Genome instability biomarkers and blood micronutrient risk profiles associated with mild cognitive impairment and Alzheimer's disease.

Successful maintenance of metabolic systems relating to accurate DNA replication and repair is critical for optimal lifelong human health. Should this homeostatic balance become impaired, genomic instability events can arise, compromising the integrity of the genome, which may result in gene expression and human disease. Both genome instability and micronutrient imbalance have been identified and implicated in diseases associated with accelerated ageing which potentially leads to an increased risk for the future development of clinically defined neurodegenerative disorders. Cognitive decline leading to the clinical diagnosis of mild cognitive impairment (MCI) has been shown to predict an increased risk in later life of developing Alzheimer's disease (AD). Knowledge on the impact of dietary factors in relation to MCI and AD risk is improving but incomplete; in particular the role of nutrient combinations (i.e. nutriomes) has not been thoroughly investigated. Currently, there is a need for preventative strategies as well as the identification of robust and reproducible diagnostic biomarkers that will allow identification of those individuals with increased risk for neurodegenerative diseases. Growing evidence suggests cells originating from different somatic tissues derived from individuals that have been clinically diagnosed with neurodegenerative disorders exhibit elevated frequencies of DNA damage compared to tissues of cognitively normal individuals which could be due to malnutrition. The objective of this review is to discuss current evidence and identify knowledge gaps relating to genome instability biomarkers and blood micronutrient profiles from human studies of MCI and AD that may be specific to and contribute to the increased risk of these diseases. This is a vital step in order to create research strategies for the future development of diagnostics that are indicative of dementia risk and to inform preventative therapies.