Study shows young blood slows Alzheimer's in mice

New research reveals that blood from younger mice can protect against Alzheimer's-like brain damage, while older blood accelerates it. Scientists conducted experiments infusing mouse blood over 30 weeks to observe effects on memory and protein buildup. The findings highlight blood's role in brain health and potential new treatments.

Alzheimer's disease, the leading cause of dementia worldwide, involves the buildup of beta-amyloid proteins that form plaques disrupting neuron communication and damaging brain tissue. Recent studies suggest these proteins appear in the bloodstream, prompting questions about blood's influence on disease progression.

Researchers from the Instituto Latinoamericano de Salud Cerebral at Universidad Adolfo Ibáñez, MELISA Institute, University of Texas Health Science Center at Houston, and Universidad Mayor tested this using Tg2576 transgenic mice, a common model for Alzheimer's. Over 30 weeks, they infused blood weekly from either young or aged donor mice to assess impacts on amyloid accumulation, memory, and behavior.

Results showed older blood worsened memory performance in the Barnes maze test and increased amyloid plaques, detected via histological and biochemical methods. Younger blood, conversely, offered protective effects, reducing these changes. A proteomic analysis of brain tissue revealed over 250 proteins with altered activity, many linked to synaptic function, endocannabinoid signaling, and calcium channel regulation.

Dr. Claudia Durán-Aniotz, from BrainLat, emphasized the broader implications: "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."

Mauricio Hernández, a proteomics specialist at MELISA Institute, highlighted the technical feat: "Within this study, we conducted a large-scale proteomic analysis that allowed us to generate excellent quality data in this complex matrix like plasma... we are proud to have contributed to the production of a robust and high-quality scientific article."

Dr. Elard Koch, Chairman of MELISA Institute, added: "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."

Published in Aging (2025; 17(11):2664), the study suggests blood-based factors could be key targets for slowing Alzheimer's, with future work identifying specific components for human application.

Makala yanayohusiana

Realistic split-image illustration showing obesity-linked faster rise in Alzheimer’s blood biomarkers versus normal weight, highlighting blood tests detecting changes earlier than brain scans.
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Obesity linked to faster rise in Alzheimer’s blood biomarkers, study finds

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New research finds that blood biomarkers associated with Alzheimer’s disease increase significantly faster in people with obesity than in those without. Drawing on five years of data from 407 volunteers, the study suggests that blood tests can detect obesity‑related changes earlier than brain scans, underscoring obesity as a major modifiable risk factor for Alzheimer’s.

Scientists at Northern Arizona University are developing a non-invasive blood test that could help detect Alzheimer’s disease before symptoms appear by examining how the brain uses glucose through tiny blood-borne microvesicles. Led by assistant professor Travis Gibbons and supported in part by the Arizona Alzheimer’s Association, the project aims to enable earlier diagnosis and intervention, similar to how doctors manage cardiovascular disease.

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A study published November 5 in Nature reports that a small subset of microglia marked by low PU.1 and expression of the receptor CD28 can dampen neuroinflammation and curb amyloid pathology in Alzheimer’s models, pointing to microglia-focused immunotherapy. The work draws on mouse experiments, human cells, and analyses of human brain tissue.

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