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Amyloid Fibrils

Amyloid Fibrils

Amyloid fibrils are aggregates of misfolded proteins. Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils.
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining,...

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Related Experiment Video

Updated: Jun 6, 2025

Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits

Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits

Published on: March 16, 2016

A Supramolecular Protein Assembly Intrinsically Rescues Memory Deficits in an Alzheimer's Disease Mouse Model.

Yuchong Hao¹, Xin Shen¹, Jiantao Liu²

¹Sino-German Joint Research Lab for Space Biomaterials and Translational Technology, Synergetic Innovation Center of Biological Optoelectronics and Healthcare Engineering, School of Life Sciences, Northwestern Polytechnical University, Youyi West Road 127, Xi'an, Shaanxi 710072, China.

|November 26, 2024

Summary

Researchers developed a novel supramolecular protein assembly capable of crossing the blood-brain barrier (BBB). This nanodisc technology effectively targets Alzheimer's disease pathology and improves cognitive function in mouse models.

Keywords:

Alzheimer’s disease blood-brain barrier nanodisc nanomedicine protein assembly

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Stereotaxic Infusion of Oligomeric Amyloid-beta into the Mouse Hippocampus

Stereotaxic Infusion of Oligomeric Amyloid-beta into the Mouse Hippocampus

Published on: June 17, 2015

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Last Updated: Jun 6, 2025

Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits

Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits

Published on: March 16, 2016

Establishment of a Valuable Mimic of Alzheimer's Disease in Rat Animal Model by Intracerebroventricular Injection of Composited Amyloid Beta Protein

Establishment of a Valuable Mimic of Alzheimer's Disease in Rat Animal Model by Intracerebroventricular Injection of Composited Amyloid Beta Protein

Published on: July 29, 2018

Stereotaxic Infusion of Oligomeric Amyloid-beta into the Mouse Hippocampus

Stereotaxic Infusion of Oligomeric Amyloid-beta into the Mouse Hippocampus

Published on: June 17, 2015

Area of Science:

Biomaterials Science
Neuroscience
Drug Delivery

Background:

Supramolecular protein assemblies are explored as intelligent drug delivery systems.
Current methods for designing blood-brain barrier (BBB)-penetrating protein assemblies are inefficient.
Targeting neurological disorders like Alzheimer's disease requires effective BBB transport.

Purpose of the Study:

To develop a novel supramolecular protein assembly capable of crossing the BBB.
To investigate the therapeutic potential of this assembly in an Alzheimer's disease mouse model.

Main Methods:

Engineered a recombinant protein based on apolipoprotein A1.
Self-assembly of the recombinant protein into nanodiscs.
Evaluation of nanodisc brain entry, amyloid-beta (Aβ) recognition, and therapeutic effects in an Alzheimer's disease mouse model.

Main Results:

The self-assembled nanodiscs efficiently crossed the BBB in an Alzheimer's disease mouse model.
Nanodiscs recognized and helped eliminate amyloid plaques (Aβ_1-42).
Treatment promoted neurogenesis and ameliorated cognitive impairment.

Conclusions:

A supramolecular recombinant-protein-based strategy enables intrinsic BBB crossing.
The developed nanodiscs offer a promising therapeutic approach for Alzheimer's disease.
This work establishes a new platform for designing versatile supramolecular biomaterials for neurological applications.