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Related Experiment Video

Updated: Mar 3, 2026

Real-Time Fluorescent Measurement of Synaptic Functions in Models of Amyotrophic Lateral Sclerosis

Real-Time Fluorescent Measurement of Synaptic Functions in Models of Amyotrophic Lateral Sclerosis

Published on: July 16, 2021

Modelling amyotrophic lateral sclerosis: progress and possibilities.

Philip Van Damme^1,2,3, Wim Robberecht^1,3, Ludo Van Den Bosch^4,2

¹KU Leuven, University of Leuven, Department of Neurosciences, Experimental Neurology, and Leuven Research Institute for Neuroscience and Disease (LIND), B-3000 Leuven, Belgium.

Disease Models & Mechanisms

|May 5, 2017

Summary

This summary is machine-generated.

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease affecting motor neurons. Research into ALS genetics and diverse model systems is crucial for understanding disease mechanisms and developing effective treatments.

Keywords:

C. elegans Fruit fly Motor neuron Neurodegeneration Zebrafish iPSCs

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ALS - Motor Neuron Disease: Mechanism and Development of New Therapies

ALS - Motor Neuron Disease: Mechanism and Development of New Therapies

Published on: July 29, 2007

Area of Science:

Neuroscience
Genetics
Cell Biology

Background:

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder characterized by progressive muscle weakness and typically a short survival time.
ALS affects approximately 90% of patients sporadically, with familial cases accounting for the remaining 10%.
Significant advancements in understanding ALS genetics have identified around 20 associated genes, including SOD1, TARDBP, FUS, and C9orf72.

Purpose of the Study:

To review various model systems utilized in ALS research.
To discuss the contributions of these models to understanding ALS disease mechanisms.
To highlight the heterogeneity of molecular pathways implicated in ALS pathogenesis.

Main Methods:

Literature review of existing research on ALS models.
Analysis of genetic associations and neuropathological findings in ALS.
Synthesis of data from diverse model systems to elucidate cellular and molecular mechanisms.

Main Results:

Model systems have revealed heterogeneous molecular pathways in ALS, including protein aggregation and cellular process defects.
Dysfunction in non-neuronal cells also plays a role in ALS pathogenesis.
Understanding genetic mutations and sporadic ALS mechanisms is advancing.

Conclusions:

Model systems are instrumental in advancing our knowledge of ALS.
Further research into emerging disease pathways and genetic factors is essential.
Accelerated progress in developing novel ALS treatments is anticipated with improved understanding.