Alzheimer's, a Ticking Timebomb. Could Nrf2 Help?

Alzheimer’s, a Ticking Timebomb. Could Nrf2 Help?

The study of demographics and aging is a fascinating field to review. During the course of the next 25 years people aged 65 and older will double. This will result in more than double the number of Alzheimer's or other dementia cases than we see today. This will be because the 85 and older age… Continue reading

The study of demographics and aging is a fascinating field to review. During the course of the next 25 years people aged 65 and older will double. This will result in more than double the number of Alzheimer's or other dementia cases than we see today. This will be because the 85 and older age group are the fastest-growing portion of America's aging population. Recognizing the impact this will have on society, the government signed into law the National Alzheimer's Project Act in 2011. This act hopes to result in the development of a National Alzheimer's Plan.

Planning for an Alzheimer's epidemic at a national level is a good idea. After all the costs associated with this disease is not a trivial one. It impacts State and Federal budgets as well as the finances families of those suffering from Alzheimer's.

Some recent studies have considered the effect of improved NRF2 activation on Alzheimer's and other brain related disease states.

The Journal of Alheimer's disease (Mar 16, 2012) reports on "a promising drug delivery strategy to protect neurons against oxidative damage as observed in Alzheimer's disease."

Alzheimer's and Oxidative Stress

In the International Journal of Alzheimers Dis. 2011 in was quoted that "Specific regions of the Alzheimer's disease (AD) brain are burdened with extracellular protein deposits, the accumulation of which is concomitant with a complex cascade of overlapping events. Many of these pathological processes produce oxidative stress."

So why would this be so concerning?

Oxidative stress is caused by an imbalance between the production of and removal of a group of molecules known as reactive oxygen species (ROS) . The resulting Oxidative stress leads to the damage of all cellular macromolecules which left unchecked will cause irreparable oxidative injury and eventually cell death. Oxidative stress has been linked to over 200 disease states and a regular review of credible databases such as Pubmed shows increasing peer reviewed scientific studies documenting this fact.

Normal aging, environmental factors within the body causes this imbalance between the production and removal of ROS. The body is steadily overwhelmed or exhausted. This particular study in 2011 states, "Oxidative stress is a central feature of AD, and, in fact, it may even be one of the first pathogenic events during disease progression. Markers of oxidative damage such as protein carbonyls and elevated lipid peroxidation precede pathological changes and are found in the brains of AD patients. Importantly, antioxidant defense is impaired in mouse models of AD; the levels and activities of protective enzymes including superoxide dismutase (SOD) and glutathione peroxidase are altered.

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