Telomere dysfunction reduces microglial numbers without fully inducing an aging phenotype

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Standard

Telomere dysfunction reduces microglial numbers without fully inducing an aging phenotype. / Khan, Asif Manzoor; Babcock, Alicia A; Saeed, Hamid; Myhre, Christa Løth; Kassem, Moustapha; Finsen, Bente.

I: Neurobiology of Aging, Bind 36, Nr. 6, 06.2015, s. 2164-75.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

Khan, AM, Babcock, AA, Saeed, H, Myhre, CL, Kassem, M & Finsen, B 2015, 'Telomere dysfunction reduces microglial numbers without fully inducing an aging phenotype', Neurobiology of Aging, bind 36, nr. 6, s. 2164-75. https://doi.org/10.1016/j.neurobiolaging.2015.03.008

APA

Khan, A. M., Babcock, A. A., Saeed, H., Myhre, C. L., Kassem, M., & Finsen, B. (2015). Telomere dysfunction reduces microglial numbers without fully inducing an aging phenotype. Neurobiology of Aging, 36(6), 2164-75. https://doi.org/10.1016/j.neurobiolaging.2015.03.008

Vancouver

Khan AM, Babcock AA, Saeed H, Myhre CL, Kassem M, Finsen B. Telomere dysfunction reduces microglial numbers without fully inducing an aging phenotype. Neurobiology of Aging. 2015 jun.;36(6):2164-75. https://doi.org/10.1016/j.neurobiolaging.2015.03.008

Author

Khan, Asif Manzoor ; Babcock, Alicia A ; Saeed, Hamid ; Myhre, Christa Løth ; Kassem, Moustapha ; Finsen, Bente. / Telomere dysfunction reduces microglial numbers without fully inducing an aging phenotype. I: Neurobiology of Aging. 2015 ; Bind 36, Nr. 6. s. 2164-75.

Bibtex

@article{55200028fed94346a9e3b4b146877a21,

title = "Telomere dysfunction reduces microglial numbers without fully inducing an aging phenotype",

abstract = "The susceptibility of the aging brain to neurodegenerative disease may in part be attributed to cellular aging of the microglial cells that survey it. We investigated the effect of cellular aging induced by telomere shortening on microglia by the use of mice lacking the telomerase RNA component (TERC) and design-based stereology. TERC knockout (KO) mice had a significantly reduced number of CD11b(+) microglia in the dentate gyrus. Because of an even greater reduction in dentate gyrus volume, microglial density was, however, increased. Microglia in TERC KO mice maintained a homogenous distribution and normal expression of CD45 and CD68 and the aging marker, ferritin, but were morphologically distinct from microglia in both adult and old wild-type mice. TERC KO mice also showed increased cellular apoptosis and impaired spatial learning. Our results suggest that individual microglia are relatively resistant to telomerase deficiency during steady state conditions, despite an overall reduction in microglial numbers. Furthermore, telomerase deficiency and aging may provide disparate cues leading to distinct changes in microglial morphology and phenotype.",

author = "Khan, {Asif Manzoor} and Babcock, {Alicia A} and Hamid Saeed and Myhre, {Christa L{\o}th} and Moustapha Kassem and Bente Finsen",

year = "2015",

month = jun,

doi = "10.1016/j.neurobiolaging.2015.03.008",

language = "English",

volume = "36",

pages = "2164--75",

journal = "Neurobiology of Aging",

issn = "0197-4580",

publisher = "Elsevier",

number = "6",

}

RIS

TY - JOUR

T1 - Telomere dysfunction reduces microglial numbers without fully inducing an aging phenotype

AU - Khan, Asif Manzoor

AU - Babcock, Alicia A

AU - Saeed, Hamid

AU - Myhre, Christa Løth

AU - Kassem, Moustapha

AU - Finsen, Bente

PY - 2015/6

Y1 - 2015/6

N2 - The susceptibility of the aging brain to neurodegenerative disease may in part be attributed to cellular aging of the microglial cells that survey it. We investigated the effect of cellular aging induced by telomere shortening on microglia by the use of mice lacking the telomerase RNA component (TERC) and design-based stereology. TERC knockout (KO) mice had a significantly reduced number of CD11b(+) microglia in the dentate gyrus. Because of an even greater reduction in dentate gyrus volume, microglial density was, however, increased. Microglia in TERC KO mice maintained a homogenous distribution and normal expression of CD45 and CD68 and the aging marker, ferritin, but were morphologically distinct from microglia in both adult and old wild-type mice. TERC KO mice also showed increased cellular apoptosis and impaired spatial learning. Our results suggest that individual microglia are relatively resistant to telomerase deficiency during steady state conditions, despite an overall reduction in microglial numbers. Furthermore, telomerase deficiency and aging may provide disparate cues leading to distinct changes in microglial morphology and phenotype.

AB - The susceptibility of the aging brain to neurodegenerative disease may in part be attributed to cellular aging of the microglial cells that survey it. We investigated the effect of cellular aging induced by telomere shortening on microglia by the use of mice lacking the telomerase RNA component (TERC) and design-based stereology. TERC knockout (KO) mice had a significantly reduced number of CD11b(+) microglia in the dentate gyrus. Because of an even greater reduction in dentate gyrus volume, microglial density was, however, increased. Microglia in TERC KO mice maintained a homogenous distribution and normal expression of CD45 and CD68 and the aging marker, ferritin, but were morphologically distinct from microglia in both adult and old wild-type mice. TERC KO mice also showed increased cellular apoptosis and impaired spatial learning. Our results suggest that individual microglia are relatively resistant to telomerase deficiency during steady state conditions, despite an overall reduction in microglial numbers. Furthermore, telomerase deficiency and aging may provide disparate cues leading to distinct changes in microglial morphology and phenotype.

U2 - 10.1016/j.neurobiolaging.2015.03.008

DO - 10.1016/j.neurobiolaging.2015.03.008

M3 - Journal article

C2 - 25892207

VL - 36

SP - 2164

EP - 2175

JO - Neurobiology of Aging

JF - Neurobiology of Aging

SN - 0197-4580

IS - 6

ER -

ID: 138763470