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Apolipoprotein D is a component of compact but not diffuse amyloid-beta plaques in Alzheimer's disease temporal cortex.
Neurobiol Dis 2005; 20(2):574-82ND

Abstract

Apolipoprotein D (apoD) is elevated in Alzheimer's disease (AD) cortex, localizing to cells, blood vessels, and neuropil deposits (plaques). The role of apoD in AD pathology and the extent of its co-distribution with diffuse (amorphous) and compact (dense fibrillar) amyloid-beta (Abeta) plaques are currently unclear. To address this issue, we combined apoD and Abeta immunohistochemistry with ThioS/X-34 staining of the beta-pleated sheet protein conformation in temporal cortex from 36 AD patients and 12 non-demented controls. ApoD-immunoreactive, Abeta-immunoreactive, and ThioS/X-34-stained plaques were detected exclusively in AD tissue. Dual-immunolabeling showed that 63% of Abeta plaques co-localized apoD. All apoD plaques contained Abeta protein and ThioS/X-34 fluorescence. Compared to controls, AD cases showed elevated vascular and intracellular apoD immunostaining which localized primarily to cells clustered within plaques and around large blood vessels. ApoD-immunoreactive cells within plaques morphologically matched MHC-II- and CD-68-immunoreactive microglia, and did not contain the astrocytic marker GFAP, which labeled a subset of apoD-immunoreactive cells surrounding plaques. These data suggest that neuropil deposits of apoD localize only to a subset of Abeta plaques, which contain compact aggregates of fibrillar Abeta. Elevated apoD in AD brain may influence Abeta aggregation, or facilitate phagocytosis and transport of Abeta fibrils from plaques to cerebral vasculature.

Authors+Show Affiliations

Department of Human Genetics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA 15261, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

15916898

Citation

Desai, Purnima P., et al. "Apolipoprotein D Is a Component of Compact but Not Diffuse Amyloid-beta Plaques in Alzheimer's Disease Temporal Cortex." Neurobiology of Disease, vol. 20, no. 2, 2005, pp. 574-82.
Desai PP, Ikonomovic MD, Abrahamson EE, et al. Apolipoprotein D is a component of compact but not diffuse amyloid-beta plaques in Alzheimer's disease temporal cortex. Neurobiol Dis. 2005;20(2):574-82.
Desai, P. P., Ikonomovic, M. D., Abrahamson, E. E., Hamilton, R. L., Isanski, B. A., Hope, C. E., ... Kamboh, M. I. (2005). Apolipoprotein D is a component of compact but not diffuse amyloid-beta plaques in Alzheimer's disease temporal cortex. Neurobiology of Disease, 20(2), pp. 574-82.
Desai PP, et al. Apolipoprotein D Is a Component of Compact but Not Diffuse Amyloid-beta Plaques in Alzheimer's Disease Temporal Cortex. Neurobiol Dis. 2005;20(2):574-82. PubMed PMID: 15916898.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Apolipoprotein D is a component of compact but not diffuse amyloid-beta plaques in Alzheimer's disease temporal cortex. AU - Desai,Purnima P, AU - Ikonomovic,Milos D, AU - Abrahamson,Eric E, AU - Hamilton,Ronald L, AU - Isanski,Barbara A, AU - Hope,Caroline E, AU - Klunk,William E, AU - DeKosky,Steven T, AU - Kamboh,M Ilyas, PY - 2004/12/15/received PY - 2005/03/31/revised PY - 2005/04/09/accepted PY - 2005/5/27/pubmed PY - 2006/1/24/medline PY - 2005/5/27/entrez SP - 574 EP - 82 JF - Neurobiology of disease JO - Neurobiol. Dis. VL - 20 IS - 2 N2 - Apolipoprotein D (apoD) is elevated in Alzheimer's disease (AD) cortex, localizing to cells, blood vessels, and neuropil deposits (plaques). The role of apoD in AD pathology and the extent of its co-distribution with diffuse (amorphous) and compact (dense fibrillar) amyloid-beta (Abeta) plaques are currently unclear. To address this issue, we combined apoD and Abeta immunohistochemistry with ThioS/X-34 staining of the beta-pleated sheet protein conformation in temporal cortex from 36 AD patients and 12 non-demented controls. ApoD-immunoreactive, Abeta-immunoreactive, and ThioS/X-34-stained plaques were detected exclusively in AD tissue. Dual-immunolabeling showed that 63% of Abeta plaques co-localized apoD. All apoD plaques contained Abeta protein and ThioS/X-34 fluorescence. Compared to controls, AD cases showed elevated vascular and intracellular apoD immunostaining which localized primarily to cells clustered within plaques and around large blood vessels. ApoD-immunoreactive cells within plaques morphologically matched MHC-II- and CD-68-immunoreactive microglia, and did not contain the astrocytic marker GFAP, which labeled a subset of apoD-immunoreactive cells surrounding plaques. These data suggest that neuropil deposits of apoD localize only to a subset of Abeta plaques, which contain compact aggregates of fibrillar Abeta. Elevated apoD in AD brain may influence Abeta aggregation, or facilitate phagocytosis and transport of Abeta fibrils from plaques to cerebral vasculature. SN - 0969-9961 UR - https://www.unboundmedicine.com/medline/citation/15916898/Apolipoprotein_D_is_a_component_of_compact_but_not_diffuse_amyloid_beta_plaques_in_Alzheimer's_disease_temporal_cortex_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0969-9961(05)00121-X DB - PRIME DP - Unbound Medicine ER -