Environmental Health Economic Analysis Annotated Bibliography
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ReviewAuthors
Huat TJ, Camats-Perna J, Newcombe EA, Valmas N, Kitazawa M, Medeiros R
Journal
Journal of Molecular Biology
Summary
In this review article, the authors explore how essential and non-essential metals affect brain physiology and immunity, as well as their roles in the accumulation of toxic Alzheimer’s disease (AD) proteinaceous species (i.e., β-amyloid and tau). The authors reviewed studies that validate the disruption of immune-related pathways as an important mechanism of toxicity by which metals can contribute to AD. They explored research on iron, copper, zinc, manganese, lead, aluminum, and cadmium. Evidence strongly supports that disruption in the homeostasis of essential metals and the accumulation of non-essential metals disturb the cellular metabolism, antioxidant defense, and immune responses, leading to the onset and progression of AD.
Population
Not available
Health Outcomes
- Alzheimer's disease (AD)
Health Outcome List:
- Not available
Environmental Agents
List of Environmental Agents:
- Reviewed publications that examined metals (iron, copper, zinc, manganese, lead, aluminum, and cadmium)
Source of Environmental Agents:
- Anthropogenic activities
Economic Evaluation / Methods and Source
Type:
- Not available
Cost Measures:
- Not available
Potential Cost Measures:
- Not available
Benefits Measures:
- Not available
Potential Benefits Measures:
- Not available
Location:
- Not available
Models Used:
- Mouse model
Models References:
- Not available
Methods Used:
- The authors performed a review of existing literature to examine research related to 6 metals and their relation to brain physiology, immunity, and their roles in the accumulation of toxic AD proteinaceous species. Metals studied were iron, copper, zinc, manganese, lead, aluminum, and cadmium.
Sources Used:
- Mouse models (Xian-Hui et al., 2015. Kitazawa et al., 2009. Sparks et al., 2006. Sparks et al., 2003. Yu et a., 2015); United Nations, Department of Economic and Social Affairs, Population Division (2017); Lifestyle factors also affect an individual’s risk of developing AD (Livingston et al., 2017); Reduced levels of LRP-1 further impair the transcytotic clearance of Aβ and exacerbate neuroinflammation (Newcombe et al., 2018); Additional sources cited in the publication.
Economic Citation / Fundings
Citation:
- Huat TJ, Camats-Perna J, Newcombe EA, Valmas N, Kitazawa M, Medeiros R. Metal Toxicity Links to Alzheimer's Disease and Neuroinflammation. Journal of Molecular Biology. 2019. 431; 9.
- Pubmed
- DOI
NIEHS Funding:
- R01ES024331
Other Funding:
- Not available