Circulating Cell Free DNA and DNA Double-Strand Breakage in Alzheimer’s Disease

Author:

Nguyen Michelle1,Wood Colby2,Rios Andres1,Salter Zach1,Reddy P. Hemachandra12345

Affiliation:

1. Department of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock, TX, USA

2. Nutritional Sciences Department, College Human Sciences, Texas Tech University, Lubbock, TX, USA

3. Department of Pharmacology and Neuroscience, Texas Tech University Health Sciences Center, Lubbock, TX, USA

4. Department of Neurology, Texas Tech University Health Sciences Center, Lubbock, TX, USA

5. Department of Public Health, Graduate School of Biomedical Sciences, Texas Tech University Health Sciences Center, Lubbock, TX, USA

Abstract

Alzheimer’s disease (AD) is an age-related neurodegenerative disease that is characterized by memory loss and multiple cognitive impairments. AD is pathologically characterized by age-dependent accumulation of amyloid-β protein and the phosphorylation of tau protein in the brains of patients with AD. Clinically, manifestations of AD include cognitive decline, dementia, alterations of high-order brain functions, and movement disorders. Double-stranded DNA breaks are a lethal form of DNA damage and are typically repaired via non-homologous end joining and homologous recombination. However, in AD brain, repair mechanism is disrupted, leading to a cascade of events, cognitive dysfunction, organ failure and reduced lifespan. Increased circulating cell-free DNA in the blood, cerebrospinal fluid, and urine in patients with AD, can be used as early detectable biomarkers for AD. The purpose of our article is to explore the potential uses of cell-free DNA and double-stranded DNA breaks as prognostic markers for AD and examine the recent research on the application of these markers in studies.

Publisher

IOS Press

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