Elevated cortical zinc in Alzheimer disease. Religa, D., Strozyk, D., Cherny, R. A., Volitakis, I., Haroutunian, V., Winblad, B., Naslund, J., & Bush, A. I. Neurology, 67(1):69–75, July, 2006. ![Elevated cortical zinc in Alzheimer disease [link]](https://bibbase.org/img/filetypes/link.svg "link")
Paper doi abstract bibtex Objective: To determine whether changes in brain biometals in Alzheimer disease (AD) and in normal brain tissue are tandemly associated with amyloid β-peptide (Aβ) burden and dementia severity. Methods: The authors measured zinc, copper, iron, manganese, and aluminum and Aβ levels in postmortem neocortical tissue from patients with AD (n = 10), normal age-matched control subjects (n = 14), patients with schizophrenia (n = 26), and patients with schizophrenia with amyloid (n = 8). Severity of cognitive impairment was assessed with the Clinical Dementia Rating Scale (CDR). Results: There was a significant, more than twofold, increase of tissue zinc in the AD-affected cortex compared with the other groups. Zinc levels increased with tissue amyloid levels. Zinc levels were significantly elevated in the most severely demented cases (CDR 4 to 5) and in cases that had an amyloid burden greater than 8 plaques/mm2. Levels of other metals did not differ between groups. Conclusions: Brain zinc accumulation is a prominent feature of advanced Alzheimer disease (AD) and is biochemically linked to brain amyloid β-peptide accumulation and dementia severity in AD.
@article{religa_elevated_2006,
title = {Elevated cortical zinc in {Alzheimer} disease},
volume = {67},
issn = {0028-3878, 1526-632X},
url = {http://www.neurology.org/content/67/1/69},
doi = {10.1212/01.wnl.0000223644.08653.b5},
abstract = {Objective: To determine whether changes in brain biometals in Alzheimer disease (AD) and in normal brain tissue are tandemly associated with amyloid β-peptide (Aβ) burden and dementia severity.
Methods: The authors measured zinc, copper, iron, manganese, and aluminum and Aβ levels in postmortem neocortical tissue from patients with AD (n = 10), normal age-matched control subjects (n = 14), patients with schizophrenia (n = 26), and patients with schizophrenia with amyloid (n = 8). Severity of cognitive impairment was assessed with the Clinical Dementia Rating Scale (CDR).
Results: There was a significant, more than twofold, increase of tissue zinc in the AD-affected cortex compared with the other groups. Zinc levels increased with tissue amyloid levels. Zinc levels were significantly elevated in the most severely demented cases (CDR 4 to 5) and in cases that had an amyloid burden greater than 8 plaques/mm2. Levels of other metals did not differ between groups.
Conclusions: Brain zinc accumulation is a prominent feature of advanced Alzheimer disease (AD) and is biochemically linked to brain amyloid β-peptide accumulation and dementia severity in AD.},
language = {en},
number = {1},
urldate = {2016-11-21TZ},
journal = {Neurology},
author = {Religa, D. and Strozyk, D. and Cherny, R. A. and Volitakis, I. and Haroutunian, V. and Winblad, B. and Naslund, J. and Bush, A. I.},
month = jul,
year = {2006},
pages = {69--75}
}
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Methods: The authors measured zinc, copper, iron, manganese, and aluminum and Aβ levels in postmortem neocortical tissue from patients with AD (n = 10), normal age-matched control subjects (n = 14), patients with schizophrenia (n = 26), and patients with schizophrenia with amyloid (n = 8). Severity of cognitive impairment was assessed with the Clinical Dementia Rating Scale (CDR). Results: There was a significant, more than twofold, increase of tissue zinc in the AD-affected cortex compared with the other groups. Zinc levels increased with tissue amyloid levels. Zinc levels were significantly elevated in the most severely demented cases (CDR 4 to 5) and in cases that had an amyloid burden greater than 8 plaques/mm2. Levels of other metals did not differ between groups. Conclusions: Brain zinc accumulation is a prominent feature of advanced Alzheimer disease (AD) and is biochemically linked to brain amyloid β-peptide accumulation and dementia severity in AD.","language":"en","number":"1","urldate":"2016-11-21TZ","journal":"Neurology","author":[{"propositions":[],"lastnames":["Religa"],"firstnames":["D."],"suffixes":[]},{"propositions":[],"lastnames":["Strozyk"],"firstnames":["D."],"suffixes":[]},{"propositions":[],"lastnames":["Cherny"],"firstnames":["R.","A."],"suffixes":[]},{"propositions":[],"lastnames":["Volitakis"],"firstnames":["I."],"suffixes":[]},{"propositions":[],"lastnames":["Haroutunian"],"firstnames":["V."],"suffixes":[]},{"propositions":[],"lastnames":["Winblad"],"firstnames":["B."],"suffixes":[]},{"propositions":[],"lastnames":["Naslund"],"firstnames":["J."],"suffixes":[]},{"propositions":[],"lastnames":["Bush"],"firstnames":["A.","I."],"suffixes":[]}],"month":"July","year":"2006","pages":"69–75","bibtex":"@article{religa_elevated_2006,\n\ttitle = {Elevated cortical zinc in {Alzheimer} disease},\n\tvolume = {67},\n\tissn = {0028-3878, 1526-632X},\n\turl = {http://www.neurology.org/content/67/1/69},\n\tdoi = {10.1212/01.wnl.0000223644.08653.b5},\n\tabstract = {Objective: To determine whether changes in brain biometals in Alzheimer disease (AD) and in normal brain tissue are tandemly associated with amyloid β-peptide (Aβ) burden and dementia severity.\nMethods: The authors measured zinc, copper, iron, manganese, and aluminum and Aβ levels in postmortem neocortical tissue from patients with AD (n = 10), normal age-matched control subjects (n = 14), patients with schizophrenia (n = 26), and patients with schizophrenia with amyloid (n = 8). Severity of cognitive impairment was assessed with the Clinical Dementia Rating Scale (CDR).\nResults: There was a significant, more than twofold, increase of tissue zinc in the AD-affected cortex compared with the other groups. Zinc levels increased with tissue amyloid levels. Zinc levels were significantly elevated in the most severely demented cases (CDR 4 to 5) and in cases that had an amyloid burden greater than 8 plaques/mm2. Levels of other metals did not differ between groups.\nConclusions: Brain zinc accumulation is a prominent feature of advanced Alzheimer disease (AD) and is biochemically linked to brain amyloid β-peptide accumulation and dementia severity in AD.},\n\tlanguage = {en},\n\tnumber = {1},\n\turldate = {2016-11-21TZ},\n\tjournal = {Neurology},\n\tauthor = {Religa, D. and Strozyk, D. and Cherny, R. A. and Volitakis, I. and Haroutunian, V. and Winblad, B. and Naslund, J. and Bush, A. 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