Telomere shortening leads to earlier age of onset in ALS mice | Zendy

Birgit Linkus | Zendy; Diana Wiesner | Zendy; Martina Meßner | Zendy; Alexander Karabatsiakis | Zendy; Annika Scheffold | Zendy; K. Lenhard Rudolph | Zendy; Dietmar Rudolf Thal | Zendy; Jochen H. Weishaupt | Zendy; Albert C. Ludolph | Zendy; Karin M. Danzer | Zendy

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Telomere shortening leads to earlier age of onset in ALS mice

Author(s) -

Birgit Linkus,

Diana Wiesner,

Martina Meßner,

Alexander Karabatsiakis,

Annika Scheffold,

K. Lenhard Rudolph,

Dietmar Rudolf Thal,

Jochen H. Weishaupt,

Albert C. Ludolph,

Karin M. Danzer

Publication year - 2016

Publication title -

aging

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.473

H-Index - 90

ISSN - 1945-4589

DOI - 10.18632/aging.100904

Subject(s) - telomerase , telomere , amyotrophic lateral sclerosis , genetically modified mouse , microglia , phenotype , knockout mouse , biology , transgene , immunology , medicine , cancer research , pathology , gene , genetics , inflammation , disease

Telomere shortening has been linked to a variety of neurodegenerative diseases. Recent evidence suggests that reduced telomerase expression results in shorter telomeres in leukocytes from sporadic patients with amyotrophic lateral sclerosis (ALS) compared with healthy controls. Here, we have characterized telomere length in microglia, astroglia and neurons in human post mortem brain tissue from ALS patients and healthy controls. Moreover, we studied the consequences of telomerase deletion in a genetic mouse model for ALS. We found a trend towards longer telomeres in microglia in the brains of ALS patients compared to non-neurologic controls. Knockout of telomerase leading to telomere shortening accelerated the ALS phenotype inSOD1G93A-transgenic mice. Our results suggest that telomerase dysfunction might contribute to the age-related risk for ALS.

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