Nanoparticles reduced amyloid-β and improved cognition in an Alzheimer’s mouse model, researchers report

Researchers from the Institute for Bioengineering of Catalonia and collaborating institutions report that engineered “supramolecular” nanoparticles restored aspects of blood-brain barrier function in Alzheimer’s-model mice, rapidly lowering brain amyloid-β and producing improvements on behavioral and memory tests.

An international research team reported results in mice suggesting a nanotechnology-based approach may help the brain clear Alzheimer’s-linked waste proteins by targeting the blood-brain barrier (BBB), a protective interface that regulates what enters and leaves the brain.

According to a research summary released by the Institute for Bioengineering of Catalonia (IBEC) and published by ScienceDaily, the scientists designed bioactive nanoparticles—described as “supramolecular drugs”—intended to modulate BBB transport rather than simply serve as drug carriers. The work was led by researchers at IBEC and West China Hospital of Sichuan University, with collaborators in the United Kingdom, and was published in Signal Transduction and Targeted Therapy.

The study focused on the BBB transport protein LRP1. Under normal conditions, LRP1 can bind amyloid-β (Aβ) and help move it out of the brain. The researchers reported engineering nanoparticles to mimic natural molecules that interact with LRP1, with the aim of “resetting” this transport pathway and improving Aβ clearance.

In experiments using genetically engineered mice that develop high levels of Aβ and cognitive decline, the animals received three nanoparticle doses. The team reported that brain Aβ fell by about 50% to 60% one hour after an injection. In longer follow-up experiments described in the summary, the researchers reported improved performance on behavioral and memory testing months after treatment, including a case in which an older treated mouse later behaved similarly to a healthy mouse on the tests used.

The researchers cautioned that the findings are limited to animal models and that many Alzheimer’s approaches that show promise in mice do not translate to effective human treatments.

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