Telomere length and oxidative stress variations in a murine model of Alzheimer's disease progression.
Katia Martínez-GonzálezAzul Islas-HernándezJosé Darío Martínez-EzquerroFederico Bermudez-RattoniPaola García-delaTorrePublished in: The European journal of neuroscience (2020)
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 <tm1Mpm> 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.
Keyphrases
- oxidative stress
- induced apoptosis
- endoplasmic reticulum stress
- cell cycle arrest
- dna damage
- diabetic rats
- signaling pathway
- ischemia reperfusion injury
- peripheral blood
- wild type
- cognitive decline
- risk factors
- white matter
- type diabetes
- cell death
- escherichia coli
- mild cognitive impairment
- cognitive impairment
- multiple sclerosis
- resting state
- physical activity
- cell proliferation
- adipose tissue
- brain injury
- heat shock
- functional connectivity
- blood brain barrier
- subarachnoid hemorrhage