Patterns of Acquiring Parkinsonism-Dementia Complex on Guam

Zhang, Zhenxin; Anderson, Dallas W.; Lavine, Lawrence; Mantel, Nathan

doi:10.1001/archneur.1990.00530090097019

Cited by 28 publications

(14 citation statements)

References 17 publications

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“…The incidence of PDC peaked in 1960-1964 for males and in 1975-1979 for females, and decreased more gradually than the incidence of ALS. Incidence of PDC was notably higher in 1980-1989 than some previous reports have indicated [4,5,26], but was similar to figures reported by the 15-year cohort study for the period 1968-1983 [27] and the recent follow-up by Plato et al [23]. A major reason for the discrepancy in the incidence of ALS and PDC for the more recent period stems from the fact that the 1980 census data were not available.…”

Section: Discussionsupporting

confidence: 75%

Incidence of Amyotrophic Lateral Sclerosis and of the Parkinsonism-Dementia Complex of Guam, 1950–1989

et al. 2004

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Studies representing the accumulated information from the first 30 years of research effort on Guam (1950–1979) have demonstrated a varying degree of decline in the incidence of amyotrophic lateral sclerosis (ALS) and the parkinsonism-dementia complex (PDC) of Guam. Analysis with more complete information for the period 1980–1989 provides more valid estimates of the later patterns in the incidence of ALS and PDC and affords a more extensive assessment of trends over a 40-year period. The annual age-adjusted incidence of ALS was 7/100,000 and the annual age-adjusted incidence of PDC was 22/100,000 in 1989. The incidence was much higher for the period 1980–1989 than suggested in previous reports. These findings provide compelling evidence that this spectrum of neurodegenerative diseases continues to have a significant impact on the health of the Chamorro people of Guam.

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Section: Discussionsupporting

confidence: 75%

Incidence of Amyotrophic Lateral Sclerosis and of the Parkinsonism-Dementia Complex of Guam, 1950–1989

et al. 2004

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“…Silent toxicity may be compared to the process of carcinogenesis, in which molecular and cellular damage occurs years if not decades before any clinical manifestation of the disease [111]. In case of neurotoxicity, an example of silent toxicity is represented by the Parkinsonism-dementia known as Guam's disease, in which latencies of decades have been reported before alleged still undefined exposures and clinical signs [112]. Similarly, bovine spongiform encephalopathy (mad cow disease), a variant of Creutzfeld-Jacob disease, has been shown to have a latency of decades [113].…”

Section: Silent Neurotoxicity Indirect Neurotoxicity and Long-tementioning

confidence: 99%

Developmental Neurotoxicity: Some Old and New Issues

Giordano

Costa

2012

ISRN Toxicology

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The developing central nervous system is often more vulnerable to injury than the adult one. Of the almost 200 chemicals known to be neurotoxic, many are developmental neurotoxicants. Exposure to these compoundsin uteroor during childhood can contribute to a variety of neurodevelopmental and neurological disorders. Two established developmental neurotoxicants, methylmercury and lead, and two classes of chemicals, the polybrominated diphenyl ether flame retardants and the organophosphorus insecticides, which are emerging as potential developmental neurotoxicants, are discussed in this paper. Developmental neurotoxicants may also cause silent damage, which would manifest itself only as the individual ages, and may contribute to neurodegenerative diseases such as Parkinson’s or Alzheimer’s diseases. Guidelines for developmental neurotoxicity testing have been implemented, but there is still room for their improvement and for searching and validating alternative testing approaches.

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“…There are several examples of how the concept of silent toxicity may apply to the nervous system. In case of the Parkinsonism-dementia known as Guam's disease, latencies of decades have been reported between alleged exposure to still-undefined substances and clinical signs (180). More recently, bovine spongiform encephalopathy (mad cow disease), a prion disease associated in humans to a variant of Creutzfeld-Jakob disease, has been shown to have an incubation period (latency) of decades (181).…”

Section: The Issue Of "Silent" Neurotoxicitymentioning

confidence: 99%

Developmental Neuropathology of Environmental Agents

Costa

Aschner

Vitalone

et al. 2004

Annu. Rev. Pharmacol. Toxicol.

316

168

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The developing central nervous system (CNS) is more vulnerable to injury than the adult one. Although a great deal of research has been devoted to subtle effects of developmental exposure, such as neurobehavioral changes, this review instead focuses on a number of chemicals that have been shown, in several experimental models as well as humans, to cause morphological changes in the developing nervous system. Chemicals that are discussed include methylmercury (MeHg), lead (Pb), antiepileptic drugs, and ethanol. Additionally, the issue of silent neurotoxicity, i.e., persistent morphological and/or biochemical injury that remains clinically unapparent until later in life, is discussed.

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Patterns of Acquiring Parkinsonism-Dementia Complex on Guam

Cited by 28 publications

References 17 publications

Incidence of Amyotrophic Lateral Sclerosis and of the Parkinsonism-Dementia Complex of Guam, 1950–1989

Incidence of Amyotrophic Lateral Sclerosis and of the Parkinsonism-Dementia Complex of Guam, 1950–1989

Developmental Neurotoxicity: Some Old and New Issues

Developmental Neuropathology of Environmental Agents

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