Abundant expression of zinc transporters in the amyloid plaques of Alzheimer's disease brain
Abstract The pathological key features of Alzheimer's disease (AD) are β-amyloid peptide (Aβ)-containing senile plaques (SP) and neurofibrillary tangles. Previous studies have suggested that an extracellular elevation of the zinc concentration can initiate the deposition of Aβ and lead to the f...
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| Veröffentlicht in: | Brain research bulletin 2008-09, Vol.77 (1), p.55-60 |
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| creator | Zhang, Li-Hong Wang, Xin Stoltenberg, Meredin Danscher, Gorm Huang, Liping Wang, Zhan-You |
| description | Abstract The pathological key features of Alzheimer's disease (AD) are β-amyloid peptide (Aβ)-containing senile plaques (SP) and neurofibrillary tangles. Previous studies have suggested that an extracellular elevation of the zinc concentration can initiate the deposition of Aβ and lead to the formation of SP. In the present study, we present data showing a correlation between zinc ions, zinc transporters (ZNTs) and AD, using immersion autometallography (AMG) and double immunofluorescence for the ZNTs and Aβ. We found that all the ZNTs tested (ZNT1, 3, 4, 5, 6, 7) were extensively present in the Aβ-positive plaques in the cortex of human AD brains, and the density of autometallographic silver enhanced zinc–sulphur nanoparticles were much higher in the plaques than in the surrounding zinc enriched (ZEN) terminals. Moreover, we found an abundant expression of ZNT3 and autometallographic grains in the amyloid angiopathic vessels. The subcellular localization of ZNTs and zinc ions were not detected, due to the limited tissue preservation in the present study. In conclusion, our data provided significant morphological evidence of zinc ions and ZNTs being actively involved in the pathological processes that lead to plaque formation. |
| doi_str_mv | 10.1016/j.brainresbull.2008.03.014 |
| format | Article |
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Previous studies have suggested that an extracellular elevation of the zinc concentration can initiate the deposition of Aβ and lead to the formation of SP. In the present study, we present data showing a correlation between zinc ions, zinc transporters (ZNTs) and AD, using immersion autometallography (AMG) and double immunofluorescence for the ZNTs and Aβ. We found that all the ZNTs tested (ZNT1, 3, 4, 5, 6, 7) were extensively present in the Aβ-positive plaques in the cortex of human AD brains, and the density of autometallographic silver enhanced zinc–sulphur nanoparticles were much higher in the plaques than in the surrounding zinc enriched (ZEN) terminals. Moreover, we found an abundant expression of ZNT3 and autometallographic grains in the amyloid angiopathic vessels. The subcellular localization of ZNTs and zinc ions were not detected, due to the limited tissue preservation in the present study. In conclusion, our data provided significant morphological evidence of zinc ions and ZNTs being actively involved in the pathological processes that lead to plaque formation.</description><identifier>ISSN: 0361-9230</identifier><identifier>EISSN: 1873-2747</identifier><identifier>DOI: 10.1016/j.brainresbull.2008.03.014</identifier><identifier>PMID: 18639746</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Aged, 80 and over ; Alzheimer Disease - metabolism ; Alzheimer Disease - pathology ; Amyloid beta-Peptides - metabolism ; Autometallography ; Beta-amyloid peptide ; Brain - metabolism ; Brain - pathology ; Carrier Proteins - metabolism ; Cation Transport Proteins - metabolism ; Cerebral Cortex - metabolism ; Cerebral Cortex - pathology ; Female ; Fluorescent Antibody Technique ; Human brain ; Humans ; Immunofluorescence ; Male ; Microscopy, Fluorescence ; Neurology ; Plaque, Amyloid - metabolism ; Plaque, Amyloid - pathology ; Postmortem Changes ; Senile plaque ; Zinc - metabolism</subject><ispartof>Brain research bulletin, 2008-09, Vol.77 (1), p.55-60</ispartof><rights>Elsevier Inc.</rights><rights>2008 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c464t-4e8639bd3b400f792765d24b0f24ed01cd8b1cc8f04b92c3be67c87cb88211363</citedby><cites>FETCH-LOGICAL-c464t-4e8639bd3b400f792765d24b0f24ed01cd8b1cc8f04b92c3be67c87cb88211363</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.brainresbull.2008.03.014$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>315,782,786,3554,27933,27934,46004</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18639746$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Li-Hong</creatorcontrib><creatorcontrib>Wang, Xin</creatorcontrib><creatorcontrib>Stoltenberg, Meredin</creatorcontrib><creatorcontrib>Danscher, Gorm</creatorcontrib><creatorcontrib>Huang, Liping</creatorcontrib><creatorcontrib>Wang, Zhan-You</creatorcontrib><title>Abundant expression of zinc transporters in the amyloid plaques of Alzheimer's disease brain</title><title>Brain research bulletin</title><addtitle>Brain Res Bull</addtitle><description>Abstract The pathological key features of Alzheimer's disease (AD) are β-amyloid peptide (Aβ)-containing senile plaques (SP) and neurofibrillary tangles. Previous studies have suggested that an extracellular elevation of the zinc concentration can initiate the deposition of Aβ and lead to the formation of SP. In the present study, we present data showing a correlation between zinc ions, zinc transporters (ZNTs) and AD, using immersion autometallography (AMG) and double immunofluorescence for the ZNTs and Aβ. We found that all the ZNTs tested (ZNT1, 3, 4, 5, 6, 7) were extensively present in the Aβ-positive plaques in the cortex of human AD brains, and the density of autometallographic silver enhanced zinc–sulphur nanoparticles were much higher in the plaques than in the surrounding zinc enriched (ZEN) terminals. Moreover, we found an abundant expression of ZNT3 and autometallographic grains in the amyloid angiopathic vessels. The subcellular localization of ZNTs and zinc ions were not detected, due to the limited tissue preservation in the present study. In conclusion, our data provided significant morphological evidence of zinc ions and ZNTs being actively involved in the pathological processes that lead to plaque formation.</description><subject>Aged, 80 and over</subject><subject>Alzheimer Disease - metabolism</subject><subject>Alzheimer Disease - pathology</subject><subject>Amyloid beta-Peptides - metabolism</subject><subject>Autometallography</subject><subject>Beta-amyloid peptide</subject><subject>Brain - metabolism</subject><subject>Brain - pathology</subject><subject>Carrier Proteins - metabolism</subject><subject>Cation Transport Proteins - metabolism</subject><subject>Cerebral Cortex - metabolism</subject><subject>Cerebral Cortex - pathology</subject><subject>Female</subject><subject>Fluorescent Antibody Technique</subject><subject>Human brain</subject><subject>Humans</subject><subject>Immunofluorescence</subject><subject>Male</subject><subject>Microscopy, Fluorescence</subject><subject>Neurology</subject><subject>Plaque, Amyloid - metabolism</subject><subject>Plaque, Amyloid - pathology</subject><subject>Postmortem Changes</subject><subject>Senile plaque</subject><subject>Zinc - metabolism</subject><issn>0361-9230</issn><issn>1873-2747</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkkuP1DAQhCMEYoeFv4AsDnBKaD9iOxyQRstTWokDcEOybKej9ZA4wU4Qs7-ehBkJxAVOffm6ulTVRfGEQkWByueHyiUbYsLslr6vGICugFdAxZ1iR7XiJVNC3S12wCUtG8bhoniQ8wEApK7l_eKCaskbJeSu-LJ3S2xtnAn-mFbFHMZIxo7chujJnGzM05hmTJmESOYbJHY49mNoydTbbwvmjd33tzcYBkzPMmlDRpuR_HL4sLjX2T7jo_O8LD6_ef3p6l15_eHt-6v9demFFHMpcLPjWu4EQKcapmTdMuGgYwJboL7VjnqvOxCuYZ47lMpr5Z3WjFIu-WXx9KQ7pXEzNZshZI99byOOSzay4UzyWvwTpI1QNTR0BV-cQJ_GnBN2ZkphsOloKJitBHMwf5ZgthIMcLOWsC4_Pl9Z3IDt79Vz6ivw6gTgGsr3gMlkHzB6bENCP5t2DP935-VfMr4PMXjbf8Uj5sO4pLjGbqjJzID5uL3D9g2gAWjdKP4TSdu1Hw</recordid><startdate>20080905</startdate><enddate>20080905</enddate><creator>Zhang, Li-Hong</creator><creator>Wang, Xin</creator><creator>Stoltenberg, Meredin</creator><creator>Danscher, Gorm</creator><creator>Huang, Liping</creator><creator>Wang, Zhan-You</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>7X8</scope></search><sort><creationdate>20080905</creationdate><title>Abundant expression of zinc transporters in the amyloid plaques of Alzheimer's disease brain</title><author>Zhang, Li-Hong ; Wang, Xin ; Stoltenberg, Meredin ; Danscher, Gorm ; Huang, Liping ; Wang, Zhan-You</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c464t-4e8639bd3b400f792765d24b0f24ed01cd8b1cc8f04b92c3be67c87cb88211363</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Aged, 80 and over</topic><topic>Alzheimer Disease - metabolism</topic><topic>Alzheimer Disease - pathology</topic><topic>Amyloid beta-Peptides - metabolism</topic><topic>Autometallography</topic><topic>Beta-amyloid peptide</topic><topic>Brain - metabolism</topic><topic>Brain - pathology</topic><topic>Carrier Proteins - metabolism</topic><topic>Cation Transport Proteins - metabolism</topic><topic>Cerebral Cortex - metabolism</topic><topic>Cerebral Cortex - pathology</topic><topic>Female</topic><topic>Fluorescent Antibody Technique</topic><topic>Human brain</topic><topic>Humans</topic><topic>Immunofluorescence</topic><topic>Male</topic><topic>Microscopy, Fluorescence</topic><topic>Neurology</topic><topic>Plaque, Amyloid - metabolism</topic><topic>Plaque, Amyloid - pathology</topic><topic>Postmortem Changes</topic><topic>Senile plaque</topic><topic>Zinc - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Li-Hong</creatorcontrib><creatorcontrib>Wang, Xin</creatorcontrib><creatorcontrib>Stoltenberg, Meredin</creatorcontrib><creatorcontrib>Danscher, Gorm</creatorcontrib><creatorcontrib>Huang, Liping</creatorcontrib><creatorcontrib>Wang, Zhan-You</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Brain research bulletin</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Li-Hong</au><au>Wang, Xin</au><au>Stoltenberg, Meredin</au><au>Danscher, Gorm</au><au>Huang, Liping</au><au>Wang, Zhan-You</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Abundant expression of zinc transporters in the amyloid plaques of Alzheimer's disease brain</atitle><jtitle>Brain research bulletin</jtitle><addtitle>Brain Res Bull</addtitle><date>2008-09-05</date><risdate>2008</risdate><volume>77</volume><issue>1</issue><spage>55</spage><epage>60</epage><pages>55-60</pages><issn>0361-9230</issn><eissn>1873-2747</eissn><abstract>Abstract The pathological key features of Alzheimer's disease (AD) are β-amyloid peptide (Aβ)-containing senile plaques (SP) and neurofibrillary tangles. Previous studies have suggested that an extracellular elevation of the zinc concentration can initiate the deposition of Aβ and lead to the formation of SP. In the present study, we present data showing a correlation between zinc ions, zinc transporters (ZNTs) and AD, using immersion autometallography (AMG) and double immunofluorescence for the ZNTs and Aβ. We found that all the ZNTs tested (ZNT1, 3, 4, 5, 6, 7) were extensively present in the Aβ-positive plaques in the cortex of human AD brains, and the density of autometallographic silver enhanced zinc–sulphur nanoparticles were much higher in the plaques than in the surrounding zinc enriched (ZEN) terminals. Moreover, we found an abundant expression of ZNT3 and autometallographic grains in the amyloid angiopathic vessels. The subcellular localization of ZNTs and zinc ions were not detected, due to the limited tissue preservation in the present study. In conclusion, our data provided significant morphological evidence of zinc ions and ZNTs being actively involved in the pathological processes that lead to plaque formation.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>18639746</pmid><doi>10.1016/j.brainresbull.2008.03.014</doi><tpages>6</tpages></addata></record> |
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| subjects | Aged, 80 and over Alzheimer Disease - metabolism Alzheimer Disease - pathology Amyloid beta-Peptides - metabolism Autometallography Beta-amyloid peptide Brain - metabolism Brain - pathology Carrier Proteins - metabolism Cation Transport Proteins - metabolism Cerebral Cortex - metabolism Cerebral Cortex - pathology Female Fluorescent Antibody Technique Human brain Humans Immunofluorescence Male Microscopy, Fluorescence Neurology Plaque, Amyloid - metabolism Plaque, Amyloid - pathology Postmortem Changes Senile plaque Zinc - metabolism |
| title | Abundant expression of zinc transporters in the amyloid plaques of Alzheimer's disease brain |
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