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Telomere length and oxidative stress variations in a murine model of Alzheimer’s disease progression
Author(s) -
MartínezGonzález Katia,
IslasHernández Azul,
MartínezEzquerro José Darío,
BermúdezRattoni Federico,
GarciadelaTorre Paola
Publication year - 2020
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/ejn.14877
Subject(s) - telomere , oxidative stress , genetically modified mouse , ageing , transgene , biology , dementia , alzheimer's disease , telomerase , senescence , medicine , hippocampus , psen1 , endocrinology , disease , genetics , presenilin , gene
Alzheimer's disease (AD) is the most common cause of dementia, and ageing is its major risk factor. Changes in telomere length have been associated with ageing and some degenerative diseases. Our aim was to explore some of the molecular changes caused by the progression of AD in a transgenic murine model (3xTg‐AD; B6; 129‐Psen1 Tg (APPSwe, tauP301L) 1Lfa). Telomere length was assessed by qPCR in both brain tissue and peripheral blood cells and compared between three age groups: 5, 9 and 13 months. In addition, a possible effect of oxidative stress on telomere length and AD progression was explored. Shorter telomeres were found in blood cells of older transgenic mice compared to younger and wild‐type mice but no changes in telomere length in the hippocampus. An increase in oxidative stress with age was found for all strains, but no correlation was found between oxidative stress and shorter telomere length for transgenic mice. Telomere length and oxidative stress are affected by AD progression in the 3xTg‐AD murine model. Changes in blood cells are more noticeable than changes in brain tissue, suggesting that systemic changes can be detected early in the disease in this murine model.