500 Aggregations of amyloid beta-proteins in the presence of metal ions

Yano, Koji; Hirosawa, Nobue; Sakamoto, Youichi; Katayama, Hiroki; Moriguchi, Takeshi

doi:10.1016/s0378-4274(03)90499-1

Cited by 17 publications

(17 citation statements)

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“…The mechanism underlying the association between Cd concentration and AD has not been elucidated. However, growing evidence indicates that Cd plays a role in the accumulation of A␤ plaques and tau protein [50], which is the main pathological feature of AD [51]. Jiang et al reported the impact of Cd on the formation of neurofibrillary tangles [52].…”

Section: Discussionmentioning

confidence: 99%

Circulatory Levels of Toxic Metals (Aluminum, Cadmium, Mercury, Lead) in Patients with Alzheimer’s Disease: A Quantitative Meta-Analysis and Systematic Review

Zhang

Liu

et al. 2018

JAD

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Section: Discussionmentioning

confidence: 99%

Circulatory Levels of Toxic Metals (Aluminum, Cadmium, Mercury, Lead) in Patients with Alzheimer’s Disease: A Quantitative Meta-Analysis and Systematic Review

Zhang

Liu

et al. 2018

JAD

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“…Although AD pathogenesis is multifactorial and complex, studies suggest that toxic metals may represent a possible cause of AD [ 21 – 23 ]. There is growing evidence that cadmium plays a role in the accumulation of Aβ plaques and tau protein [ 24 – 26 ], as the main pathological components of AD [ 1 , 2 ]. Syme and Viles (2006) found that Cd(II) caused the 1H NMR chemical shift of the Val12 γCH3 protons in Aβ (1–16) that is similar to that observed for Zn(II), which is known to be an important inducer of amyloid production [ 25 , 27 ].…”

Section: Discussionmentioning

confidence: 99%

Blood cadmium levels and Alzheimer’s disease mortality risk in older US adults

Min

2016

Environ Health

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BackgroundCadmium, a ubiquitous environmental pollutant, exhibits potential neurotoxic risk. Although compelling evidence suggests cadmium accumulation has a role in the formation of amyloid-β plaques and neurofibrillary tangles, which are the hallmarks of Alzheimer's disease (AD) pathogenesis, the supporting evidence in humans is limited and conflicting. In this study, we investigated the association between blood cadmium levels and AD mortality among older adults by analyzing the prospective data from the 1999–2004 Third National Health and Nutrition Examination Survey (NHANES) and the Linked Mortality File.MethodsThe data were obtained from the 1999–2004 NHANES and the NHANES (1999–2004) Linked Mortality File. A total of 4,064 participants aged ≥60 years old with available blood cadmium data and no other missing information on their questionnaires at baseline were included in this study. AD was denoted as G30 based on the ICD-10 underlying causes of death.ResultsOf the 4,064 participants, 51 subjects died as a result of AD. Compared with participants with low blood cadmium levels (≤0.3 μg/L), those with high cadmium levels (>0.6 μg/L) exhibited a 3.83-fold (hazard ratio = 3.83; 95 % CI = 1.39–10.59) increased risk of AD mortality. In the Kaplan–Meier survival curves for cumulative AD mortality, higher levels of blood cadmium showed marginally significant association with increased mortality at baseline and in patients over 60 years of age (p = 0.0684).ConclusionsWe observed a significant association between blood cadmium levels and AD mortality among older adults in the US. Our findings suggest that environmental exposure to cadmium may be a risk factor for AD.

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“…The chemical mechanisms of neurotoxicity are several: Hg(II) binds to soft Lewis base amino acids cysteine and methionine in various proteins, notably tubulin, the structural protein component of microtubules in the cytoskeleton that are produced by tau protein, thereby inhibiting binding of guanosine triphosphate (GTP) , and ADP ribolyzation of tubulin, both required for normal microtubule formation and hence cytoskeleton integrity, thus leading to cell degeneration . Such a cascade would also cause tau hyperphosphorylation and neurofibrillar tangles as a consequence of heavy metal exposure to the CNS, which is indeed observed upon Hg exposure, − in concurrence with increased Aβ secretion, Hg-induced Aβ aggregation, tubulin dysfunction, and apoptosis …”

Section: Exogenous Metal Exposure and Alzheimer’s Diseasementioning

confidence: 99%