Serum zinc, senile plaques, and neurofibrillary tangles

Tully, Christine L.; Snowdon, David A.; Markesbery, William R.

doi:10.1097/00001756-199511000-00002

Cited by 42 publications

(17 citation statements)

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“…In serum by contrast, the literature generally reported either no change (Dong et al 2008;Gerhardsson et al 2008;Gonzalez et al 1999;Ozcankaya and Delibas 2002) or a decrease (this study) in AD compared to controls. This contrast was supported by a report of a significant negative correlation between amyloid plaque numbers and serum zinc concentration in AD (Tully et al 1995). Brain zinc levels positively correlated with levels of Ab peptide (which forms amyloid plaques), plaque numbers, and dementia severity in AD (Religa et al 2006).…”

Section: Discussionmentioning

confidence: 59%

Serum zinc is decreased in Alzheimer’s disease and serum arsenic correlates positively with cognitive ability

et al. 2009

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Zinc, copper, and iron aggregate Abeta and accumulate in Alzheimer's disease (AD) plaques. Some metals are increased in AD vs. control serum. The authors examined levels of 12 metals in serum of 44 AD and 41 control subjects. Zinc decreased from 12.3 to 10.9 micromol/L (means, p = 0.0007). Arsenic positively correlated with Mini-Mental State Examination score (p < 0.0001). Zinc deposition in brain amyloid might deplete zinc from other body compartments, such as serum. The arsenic correlation might be caused by the major contribution of seafood consumption to intake of both arsenic and docosahexaenoic acid, of which the latter may delay AD.

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Section: Discussionmentioning

confidence: 59%

Serum zinc is decreased in Alzheimer’s disease and serum arsenic correlates positively with cognitive ability

et al. 2009

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“…We first evaluated data from the UK ADC (12) and the Nun Study (23, 25) to compare counts of NFTs and NPs from individual cases (Fig. 1).…”

Section: Resultsmentioning

confidence: 99%

“…All clinical diagnoses were documented by the clinicians at a consensus conference that included neurologists, neuropsychologists, and social workers. The Nun study of the School Sisters of Notre Dame in the United States is a longitudinal study of 493 participants ranging in ages from 75 to 102 years (mean = 83 years) and has been described elsewhere (22, 23). Neuropathologic evaluations were conducted by a single blinded neuropathologist (W.R.M.)…”

Section: Methodsmentioning

confidence: 99%

Brains With Medial Temporal Lobe Neurofibrillary Tangles But No Neuritic Amyloid Plaques Are a Diagnostic Dilemma But May Have Pathogenetic Aspects Distinct From Alzheimer Disease

Nelson¹,

Abner²,

Schmitt³

et al. 2009

J Neuropathol Exp Neurol

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Brains that have many neurofibrillary tangles (NFTs) in medial temporal lobe structures (Braak Stages III or IV) but no cortical neuritic plaques (NPs) may be a diagnostic dilemma; they also raise questions about the "amyloid cascade hypothesis" of Alzheimer disease (AD) in which NFT development is thought to occur downstream of the development of amyloid plaques. To determine the clinical, demographic, and biological factors related to NFT+/NP− cases, we analyzed 26 NFT +/NP− patient brains identified from the University of Kentucky AD Center autopsy cohort (n = 502); most of these patients were at least 85 years old and lacked profound antemortem cognitive impairment. A subset of the cases had neurofibrillary tangles in the medulla oblongata. Aberrant TAR-DNA binding protein-43 immunohistochemical staining was seen in 5 of the 26 cases with the clinical diagnoses of AD or mild cognitive impairment. We also queried cases in the National Alzheimer's Coordinating Center Registry (n = 5,108) and found 219 NFT+/NP− cases. Those patients had a relatively high likelihood of belonging to a birth cohort with the highest incidence of influenza infection during the 1918-1919 pandemic. This observation may link the pathogenesis in NFT+/NP− cases to encephalitis during childhood. We conclude that NFT+/NP-cases comprise approximately 5% of aged individuals in multiple data sets; these cases are not necessarily within the spectrum of AD.

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“…Changes reported in Alzheimer's disease include decreased temporal lobe zinc concentrations [11], elevated cerebrospinal fluid zinc and copper concentrations [12,13], increased hepatic zinc with decreased zinc bound to metallothionein [14], and decreased concentrations of astrocytic growth inhibitory factor, a metallothionein-like protein that chelates zinc [15]. In a group of nuns who received no supplemental zinc, serum zinc concentrations were found to have moderate to strong negative correlations with senile plaque and neurofibrillary tangle counts in each of seven brain regions [16]. Burnet [17] has hypothesized that many of the neurologic symptoms associated with dementia are caused by a lack of zinc and consequent impairment of metalloenzymes associated with DNA and RNA metabolism.…”

Section: Introductionmentioning

confidence: 99%

Effect of dietary zinc and copper on ?-Amyloid precursor protein expression in the rat brain

Davis

1997

J. Trace Elem. Exp. Med.

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The β‐amyloid precursor protein (APP) is the source of the amyloid β‐peptide that accumulates in the brain in Alzheimer's disease. Recently, APP has been shown to bind zinc and copper, and this binding has been suggested to control APP conformation and stability. In vitro studies show that zinc ions cause β‐amyloid protein to form plaques resembling the amyloid plaques found in the brains of patients with Alzheimer's disease. This suggests a role for zinc and/or copper in the neuropathogenesis of Alzheimer's disease. Male Sprague‐Dawley rats (100 ± 10 g) were fed diets containing 5, 35, or 350 μg zinc/g diet, and 1.5, 3 or 6 μg copper/g diet for 6 weeks. Brain APP expression was determined by using Western blots. Proteins were separated on 8.5% SDS‐PAGE, and the APP immunoreactive species were detected by using anti‐Alzheimer precursor protein A4 clone 22C11. Alterations in dietary zinc and copper significantly (P < 0.05) affected ceruloplasmin, red blood cell and extracellular superoxide dismutase activities, and tissue mineral concentrations. Although brain zinc concentrations were 13% lower (P < 0.005) in animals fed low dietary zinc than in animals fed high dietary zinc, and brain copper concentrations were 11% lower (P < 0.0001) in animals fed low dietary copper than in animals fed high dietary copper, there were no significant differences in the expression of APP among the different dietary treatments. Therefore, it seems that dietary zinc and copper do not affect APP expression in the rat brain. J. Trace Elem. Exp. Med. 10:249–258, 1997. © 1997 Wiley‐Liss, Inc. This article is a US Government work and, as such, is in the public domain in the United States of America.

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Serum zinc, senile plaques, and neurofibrillary tangles

Cited by 42 publications

References 0 publications

Serum zinc is decreased in Alzheimer’s disease and serum arsenic correlates positively with cognitive ability

Serum zinc is decreased in Alzheimer’s disease and serum arsenic correlates positively with cognitive ability

Brains With Medial Temporal Lobe Neurofibrillary Tangles But No Neuritic Amyloid Plaques Are a Diagnostic Dilemma But May Have Pathogenetic Aspects Distinct From Alzheimer Disease

Effect of dietary zinc and copper on ?-Amyloid precursor protein expression in the rat brain

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