الفهرس 
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Abstract
AD is a progressive neurodegenerative disease affecting approximately 5.3 million people in the United States, including almost half of the population at 85 years and older. AD is the fifth leading cause of death among older adults, and about 200 billion dollars are spent annually on direct care of individuals living with dementia.
Reactive oxygen species (ROS) is a major risk factor of Alzheimer. Oxidative stress occurs when ROS and reactive nitrogen species (RNS) increases and/or antioxidant defense system decreases. Total anti-oxidant (TAC) is marker of DNA oxidation. These data will explain pathogenesis, prevention and help in the treatment for AD.
The aim of this study is to evaluate the telomere length and serum level of 8-hydroxy-2-deoxyguanosine (8-OHdG) as aging markers in patients with Alzheimer disease
In this study we investigated 90 individuals categorized into three groups: group 1 (Patients group): 30 patients. group II (age matched group): 30 age matched apparently healthy subjects. group III (pre geriatric group): 30 apparently healthy subjects their age between (30-60) years old. All patients were submitted to the following :Full history taking including DM, hypertension, smoking, history of memory problem, family history of AD and routine laboratory investigations including: Fasting blood sugar, TSH lipid profile(total cholesterol, TG,LDL,HDL), determination of the TAC is performed by the reaction of antioxidants in the sample with a defined amount of exogenously provide hydrogen peroxide (H2O2) colorimetrically, measurement of plasma levels of 8-OHdG by Enzyme linked Immunosorbent Assay [ELISA] and telomere length analysis by real time PCR.
There was statistical significant decrease in total antioxidant capacity in AD patients compared to age matched group and pregeriatric group.
There was statistical significant increase in plasma 8-OHdG concentration in AD patients compared to age matched group and pregeriatric group.
The relative TL (T/S ratio after normalization to single copy gene) significantly shortened with Alzheimer disease.
These findings needed to be confirmed by further prospective longitudinal studies with adequate sample size