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Alzheimer Disease ll: Pathophysiology

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Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and microglia. Abnormal...

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Stereotaxic Infusion of Oligomeric Amyloid-beta into the Mouse Hippocampus

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[Morpho-functional changes in the goldfish Mauthner neurons after beta-amyloid application].

N A Kokanova, G Z Mikhaĭlova, R Sh Shtanchaev

Morfologiia (Saint Petersburg, Russia)

|April 3, 2010

Summary

Beta-amyloid peptide disrupts goldfish motor control and Mauthner cell (MC) structure. This peptide causes motor asymmetry changes, suggesting MCs are key to understanding amyloidosis structural effects.

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Published on: March 16, 2016

Area of Science:

Neuroscience
Cell Biology
Biochemistry

Context:

Amyloidosis is a group of diseases characterized by the deposition of amyloid protein aggregates in various organs and tissues.
Beta-amyloid peptide is a key component of amyloid plaques found in the brains of Alzheimer's disease patients.
Mauthner cells (MCs) are large neurons in fish that control the startle response and are involved in motor control.

Purpose:

To investigate the impact of aggregated beta-amyloid peptide fragment 25-35 on the three-dimensional structure and volume of Mauthner cells (MCs).
To assess the effect of beta-amyloid on motor asymmetry in goldfish.
To explore the relationship between structural changes in MCs and motor behavior under beta-amyloid influence.

Summary:

Application of beta-amyloid peptide fragment 25-35 altered goldfish motor asymmetry, often inverting it and decoupling it from the structural asymmetry of Mauthner cells.
Structural changes in MCs included dystrophy or hypertrophy of individual neurons and dendrites, leading to altered proportions.
The study suggests that beta-amyloid's injurious effect on MCs may stem from mechanical deformation by amyloid fibrils, creating a structural discordance with motor behavior.

Impact:

Mauthner cells serve as a suitable model for studying the structural alterations associated with amyloidosis.
Findings provide insights into the neurobiological mechanisms underlying behavioral changes in amyloid-related disorders.
This research highlights the potential for mechanical forces exerted by amyloid fibrils to disrupt neuronal structure and function.