The Pathogenic Aβ43 Is Enriched in Familial and Sporadic Alzheimer Disease
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{"title"=>"The Pathogenic Aβ43 Is Enriched in Familial and Sporadic Alzheimer Disease", "type"=>"journal", "authors"=>[{"first_name"=>"Anna", "last_name"=>"Sandebring", "scopus_author_id"=>"26640710800"}, {"first_name"=>"Hedvig", "last_name"=>"Welander", "scopus_author_id"=>"16647721400"}, {"first_name"=>"Bengt", "last_name"=>"Winblad", "scopus_author_id"=>"36048831500"}, {"first_name"=>"Caroline", "last_name"=>"Graff", "scopus_author_id"=>"57200995035"}, {"first_name"=>"Lars O.", "last_name"=>"Tjernberg", "scopus_author_id"=>"6701503248"}], "year"=>2013, "source"=>"PLoS ONE", "identifiers"=>{"issn"=>"19326203", "scopus"=>"2-s2.0-84873728856", "pui"=>"368331365", "doi"=>"10.1371/journal.pone.0055847", "isbn"=>"1932-6203 (Electronic)\\r1932-6203 (Linking)", "sgr"=>"84873728856", "pmid"=>"23409063"}, "id"=>"2cd311c6-d1bc-3f80-bc6b-eb729178a12d", "abstract"=>"The amyloid-cascade hypothesis posits that the role of amyloid β-peptide (Aβ) in Alzheimer disease (AD) involves polymerization into structures that eventually are deposited as amyloid plaques. During this process, neurotoxic oligomers are formed that induce synaptic loss and neuronal death. Several different isoforms of Aβ are produced, of which the 40 and 42 residue variants (Aβ40 and Aβ42) are the most common. Aβ42 has a strong tendency to form neurotoxic aggregates and is involved in AD pathogenesis. Longer Aβ isoforms, like the less studied Aβ43, are gaining attention for their higher propensity to aggregate into neurotoxic oligomers. To further investigate Aβ43 in AD, we conducted a quantitative study on Aβ43 levels in human brain. We homogenized human brain tissue and prepared fractions of various solubility; tris buffered saline (TBS), sodium dodecyl sulfate (SDS) and formic acid (FA). Levels of Aβ43, as well as Aβ40 and Aβ42, were quantified using ELISA. We compared quantitative data showing Aβ levels in occipital and frontal cortex from sporadic (SAD) and familial (FAD) AD cases, as well as non-demented (ND) controls. Results showed Aβ43 present in each fraction from the SAD and FAD cases, while its level was lower than the detection limit in the majority of the ND-cases. Aβ42 and Aβ43 were enriched in the less soluble fractions (SDS and FA) of SAD and FAD cases in both occipital and frontal cortex. Thus, although the total levels of Aβ43 in human brain are low compared to Aβ40 and Aβ42, we suggest that Aβ43 could initiate the formation of oligomers and amyloid plaques and thereby be crucial to AD pathogenesis.", "link"=>"http://www.mendeley.com/research/pathogenic-a%CE%B243-enriched-familial-sporadic-alzheimer-disease", "reader_count"=>37, "reader_count_by_academic_status"=>{"Unspecified"=>2, "Professor > Associate Professor"=>2, "Researcher"=>8, "Student > Ph. D. Student"=>9, "Student > Postgraduate"=>1, "Student > Master"=>3, "Other"=>2, "Student > Bachelor"=>10}, "reader_count_by_user_role"=>{"Unspecified"=>2, "Professor > Associate Professor"=>2, "Researcher"=>8, "Student > Ph. D. Student"=>9, "Student > Postgraduate"=>1, "Student > Master"=>3, "Other"=>2, "Student > Bachelor"=>10}, "reader_count_by_subject_area"=>{"Unspecified"=>5, "Biochemistry, Genetics and Molecular Biology"=>4, "Agricultural and Biological Sciences"=>15, "Medicine and Dentistry"=>6, "Neuroscience"=>5, "Psychology"=>1, "Chemistry"=>1}, "reader_count_by_subdiscipline"=>{"Medicine and Dentistry"=>{"Medicine and Dentistry"=>6}, "Neuroscience"=>{"Neuroscience"=>5}, "Chemistry"=>{"Chemistry"=>1}, "Psychology"=>{"Psychology"=>1}, "Agricultural and Biological Sciences"=>{"Agricultural and Biological Sciences"=>15}, "Biochemistry, Genetics and Molecular Biology"=>{"Biochemistry, Genetics and Molecular Biology"=>4}, "Unspecified"=>{"Unspecified"=>5}}, "reader_count_by_country"=>{"United States"=>1, "Poland"=>1}, "group_count"=>2}

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Figshare

  • {"files"=>["https://ndownloader.figshare.com/files/491413"], "description"=>"<p>a) Total Aβ42 level was divided by total Aβ40 level and by total Aβ43; b) Aβ43 total level was divided by total Aβ40 concentrations. *<0.05; **<0.01.</p>", "links"=>[], "tags"=>["chemistry", "geriatrics", "neuroscience", "neurological disorders", "Biochemistry"], "article_id"=>161933, "categories"=>["Medicine", "Biochemistry", "Neuroscience", "Chemistry"], "users"=>["Anna Sandebring", "Hedvig Welander", "Bengt Winblad", "Caroline Graff", "Lars O. Tjernberg"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0055847.g006", "stats"=>{"downloads"=>1, "page_views"=>12, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_A_946_42_A_946_40_and_A_946_43_A_946_40_ratios_/161933", "title"=>"Aβ42/Aβ40 and Aβ43/Aβ40 ratios.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2013-02-11 00:32:13"}
  • {"files"=>["https://ndownloader.figshare.com/files/484550"], "description"=>"<div><p>The amyloid-cascade hypothesis posits that the role of amyloid β-peptide (Aβ) in Alzheimer disease (AD) involves polymerization into structures that eventually are deposited as amyloid plaques. During this process, neurotoxic oligomers are formed that induce synaptic loss and neuronal death. Several different isoforms of Aβ are produced, of which the 40 and 42 residue variants (Aβ40 and Aβ42) are the most common. Aβ42 has a strong tendency to form neurotoxic aggregates and is involved in AD pathogenesis. Longer Aβ isoforms, like the less studied Aβ43, are gaining attention for their higher propensity to aggregate into neurotoxic oligomers. To further investigate Aβ43 in AD, we conducted a quantitative study on Aβ43 levels in human brain. We homogenized human brain tissue and prepared fractions of various solubility; tris buffered saline (TBS), sodium dodecyl sulfate (SDS) and formic acid (FA). Levels of Aβ43, as well as Aβ40 and Aβ42, were quantified using ELISA. We compared quantitative data showing Aβ levels in occipital and frontal cortex from sporadic (SAD) and familial (FAD) AD cases, as well as non-demented (ND) controls. Results showed Aβ43 present in each fraction from the SAD and FAD cases, while its level was lower than the detection limit in the majority of the ND-cases. Aβ42 and Aβ43 were enriched in the less soluble fractions (SDS and FA) of SAD and FAD cases in both occipital and frontal cortex. Thus, although the total levels of Aβ43 in human brain are low compared to Aβ40 and Aβ42, we suggest that Aβ43 could initiate the formation of oligomers and amyloid plaques and thereby be crucial to AD pathogenesis.</p> </div>", "links"=>[], "tags"=>["pathogenic", "enriched", "familial", "sporadic", "alzheimer", "disease"], "article_id"=>156501, "categories"=>["Medicine", "Biochemistry", "Neuroscience", "Chemistry"], "users"=>["Anna Sandebring", "Hedvig Welander", "Bengt Winblad", "Caroline Graff", "Lars O. Tjernberg"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0055847", "stats"=>{"downloads"=>0, "page_views"=>45, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/The_Pathogenic_A_43_Is_Enriched_in_Familial_and_Sporadic_Alzheimer_Disease__/156501", "title"=>"The Pathogenic Aβ43 Is Enriched in Familial and Sporadic Alzheimer Disease", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2013-02-11 01:48:21"}
  • {"files"=>["https://ndownloader.figshare.com/files/491164"], "description"=>"<p>Fractions of human brain homogenates from non-demented (ND), sporadic Alzheimer disease (SAD) and familial Alzheimer disease (FAD) were analyzed with an Aβ42-specific ELISA. Colored symbols each represents one case as listed in <a href=\"http://www.plosone.org/article/info:doi/10.1371/journal.pone.0055847#pone-0055847-g001\" target=\"_blank\"><b>Figure 1</b></a> and horizontal lines indicate the mean value of each group. Data is expressed as nmol or pmol/g of protein. <b>a</b>) TBS-soluble Aβ42 in frontal cortex; <b>b</b>) TBS-soluble Aβ42 in occipital cortex; <b>c</b>) SDS-soluble Aβ42 in frontal cortex; <b>d</b>) SDS-soluble Aβ42 in occipital cortex; <b>e</b>) FA-soluble Aβ42 in frontal cortex; <b>f</b>) FA-soluble Aβ42 in occipital cortex; <b>g</b>) Total Aβ42 (TBS+SDS+FA) in frontal cortex; <b>h</b>) Total Aβ42 (TBS+SDS+FA) in occipital cortex *<0.05; **<0.01.</p>", "links"=>[], "tags"=>["plots"], "article_id"=>161684, "categories"=>["Medicine", "Biochemistry", "Neuroscience", "Chemistry"], "users"=>["Anna Sandebring", "Hedvig Welander", "Bengt Winblad", "Caroline Graff", "Lars O. Tjernberg"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0055847.g003", "stats"=>{"downloads"=>0, "page_views"=>1, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_ELISA_scatter_plots_of_A_946_42_/161684", "title"=>"ELISA scatter plots of Aβ42.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2013-02-11 00:28:04"}
  • {"files"=>["https://ndownloader.figshare.com/files/491095"], "description"=>"<p>Fractions of human brain homogenates from non-demented (ND), sporadic Alzheimer disease (SAD) and familial Alzheimer disease (FAD) were analyzed with an Aβ40-specific ELISA. Colored symbols each represents one case as listed in <a href=\"http://www.plosone.org/article/info:doi/10.1371/journal.pone.0055847#pone-0055847-g001\" target=\"_blank\"><b>Figure 1</b></a> and horizontal lines indicate the mean value of each group. Data is expressed as nmol or pmol/g of protein. <b>a</b>) TBS-soluble Aβ40 in frontal cortex; <b>b</b>) TBS-soluble Aβ40 in occipital cortex; <b>c</b>) SDS-soluble Aβ40 in frontal cortex; <b>d</b>) SDS-soluble Aβ40 in occipital cortex; <b>e</b>) FA-soluble Aβ40 in frontal cortex; <b>f</b>) FA-soluble Aβ40 in occipital cortex; <b>g</b>) Total Aβ40 (TBS+SDS+FA) in frontal cortex; <b>h</b>) Total Aβ40 (TBS+SDS+FA) in occipital cortex *<0.05; **<0.01.</p>", "links"=>[], "tags"=>["plots"], "article_id"=>161617, "categories"=>["Medicine", "Biochemistry", "Neuroscience", "Chemistry"], "users"=>["Anna Sandebring", "Hedvig Welander", "Bengt Winblad", "Caroline Graff", "Lars O. Tjernberg"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0055847.g002", "stats"=>{"downloads"=>0, "page_views"=>1, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_ELISA_scatter_plots_of_A_946_40_/161617", "title"=>"ELISA scatter plots of Aβ40.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2013-02-11 00:26:57"}
  • {"files"=>["https://ndownloader.figshare.com/files/491317"], "description"=>"<p>Absolute levels of Aβ in SDS-soluble and FA-soluble fractions were divided by levels in TBS-soluble fractions. ND: non-demented; SAD: sporadic Alzheimer disease; FAD: familial Alzheimer disease. <b>a</b>) Enrichment of insoluble Aβ in human frontal cortex; <b>b</b>) Enrichment of insoluble Aβ in human occipital cortex. *<0.05; **<0.01; #<0.05; ##<0.01.</p>", "links"=>[], "tags"=>["plots", "enrichment"], "article_id"=>161835, "categories"=>["Medicine", "Biochemistry", "Neuroscience", "Chemistry"], "users"=>["Anna Sandebring", "Hedvig Welander", "Bengt Winblad", "Caroline Graff", "Lars O. Tjernberg"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0055847.g005", "stats"=>{"downloads"=>0, "page_views"=>1, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Scatter_plots_representing_the_enrichment_of_A_946_40_A_946_42_and_A_946_43_in_human_brain_/161835", "title"=>"Scatter plots representing the enrichment of Aβ40, Aβ42 and Aβ43 in human brain.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2013-02-11 00:30:35"}
  • {"files"=>["https://ndownloader.figshare.com/files/491016"], "description"=>"<p>ND = non-demented; SAD = sporadic Alzheimer disease; FAD = familial Alzheimer disease; y = years; M = male; F = female; PMI = postmortem interval; h = hours; Clinic = clinical neurological diagnosis; dem = demented; APPswe = Swedish mutation in <i>APP</i>; PS1I143T = I143T mutation in <i>PSEN1</i>; NP = neuropathological diagnosis; NH = neurologically healthy; pro AD = probable AD; pos AD = possible AD; def AD = definite AD. NH* = case excluded from grouped analysis.</p>", "links"=>[], "tags"=>["chemistry", "geriatrics", "neuroscience", "neurological disorders", "Biochemistry"], "article_id"=>161532, "categories"=>["Medicine", "Biochemistry", "Neuroscience", "Chemistry"], "users"=>["Anna Sandebring", "Hedvig Welander", "Bengt Winblad", "Caroline Graff", "Lars O. Tjernberg"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0055847.g001", "stats"=>{"downloads"=>1, "page_views"=>12, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Study_Subject_Data_/161532", "title"=>"Study Subject Data.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2013-02-11 00:25:32"}
  • {"files"=>["https://ndownloader.figshare.com/files/491237"], "description"=>"<p>Fractions of human brain homogenates from non-demented (ND), sporadic Alzheimer disease (SAD) and familial Alzheimer disease (FAD) were analyzed with an Aβ43-specific ELISA. Colored symbols each represents one case as listed in <a href=\"http://www.plosone.org/article/info:doi/10.1371/journal.pone.0055847#pone-0055847-g001\" target=\"_blank\"><b>Figure 1</b></a> and horizontal lines indicate the mean value of each group. Data is expressed as nmol or pmol/g of protein. <b>a</b>) TBS-soluble Aβ43 in frontal cortex; <b>b</b>) TBS-soluble Aβ43 in occipital cortex; <b>c</b>) SDS-soluble Aβ43 in frontal cortex; <b>d</b>) SDS-soluble Aβ43 in occipital cortex; <b>e</b>) FA-soluble Aβ43 in frontal cortex; <b>f</b>) FA-soluble Aβ43 in occipital cortex; <b>g</b>) Total Aβ43 (TBS+SDS+FA) in frontal cortex; <b>h</b>) Total Aβ43 (TBS+SDS+FA) in occipital cortex *<0.05; **<0.01.</p>", "links"=>[], "tags"=>["plots"], "article_id"=>161756, "categories"=>["Medicine", "Biochemistry", "Neuroscience", "Chemistry"], "users"=>["Anna Sandebring", "Hedvig Welander", "Bengt Winblad", "Caroline Graff", "Lars O. Tjernberg"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0055847.g004", "stats"=>{"downloads"=>1, "page_views"=>4, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_ELISA_scatter_plots_of_A_946_43_/161756", "title"=>"ELISA scatter plots of Aβ43.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2013-02-11 00:29:16"}

PMC Usage Stats | Further Information

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Relative Metric

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