ArticleMolecular psychiatry2022
Preventive and therapeutic reduction of amyloid deposition and behavioral impairments in a model of Alzheimer's disease by whole blood exchange.
Article in Molecular psychiatry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 30 citations in OpenAlex.
- Spectroscopic Insights into Lysozyme Structural Modulation by Polyphenols: A Combined FTIR and VCD Study.Molecules (Basel, Switzerland) · 2026Article
- Stem Cell and Stem Cell-Derived Extracellular Vesicles: Therapeutic Potential and Mechanistic Insights in Anti-Aging.Stem cell reviews and reports · 2026Review
- The liver-brain axis: A multidimensional regulatory network implicated in Alzheimer's disease pathogenesis and clinical implications.Animal models and experimental medicine · 2026Review
- Vitronectin Modulates Plasma Aβ Oligomerization Propensity Within Altered Albumin Interactome Networks in Alzheimer's Disease.International journal of molecular sciences · 2026Article
- Splenic treg-related immunoregulation in the spleen-brain axis of alzheimer's disease: mechanisms and translational strategies.Molecular biology reports · 2026Review
- First application of whole blood exchange-lymphoplasmapheresis combined transfusion for restoring immune homeostasis of ceftriaxone-induced hemolytic crisis: a case report.Frontiers in immunology · 2026Article
- Systemic proteomic and organ aging signatures associated with plasma Aβ oligomerization in a Korean cohort: a cross-sectional study.Frontiers in aging neuroscience · 2026Article
- The diagnostic value of plasma Aβ42 and Aβ40 in Alzheimer's disease: current status, challenges, and impacting variables.Journal of neurology · 2025Review
- Impacts of systemic milieu on cerebrovascular and brain aging: insights from heterochronic parabiosis, blood exchange, and plasma transfer experiments.GeroScience · 2025Review
- Article
- Liver-specific expression of ANGPTL8 promotes Alzheimer's disease progression through activating microglial pyroptosis.Journal of neuroinflammation · 2025Article
- Stroke Exacerbates Respiratory Disorder and Cognition Impairment in Mice with Cerebral Amyloid Angiopathy.Aging and disease · 2025Article
- Antiageing strategy for neurodegenerative diseases: from mechanisms to clinical advances.Signal transduction and targeted therapy · 2025Review
- Improvements in Exercise for Alzheimer's Disease: Highlighting FGF21-Induced Cerebrovascular Protection.Neurochemical research · 2025Review
- Peripheral proteinopathy in neurodegenerative diseases.Translational neurodegeneration · 2025Review
- Peripheral administration of blood from tau transgenic animals exacerbates brain tau-associated pathology.PloS one · 2025Article
- Bidirectional Crosstalk between the Heart and Brain in Alzheimer's Disease.Aging and disease · 2024Review
- Insights into AlphaFold's breakthrough in neurodegenerative diseases.Irish journal of medical science · 2024Review
- Trajectory of brain-derived amyloid beta in Alzheimer's disease: where is it coming from and where is it going?Translational neurodegeneration · 2024Review
- Targeting Astrogliosis in the Retrotrapezoid Nucleus: A Novel Approach to Ameliorate Respiratory Dysfunction and Alzheimer's Pathology in Mice.Aging and disease · 2024Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Alzheimer's disease (AD) is the major form of dementia in the elderly population. The main neuropathological changes in AD patients are neuronal death, synaptic alterations, brain inflammation, and the presence of cerebral protein aggregates in the form of amyloid plaques and neurofibrillary tangles. Compelling evidence suggests that the misfolding, aggregation, and cerebral deposition of amyloid-beta (Aβ) plays a central role in the disease. Thus, prevention and removal of misfolded protein aggregates is considered a promising strategy to treat AD. In the present study, we describe that the development of cerebral amyloid plaques in a transgenic mice model of AD (Tg2576) was significantly reduced by 40-80% through exchanging whole blood with normal blood from wild type mice having the same genetic background. Importantly, such reduction resulted in improvement in spatial memory performance in aged Tg2576 mice. The exact mechanism by which blood exchange reduces amyloid pathology and improves memory is presently unknown, but measurements of Aβ in plasma soon after blood exchange suggest that mobilization of Aβ from the brain to blood may be implicated. Our results suggest that a target for AD therapy may exist in the peripheral circulation, which could open a novel disease-modifying intervention for AD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.