The calcium-magnesium-deficient rat: A study on the distribution of calcium in the spinal cord using the electron probe microanalyser

Nakagawa, Shiro; Yoshida, Sohei; Suematsu, Chiharu; Shimizu, Eiichi; Hirohata, Tajimi; Kumamoto, Tetsuzo; Yase, Yoshiro; Kawai, Ken‐ichi; Iwata, S.

doi:10.1007/bf01922343

Cited by 12 publications

(1 citation statement)

References 6 publications

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“…Kumamoto et al (1975) fed rats for 6 weeks on a diet that contained 0.4% of the normal Ca and 20% of the normal Mg. Kumamoto et al (1975) found increased Ca in spinal cord, kidney, and muscle tissues and decreased Ca in blood serum, cerebellum, liver and intestines. Nakagawa et al (1977) measured Ca levels in spinal cords of these rats by electron probe microanalysis and demonstrated a 6-fold rise in Ca in the Ca and Mg deficient rat spinal cords as well as a 6-fold elevation in number of motor neurons affected when compared with controls. Garruto et al (1989) fed 6 cynomolgus monkeys variations of a base diet containing one-third the normal amount of Ca.…”

Section: Alternate Hypotheses Of Causal Factors Related To Als/pdcmentioning

confidence: 99%

A critical review of the postulated role of the non-essential amino acid, β-N-methylamino-L-alanine, in neurodegenerative disease in humans

Chernoff

Hill

Diggs

et al. 2017

Journal of Toxicology and Environmental Health, Part B

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The compound BMAA (β-N-methylamino-L-alanine) has been postulated to play a significant role in four serious neurological human diseases: Amyotrophic Lateral Sclerosis/Parkinsonism Dementia Complex (ALS/PDC) found on Guam, and ALS, Parkinsonism, and dementia that occur globally. ALS/PDC with symptoms of all three diseases first came to the attention of the scientific community during and after World War II. It was initially associated with cycad flour used for food because BMAA is a product of symbiotic cycad root-dwelling cyanobacteria. Human consumption of flying foxes that fed on cycad seeds was later suggested as a source of BMAA on Guam and a cause of ALS/PDC. Subsequently, the hypothesis was expanded to include a causative role for BMAA in other neurodegenerative diseases including Alzheimer's disease (AD) through exposures attributed to proximity to freshwaters and/or consumption of seafood due to its purported production by most species of cyanobacteria. The hypothesis that BMAA is the critical factor in the genesis of these neurodegenerative diseases received considerable attention in the medical, scientific, and public arenas. This review examines the history of ALS/PDC and the BMAA-human disease hypotheses; similarities and differences between ALS/PDC and the other diseases with similar symptomologies; the relationship of ALS/PDC to other similar diseases, studies of BMAA-mediated effects in lab animals, inconsistencies and data gaps in the hypothesis; and other compounds and agents that were suggested as the cause of ALS/PDC on Guam. The review concludes that the hypothesis of a causal BMAA neurodegenerative disease relationship is not supported by existing data.

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Section: Alternate Hypotheses Of Causal Factors Related To Als/pdcmentioning

confidence: 99%

A critical review of the postulated role of the non-essential amino acid, β-N-methylamino-L-alanine, in neurodegenerative disease in humans

Chernoff

Hill

Diggs

et al. 2017

Journal of Toxicology and Environmental Health, Part B

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Amyotrophic leteral sclerosis: Part 2. Etiopathogenesis

Tandan

Bradley

1985

Annals of Neurology

139

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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.

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Disorders of the Anterior Horn Cell

Mitchell¹

1997

Spinal Cord Disease

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The calcium-magnesium-deficient rat: A study on the distribution of calcium in the spinal cord using the electron probe microanalyser

Abstract: Using the scanning electron probe X-ray microanalysis technique, calcium distribution in the spinal cord of the calcium-magnesium-deficient rat was studied. Calcium accumulations were observed within and around the perikaryon of certain unspecified motoneurons in the spinal cord.

Cited by 12 publications

References 6 publications

A critical review of the postulated role of the non-essential amino acid, β-N-methylamino-L-alanine, in neurodegenerative disease in humans

A critical review of the postulated role of the non-essential amino acid, β-N-methylamino-L-alanine, in neurodegenerative disease in humans

Amyotrophic leteral sclerosis: Part 2. Etiopathogenesis

Disorders of the Anterior Horn Cell

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