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Lipoprotein Lipase (LPL) is Associated with Neurite Pathology and Its Levels Are Markedly Reduced in the Dentate Gyrus of Alzheimer’s Disease Brains

Lipoprotein lipase (LPL) is involved in regulation of fatty acid metabolism, and facilitates cellular uptake of lipoproteins, lipids and lipid-soluble vitamins. We evaluated LPL distribution in healthy and Alzheimer’s disease (AD) brain tissue and its relative levels in cerebrospinal fluid. LPL immu...

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Autores principales: Gong, Huilin, Dong, Weijiang, Rostad, Steven W., Marcovina, Santica M., Albers, John J., Brunzell, John D., Vuletic, Simona
Formato: Online Artículo Texto
Lenguaje:English
Publicado: SAGE Publications 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3840745/
https://www.ncbi.nlm.nih.gov/pubmed/24004859
http://dx.doi.org/10.1369/0022155413505601
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author Gong, Huilin
Dong, Weijiang
Rostad, Steven W.
Marcovina, Santica M.
Albers, John J.
Brunzell, John D.
Vuletic, Simona
author_facet Gong, Huilin
Dong, Weijiang
Rostad, Steven W.
Marcovina, Santica M.
Albers, John J.
Brunzell, John D.
Vuletic, Simona
author_sort Gong, Huilin
collection PubMed
description Lipoprotein lipase (LPL) is involved in regulation of fatty acid metabolism, and facilitates cellular uptake of lipoproteins, lipids and lipid-soluble vitamins. We evaluated LPL distribution in healthy and Alzheimer’s disease (AD) brain tissue and its relative levels in cerebrospinal fluid. LPL immunostaining is widely present in different neuronal subgroups, microglia, astrocytes and oligodendroglia throughout cerebrum, cerebellum and spinal cord. LPL immunoreactivity is also present in leptomeninges, small blood vessels, choroid plexus and ependymal cells, Schwann cells associated with cranial nerves, and in anterior and posterior pituitary. In vitro studies have shown presence of secreted LPL in conditioned media of human cortical neuronal cell line (HCN2) and neuroblastoma cells (SK-N-SH), but not in media of cultured primary human astrocytes. LPL was present in cytoplasmic and nuclear fractions of neuronal cells and astrocytes in vitro. LPL immunoreactivity strongly associates with AD-related pathology, staining diffuse plaques, dystrophic and swollen neurites, possible Hirano bodies and activated glial cells. We observed no staining associated with neurofibrillary tangles or granulovacuolar degeneration. Granule cells of the dentate gyrus and the associated synaptic network showed significantly reduced staining in AD compared to control tissue. LPL was also reduced in AD CSF samples relative to those in controls.
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spelling pubmed-38407452014-12-01 Lipoprotein Lipase (LPL) is Associated with Neurite Pathology and Its Levels Are Markedly Reduced in the Dentate Gyrus of Alzheimer’s Disease Brains Gong, Huilin Dong, Weijiang Rostad, Steven W. Marcovina, Santica M. Albers, John J. Brunzell, John D. Vuletic, Simona J Histochem Cytochem Articles Lipoprotein lipase (LPL) is involved in regulation of fatty acid metabolism, and facilitates cellular uptake of lipoproteins, lipids and lipid-soluble vitamins. We evaluated LPL distribution in healthy and Alzheimer’s disease (AD) brain tissue and its relative levels in cerebrospinal fluid. LPL immunostaining is widely present in different neuronal subgroups, microglia, astrocytes and oligodendroglia throughout cerebrum, cerebellum and spinal cord. LPL immunoreactivity is also present in leptomeninges, small blood vessels, choroid plexus and ependymal cells, Schwann cells associated with cranial nerves, and in anterior and posterior pituitary. In vitro studies have shown presence of secreted LPL in conditioned media of human cortical neuronal cell line (HCN2) and neuroblastoma cells (SK-N-SH), but not in media of cultured primary human astrocytes. LPL was present in cytoplasmic and nuclear fractions of neuronal cells and astrocytes in vitro. LPL immunoreactivity strongly associates with AD-related pathology, staining diffuse plaques, dystrophic and swollen neurites, possible Hirano bodies and activated glial cells. We observed no staining associated with neurofibrillary tangles or granulovacuolar degeneration. Granule cells of the dentate gyrus and the associated synaptic network showed significantly reduced staining in AD compared to control tissue. LPL was also reduced in AD CSF samples relative to those in controls. SAGE Publications 2013-12 /pmc/articles/PMC3840745/ /pubmed/24004859 http://dx.doi.org/10.1369/0022155413505601 Text en © The Author(s) 2013 http://creativecommons.org/licenses/by/2.5/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Articles
Gong, Huilin
Dong, Weijiang
Rostad, Steven W.
Marcovina, Santica M.
Albers, John J.
Brunzell, John D.
Vuletic, Simona
Lipoprotein Lipase (LPL) is Associated with Neurite Pathology and Its Levels Are Markedly Reduced in the Dentate Gyrus of Alzheimer’s Disease Brains
title Lipoprotein Lipase (LPL) is Associated with Neurite Pathology and Its Levels Are Markedly Reduced in the Dentate Gyrus of Alzheimer’s Disease Brains
title_full Lipoprotein Lipase (LPL) is Associated with Neurite Pathology and Its Levels Are Markedly Reduced in the Dentate Gyrus of Alzheimer’s Disease Brains
title_fullStr Lipoprotein Lipase (LPL) is Associated with Neurite Pathology and Its Levels Are Markedly Reduced in the Dentate Gyrus of Alzheimer’s Disease Brains
title_full_unstemmed Lipoprotein Lipase (LPL) is Associated with Neurite Pathology and Its Levels Are Markedly Reduced in the Dentate Gyrus of Alzheimer’s Disease Brains
title_short Lipoprotein Lipase (LPL) is Associated with Neurite Pathology and Its Levels Are Markedly Reduced in the Dentate Gyrus of Alzheimer’s Disease Brains
title_sort lipoprotein lipase (lpl) is associated with neurite pathology and its levels are markedly reduced in the dentate gyrus of alzheimer’s disease brains
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3840745/
https://www.ncbi.nlm.nih.gov/pubmed/24004859
http://dx.doi.org/10.1369/0022155413505601
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