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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, normally used to...

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Updated: May 26, 2026

A Novel In Vitro Live-imaging Assay of Astrocyte-mediated Phagocytosis Using pH Indicator-conjugated Synaptosomes

A Novel In Vitro Live-imaging Assay of Astrocyte-mediated Phagocytosis Using pH Indicator-conjugated Synaptosomes

Published on: February 5, 2018

Amyloid-β clearance: an astrocytic perspective.

Jiayi Li¹, Zhongyue Lv¹, Xiao Chen¹

¹Department of Neurology, The Affiliated Lihuili Hospital of Ningbo University, Ningbo University, Ningbo, Zhejiang, China.

Frontiers in Neuroscience

|May 25, 2026

Summary

Alzheimer's disease (AD) involves amyloid-beta (Aβ) buildup. This review explores how astrocytes, a type of brain cell, clear Aβ, offering new targets for early AD intervention.

Keywords:

Alzheimer’s disease Aβ clearance astrocyte blood–brain barrier glymphatic pathway neuroinflammation

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Last Updated: May 26, 2026

A Novel In Vitro Live-imaging Assay of Astrocyte-mediated Phagocytosis Using pH Indicator-conjugated Synaptosomes

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Published on: February 5, 2018

Cell-based Assay to Study Antibody-mediated Tau Clearance by Microglia

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Visualization of Amyloid β Deposits in the Human Brain with Matrix-assisted Laser Desorption/Ionization Imaging Mass Spectrometry

Visualization of Amyloid β Deposits in the Human Brain with Matrix-assisted Laser Desorption/Ionization Imaging Mass Spectrometry

Published on: March 7, 2019

Area of Science:

Neuroscience
Neurodegenerative Diseases
Cell Biology

Background:

Alzheimer's disease (AD) is a leading cause of mortality and socioeconomic burden.
Pathological hallmark of AD is amyloid-beta (Aβ) imbalance, leading to aggregation and neurodegeneration years before symptoms.
Current therapies targeting Aβ production show limited success; early Aβ clearance interventions are gaining traction.

Purpose of the Study:

To review astrocyte-mediated Aβ clearance mechanisms.
To explore astrocyte roles in blood-brain barrier maintenance and glymphatic drainage.
To identify astrocyte phenotypic changes and functional decline in AD pathology.

Main Methods:

Literature review synthesizing recent findings on astrocyte-AD pathology.
Focus on molecular mechanisms of astrocyte Aβ uptake and degradation.
Analysis of astrocyte roles in blood-brain barrier integrity and glymphatic transport.

Main Results:

Astrocytes clear Aβ via endocytosis and intracellular degradation.
Astrocyte function in blood-brain barrier maintenance and aquaporin-4 (AQP4)-dependent glymphatic drainage is crucial for Aβ clearance.
Astrocyte phenotypic plasticity and pathological decline dynamically modulate Aβ clearance capacity.

Conclusions:

Astrocytes play a significant, underexplored role in Aβ clearance.
Understanding astrocyte mechanisms provides a basis for astrocyte-targeted early AD interventions.
Targeting astrocyte functions offers a promising translational approach for AD therapy.