Amyotrophic lateral sclerosis

Part 2. Etiopathogenesis

R. Tandan, Walter G Bradley

Research output: Contribution to journalArticle

129 Citations (Scopus)

Abstract

The pathogenesis of the motor neuronal degeneration in amyotrophic lateral sclerosis (ALS) is unclear, though several possible etiological factors are currently being investigated. A unifying hypothesis will have to explain the diverse geographical occurrence, clinical features, and selective vulnerability and relative resistance of different neuronal populations in the disease. It is possible that different biochemical defects underlie this diversity, or alternatively that the many factors incriminated in the etiology may act upon an underlying genetic-biochemical abnormality to trigger premature neuronal death. Viruses, metals, endogenous toxins, immune dysfunction, endocrine abnormalities, impaired DNA repair, altered axonal transport, and trauma have all been etiologically linked with ALS, but convincing research evidence of a causative role for any of these factors is yet to be demonstrated.

Original languageEnglish
Pages (from-to)419-431
Number of pages13
JournalAnnals of Neurology
Volume18
Issue number4
StatePublished - Dec 1 1985
Externally publishedYes

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Amyotrophic Lateral Sclerosis
Axonal Transport
Premature Mortality
DNA Repair
Molecular Biology
Metals
Viruses
Wounds and Injuries
Research
Population

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Amyotrophic lateral sclerosis : Part 2. Etiopathogenesis. / Tandan, R.; Bradley, Walter G.

In: Annals of Neurology, Vol. 18, No. 4, 01.12.1985, p. 419-431.

Research output: Contribution to journalArticle

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