Extracorporeal Apheresis and Alzheimer’s Disease Research

Long Covid Treatment

Extracorporeal Apheresis and Alzheimer’s Disease Research

A 2020 Molecular Psychiatry review exploring extracorporeal apheresis, inflammation and lipid pathways in Alzheimer’s disease research.

Access the full study via the Molecular Psychiatry journal.

Study Overview

In 2020, a perspective review published in Molecular Psychiatry examined the potential biological rationale for extracorporeal apheresis in the context of Alzheimer’s disease. The authors explored how lipid metabolism, inflammation, oxidative stress, and vascular function may interact in neurodegenerative conditions.

The paper does not present a randomised clinical trial. Rather, it outlines theoretical mechanisms and proposes further research into how plasma filtration approaches may influence systemic inflammatory and metabolic pathways relevant to neurological disease.

What the Review Discussed

The authors considered several biological factors:

• Chronic systemic inflammation
• Lipid transport and cholesterol metabolism
• Oxidative stress
• Blood–brain barrier integrity
• Vascular and metabolic signalling

The review proposed that removing selected plasma components through extracorporeal filtration could potentially influence these pathways. However, the article emphasised the need for structured clinical trials to evaluate safety, outcomes, and efficacy in defined patient populations.

Important Context

This publication is a hypothesis-driven review article. It does not demonstrate clinical effectiveness in Alzheimer’s disease.

The authors conclude that controlled studies would be required to determine whether extracorporeal apheresis could have a measurable clinical role in neurodegenerative conditions.

Research in this area remains ongoing internationally.

Reference

Bornstein SR et al. (2020). Extracorporeal apheresis therapy for Alzheimer disease—targeting lipids, stress, and inflammation. Molecular Psychiatry, 25, 275–282.
DOI: 10.1038/s41380-019-0542-x