Risk of Alzheimer's disease with metal concentrations in whole blood and urine: A case–control study using propensity score matching

Yang, Yu‐Wan; Liou, Saou-Hsing; Hsueh, Yu Mei; Lyu, Wun-Sin; Liu, Chiu-Shong; Liu, Huei-Ju; Chung, Mu‐Chi; Hung, Peir-Haur; Chung, Chi Jung

doi:10.1016/j.taap.2018.07.015

Cited by 59 publications

(27 citation statements)

References 56 publications

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“…Hence, it is reasonable to suspect that, at least in areas where soil Se can be low, people consume locally produced foods, and suboptimal Se status consequently is common, Se intake will correlate inversely with risk for AD or cognitive decline. Some epidemiology from regions where soil Se is frequently low supports this view [91][92][93][94]. People with plasma Se below 100 ng/mL and intakes below 70 mcg daily are most likely to benefit from supplemental Se.…”

Section: Phase Two Induction and Support For Glutathione Synthesismentioning

confidence: 98%

A Fundamental Role for Oxidants and Intracellular Calcium Signals in Alzheimer’s Pathogenesis—And How a Comprehensive Antioxidant Strategy May Aid Prevention of This Disorder

McCarty

DiNicolantonio

Lerner

2021

IJMS

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Oxidative stress and increased cytoplasmic calcium are key mediators of the detrimental effects on neuronal function and survival in Alzheimer’s disease (AD). Pathways whereby these perturbations arise, and then prevent dendritic spine formation, promote tau hyperphosphorylation, further amplify amyloid β generation, and induce neuronal apoptosis, are described. A comprehensive program of nutraceutical supplementation, comprised of the NADPH oxidase inhibitor phycocyanobilin, phase two inducers, the mitochondrial antioxidant astaxanthin, and the glutathione precursor N-acetylcysteine, may have important potential for antagonizing the toxic effects of amyloid β on neurons and thereby aiding prevention of AD. Moreover, nutraceutical antioxidant strategies may oppose the adverse impact of amyloid β oligomers on astrocyte clearance of glutamate, and on the ability of brain capillaries to export amyloid β monomers/oligomers from the brain. Antioxidants, docosahexaenoic acid (DHA), and vitamin D, have potential for suppressing microglial production of interleukin-1β, which potentiates the neurotoxicity of amyloid β. Epidemiology suggests that a health-promoting lifestyle, incorporating a prudent diet, regular vigorous exercise, and other feasible measures, can cut the high risk for AD among the elderly by up to 60%. Conceivably, complementing such lifestyle measures with long-term adherence to the sort of nutraceutical regimen outlined here may drive down risk for AD even further.

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Section: Phase Two Induction and Support For Glutathione Synthesismentioning

confidence: 98%

A Fundamental Role for Oxidants and Intracellular Calcium Signals in Alzheimer’s Pathogenesis—And How a Comprehensive Antioxidant Strategy May Aid Prevention of This Disorder

McCarty

DiNicolantonio

Lerner

2021

IJMS

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“…In addition, in C57BL/6 J male mice treated with arsenite for 6 months, it was observed that arsenite induced ferroptotic cell death in neurons by the accumulation of reactive oxygen species and lipid peroxidation products, disruption of Fe 2+ homeostasis, depletion of glutathione and adenosine triphosphate, inhibition of system xc − , activation of mitogen-activated protein kinases and mitochondrial voltage-dependent anion channel pathways, and upregulation of endoplasmic reticulum stress [122]. This is an important issue because arsenite (inorganic arsenic) has been associated with neural loss and Alzheimer's and Parkinson's diseases as well as amyotrophic lateral sclerosis (ALS) [123][124][125][126][127][128][129][130]. An in vitro study showed that exposure to paraquat and maneb induced ferroptosis in dopaminergic SHSY5Y cells, associated with the activation of NADPH oxidase.…”

Section: Ferroptosis In Neurodegenerative Diseasesmentioning

confidence: 99%

Ferroptosis Mechanisms Involved in Neurodegenerative Diseases

Reichert

Freitas

Sampaio-Silva

et al. 2020

IJMS

252

148

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Ferroptosis is a type of cell death that was described less than a decade ago. It is caused by the excess of free intracellular iron that leads to lipid (hydro) peroxidation. Iron is essential as a redox metal in several physiological functions. The brain is one of the organs known to be affected by iron homeostatic balance disruption. Since the 1960s, increased concentration of iron in the central nervous system has been associated with oxidative stress, oxidation of proteins and lipids, and cell death. Here, we review the main mechanisms involved in the process of ferroptosis such as lipid peroxidation, glutathione peroxidase 4 enzyme activity, and iron metabolism. Moreover, the association of ferroptosis with the pathophysiology of some neurodegenerative diseases, namely Alzheimer’s, Parkinson’s, and Huntington’s diseases, has also been addressed.

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“…In contrast to the potential therapeutic effects of the chemicals mentioned above, arsenic was also identified in our chemical analysis. Arsenic is a chemical that has been documented to increase the risk of developing AD [120]. A study conducted on patients in Taiwan found that individuals living in locations with higher concentrations of arsenic, and a resultant increased urinary percent excretion of arsenic, were at a significantly higher risk of AD [120].…”

Section: Chemicalsmentioning

confidence: 99%

Key Disease Mechanisms Linked to Alzheimer’s Disease in the Entorhinal Cortex

Bottero

Powers

Yalamanchi

et al. 2021

IJMS

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Alzheimer’s disease (AD) is a chronic, neurodegenerative brain disorder affecting millions of Americans that is expected to increase in incidence with the expanding aging population. Symptomatic AD patients show cognitive decline and often develop neuropsychiatric symptoms due to the accumulation of insoluble proteins that produce plaques and tangles seen in the brain at autopsy. Unexpectedly, some clinically normal individuals also show AD pathology in the brain at autopsy (asymptomatic AD, AsymAD). In this study, SWItchMiner software was used to identify key switch genes in the brain’s entorhinal cortex that lead to the development of AD or disease resilience. Seventy-two switch genes were identified that are differentially expressed in AD patients compared to healthy controls. These genes are involved in inflammation, platelet activation, and phospholipase D and estrogen signaling. Peroxisome proliferator-activated receptor γ (PPARG), zinc-finger transcription factor (YY1), sterol regulatory element-binding transcription factor 2 (SREBF2), and early growth response 1 (EGR1) were identified as transcription factors that potentially regulate switch genes in AD. Comparing AD patients to AsymAD individuals revealed 51 switch genes; PPARG as a potential regulator of these genes, and platelet activation and phospholipase D as critical signaling pathways. Chemical–protein interaction analysis revealed that valproic acid is a therapeutic agent that could prevent AD from progressing.

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Risk of Alzheimer's disease with metal concentrations in whole blood and urine: A case–control study using propensity score matching

Cited by 59 publications

References 56 publications

A Fundamental Role for Oxidants and Intracellular Calcium Signals in Alzheimer’s Pathogenesis—And How a Comprehensive Antioxidant Strategy May Aid Prevention of This Disorder

A Fundamental Role for Oxidants and Intracellular Calcium Signals in Alzheimer’s Pathogenesis—And How a Comprehensive Antioxidant Strategy May Aid Prevention of This Disorder

Ferroptosis Mechanisms Involved in Neurodegenerative Diseases

Key Disease Mechanisms Linked to Alzheimer’s Disease in the Entorhinal Cortex

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