%0 Journal Article %1 simpson2010astrocytebrain. %A Simpson, JE %A Ince, PG %A Lace, G %A Forster, G %A Shaw, PJ %A Matthews, F %A Savva, G %A Brayne, C %A Wharton, SB %A Function, MRC Cognitive %A Group, Ageing Neuropathology Study %C Academic Unit of Pathology, University of Sheffield Medical School, Beech Hill Road, Sheffield S10 2RX, UK. %D 2010 %J Neurobiol Aging %K imported %N 4 %P 578--590 %R 10.1016/j.neurobiolaging.2008.05.015 %T Astrocyte phenotype in relation to Alzheimer-type pathology in the ageing brain. %U http://www.ncbi.nlm.nih.gov/pubmed/18586353 %V 31 %X Astrocyte pathology occurs in association with Alzheimer's disease (AD) and in brain ageing, but is poorly characterised. We sought to define the detailed cellular pathology of astrocytes, the extent of population variation and the relationship to Alzheimer-type changes in a population-based cohort. Three staining patterns were associated with GFAP and excitatory amino acid transporter 2 (EAAT2): minimal, moderate or extensive immunoreactivity. GFAP and EAAT2 expression were inversely related (p=0.015), with trends to increased expression of GFAP (p=0.019) and decreased expression of EAAT2 (p=ns) with increasing Braak stage. GFAP and EAAT2 correlated incompletely with beta-amyloid and tau immunoreactivity. However, gliosis increased with increasing burden of neuritic (p=0.011), but not diffuse (p=ns), plaques. Double-staining revealed distinct subsets of astrocytes; GFAP(+)EAAT(-), GFAP(-)EAAT(+), or GFAP(+)EAAT(+). In contrast to the variation in GFAP and EAAT2, levels of EAAT1 and S100B showed consistent staining patterns. Alzheimer-type pathology only partially explains the variation in gliosis and astrocyte functional markers, suggesting that other factors contribute to the population variance in astrocyte pathology.

@article{simpson2010astrocytebrain., abstract = {Astrocyte pathology occurs in association with Alzheimer's disease (AD) and in brain ageing, but is poorly characterised. We sought to define the detailed cellular pathology of astrocytes, the extent of population variation and the relationship to Alzheimer-type changes in a population-based cohort. Three staining patterns were associated with GFAP and excitatory amino acid transporter 2 (EAAT2): minimal, moderate or extensive immunoreactivity. GFAP and EAAT2 expression were inversely related (p=0.015), with trends to increased expression of GFAP (p=0.019) and decreased expression of EAAT2 (p=ns) with increasing Braak stage. GFAP and EAAT2 correlated incompletely with beta-amyloid and tau immunoreactivity. However, gliosis increased with increasing burden of neuritic (p=0.011), but not diffuse (p=ns), plaques. Double-staining revealed distinct subsets of astrocytes; GFAP(+)EAAT(-), GFAP(-)EAAT(+), or GFAP(+)EAAT(+). In contrast to the variation in GFAP and EAAT2, levels of EAAT1 and S100B showed consistent staining patterns. Alzheimer-type pathology only partially explains the variation in gliosis and astrocyte functional markers, suggesting that other factors contribute to the population variance in astrocyte pathology.}, added-at = {2013-08-12T12:53:15.000+0200}, address = {Academic Unit of Pathology, University of Sheffield Medical School, Beech Hill Road, Sheffield S10 2RX, UK.}, author = {Simpson, JE and Ince, PG and Lace, G and Forster, G and Shaw, PJ and Matthews, F and Savva, G and Brayne, C and Wharton, SB and Function, MRC Cognitive and Group, Ageing Neuropathology Study}, biburl = {https://www.bibsonomy.org/bibtex/271c11fcfc3f6c00b8da40659671304aa/sokratesagogo}, doi = {10.1016/j.neurobiolaging.2008.05.015}, eissn = {1558-1497}, interhash = {f09306d02245547e0954ded17f254ffc}, intrahash = {71c11fcfc3f6c00b8da40659671304aa}, journal = {Neurobiol Aging}, keyword = {Aged}, keywords = {imported}, language = {eng}, month = Apr, number = 4, organization = {United States}, pages = {578--590}, pii = {S0197-4580(08)00170-X}, timestamp = {2013-08-12T12:53:46.000+0200}, title = {Astrocyte phenotype in relation to Alzheimer-type pathology in the ageing brain.}, url = {http://www.ncbi.nlm.nih.gov/pubmed/18586353}, volume = 31, year = 2010 }