Blood-borne influence: Aged blood accelerated amyloid accumulation and cognitive decline in Alzheimer’s model mice. Protective effect: Young blood altered brain protein profiles consistent with better synaptic and neuronal function. Therapeutic potential: Results point to blood-derived factors as a new frontier for Alzheimer’s interventions.
Source: Melisa Institute
Alzheimer’s disease is the most common form of dementia worldwide and remains one of the biggest public health challenges.
New research, published in the journal Aging-US, reveals that blood from old mice can accelerate the progression of the disease, while young blood can have protective effects.
The study was led by researchers from the Latin American Institute of Brain Health (BrainLat) of the Adolfo Ibáñez University in conjunction with the MELISA Institute, the Health Sciences Center of the University of Texas in Houston and the Universidad Mayor.
Alzheimer’s is characterized by the abnormal accumulation of beta-amyloid protein (Aβ) in the brain, forming plaques that alter communication between neurons and generate neurodegenerative processes.
Although this protein originates in the central nervous system, recent studies have suggested that it may also be present in the blood, opening new possibilities for understanding how the disease progresses.
To explore this hypothesis, the team used Tg2576 transgenic mice (a model widely used in Alzheimer’s research), which received weekly blood infusions from young and old mice for 30 weeks to evaluate whether factors present in the blood could modulate amyloid accumulation and the animals’ behavior.
“This collaborative work between several institutions reinforces the importance of understanding how systemic factors condition the brain environment and directly impact the 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 directed at the blood-brain axis,” explained Dr. Claudia Durán-Aniotz, from the Latin American Institute of Brain Health (BrainLat) of the Adolfo Ibáñez University.
The team assessed cognitive performance using the Barnes test, amyloid plaque accumulation with histological and biochemical techniques, and performed a comprehensive proteomic analysis of the treated brains.
This analysis revealed more than 250 differentially expressed proteins, linked to synaptic functions, endocannabinoid signaling and calcium channels, which could explain the observed changes.
Regarding the participation of the MELISA Institute in this research, Mauricio Hernández, proteomics expert at the research and biotechnology center, commented that “within this study we carried out a large-scale proteomic analysis that allowed us to generate data of excellent quality in this complex matrix such as 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.”
These results reinforce the idea that factors circulating in the blood can directly influence the progression of neurodegenerative diseases such as Alzheimer’s. Understanding these mechanisms will allow the identification of new therapeutic targets and preventive strategies. The next step will be to determine exactly what these factors are and if it is possible to intervene on them in humans.
“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,” emphasized Dr. Elard Koch, president of the MELISA Institute.
Funds:
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 MULTISOCIO CONSORTIUM TO EXPAND RESEARCH IN DEMENTIA IN LATIN AMERICA (ReDLat), supported by NIH Research Grant R01AG057234 funded by the National Institute on Aging (NIA) and the Fogarty International Center (FIC), a grant from the Alzheimer’s Association (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, the Rainwater Charitable Foundation, the Bluefield Project to Cure Frontotemporal Dementia, or the Global Brain Health Institute.
RM and team’s contribution to this work was supported by NIH grants RF1AG072491 and RF1AG059321. The UW was supported by ANID/FONDECYT Regular 1240176.
Key questions answered:
A: Mice that received blood from older donors showed more rapid accumulation of amyloid plaque, altered brain protein profiles, and poorer performance on cognitive tests. These changes suggest that factors circulating in aged blood actively promote processes related to the progression of Alzheimer’s.
A: Young blood shifted brain protein expression toward patterns associated with healthier synaptic signaling and reduced disease-related dysfunction. These protective effects point to specific molecular factors that may slow or counteract neurodegeneration.
A: The findings reveal that the blood-brain axis plays an important role in boosting or slowing the progression of Alzheimer’s. Identifying the exact blood-borne molecules involved could lead to new therapeutic targets or preventive strategies aimed at modifying systemic factors rather than the brain alone.
Editorial notes:
This article was edited by a Neuroscience News editor. Magazine article reviewed in its entirety. Additional context added by our staff.
About this news about Alzheimer’s research
Author: Damián Vallejos
Source: Melisa Institute
Contact: Damián Vallejos – Melisa Institute
Image: Image is credited to Neuroscience News.
Original research: Open access.
“Blood infusion from young and old mice modulates amyloid pathology” by Claudia Durán-Aniotz et al. Aging-USA
Abstract
Blood infusion from young and old mice modulates amyloid pathology
Alzheimer’s disease (AD) is a neurodegenerative disease characterized by the accumulation of misfolded proteins in the brain.
Recently, attention has been drawn to the impact of blood components on the progression of this disease.
This study investigates the effects of infusion of blood from young and old wild-type mice into transgenic mice modeling AD cerebral amyloidosis.
Memory problems and Aβ accumulation were observed in mice infused with blood from old donors.
A proteomic analysis in the brain of these mice identified alterations in components related to synaptogenesis and the endocannabinoid system. The α2δ2 protein, associated with neuronal calcium regulation, was validated as a possible mediator of the observed effects.
This study highlights the influence of blood on AD pathology and the identification of possible therapeutic targets.
