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Eye-Tracking Control to Assess Cognitive Functions in Patients with Amyotrophic Lateral Sclerosis

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Amyotrophic lateral sclerosis as a synaptopathy.

Matthew J Fogarty¹

¹Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, MN, USA; School of Biomedical Sciences, The University of Queensland, St. Lucia, Australia.

Neural Regeneration Research

|December 12, 2018

Summary

Amyotrophic lateral sclerosis (ALS) may stem from synaptic dysfunction, a synaptopathy. Research in rodent models examines synaptic changes in neurons, supporting this hypothesis and its consistency with other ALS mechanisms.

Keywords:

corticospinal dendrites dendritic spines excitotoxicity motor cortex motor neuron neuromuscular junction synaptic transmission

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Area of Science:

Neuroscience
Neurology
Cellular Biology

Background:

Synapses are crucial for neuronal communication, forming circuits that govern neural outputs.
Synaptic dysfunction, termed synaptopathy, is implicated in various neurological disorders.
Amyotrophic lateral sclerosis (ALS) is a potential synaptopathy affecting the neuromotor system.

Purpose of the Study:

To review synaptic observations in rodent models of ALS.
To provide a framework for evaluating the synaptopathy hypothesis in ALS.
To explore the link between synaptic dysfunction and other proposed ALS pathogenic mechanisms.

Main Methods:

Review of existing research on synaptic changes in rodent models of ALS.
Analysis of morphological and functional synaptic alterations in vulnerable neuronal populations.
Comparison of the synaptopathy hypothesis with other ALS pathogenesis theories.

Main Results:

Detailed synaptic dysfunctions observed in corticospinal and motor neurons in rodent models.
Consistency of synaptic dysfunction with glutamate excitotoxicity, protein aggregation, and mitochondrial issues.
Synaptopathy aligns with evidence of disease spread and prion-like propagation in ALS.

Conclusions:

The synaptopathy hypothesis offers a unifying framework for understanding ALS.
Further research into synaptic pathology is critical for ALS diagnosis and treatment.
Investigating synaptic changes across different neuronal populations and disease stages is warranted.