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Amyotrophic lateral sclerosis is a multifactorial disease

¹Neuromuscular Diseases Unit, Vancouver General Hospital, British Columbia, Canada.

|July 1, 1995

Summary

Amyotrophic lateral sclerosis (ALS) likely involves an initial trigger followed by a cascade of aging-related failures. This leads to neurodegeneration, with environmental factors and glutamate excitotoxicity potentially playing key roles.

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Area of Science:

Neuroscience
Pathology

Background:

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by progressive motor neuron loss.
The disease pathogenesis is thought to be biphasic, involving an initial trigger and a subsequent terminal cascade.

Purpose of the Study:

To explore the multifactorial pathogenic mechanisms underlying amyotrophic lateral sclerosis (ALS).
To investigate the role of aging, environmental factors, and specific cellular processes in ALS pathogenesis.

Main Methods:

The study presents a theoretical framework based on existing evidence and postulates mechanisms.
It discusses the potential involvement of aging, gene product accumulation, receptor integrity failure, excitotoxicity, and free radical damage.
The role of glutamate transporters, calcium binding proteins, corticomotoneurons, interneurons, and glia cells is considered.

Main Results:

Aging contributes to the accumulation of defective gene products, leading to cellular dysfunction.
Failure of receptor integrity, excitotoxicity, free radical accumulation, and impaired neurotrophism are implicated in the terminal cascade.
Environmental factors may act as cumulative triggers for ALS.

Conclusions:

The corticomotoneuron or its modulating interneurons are postulated as primary targets in ALS.
Glial cells may contribute to motor neuron demise.
Disordered corticomotoneurons may lead to excessive glutamate release, causing excitotoxicity and subsequent neuronal death.

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