Perhaps one of the greatest worries of small plane pilots is engine failure. When the engine fails to make the plane fly, a crash often ensues. Some new research shows that the mechanism which causes brain cells to die off in Alzheimer’s disease is the failure of the cells “engine” called the mitochondria. (1)
The requirement for living cells to have oxygen and glucose for survival is that these molecules are used in the cell mitochondria to produce energy in the form of ATP to run and repair the cell on an ongoing basis.
A by-product of inefficient energy processing by the cell mitochondria are free radicals which damage and eventually kill the cell.
The dominant theory of the mechanism driving Alzheimer’s disease is the production and build-up of abnormal proteins like beta amyloid. While this protein is definitely associated with the disease several factors suggest that it is not the primary cause of neuron or cell loss in the brain. The first has been the demonstration of extensive beta amyloid in the brain of some older persons who show no cognitive decline. Additionally, some patients with the disease show very little beta amyloid build up. The most striking piece of evidence has been the clinical trials of several drugs which produce a marked removal of brain beta amyloid but have no impact on the disease progression.
The search for the mechanisms that are the cause of cell death in Alzheimer’s has recently turned to the mitochondria in neurons. The idea that this structure could be the link was suggested by the brain’s inordinately high requirement for energy. While the brain is only 2% of body weight, it accounts for 20% of the body’s oxygen consumption for energy production.
Researchers looked at mitochondrial gene expression which is an indicator of the cells energy production process.(1) They found that gene expression was markedly reduced signaling energy failure. Answers always led to more questions. The natural one was why was this energy failure and cell death happening? As it turned out beta amyloid was altering mitochondrial gene expression and the cascade of ending in cell death.
This understanding helps reflect several dilemmas. The first was that beta amyloid generally is present in the diseased brain although the levels do not correspond to the loss of brain cells and cognitive function. Some persons have more resilient mitochondrial function and may be less affected by higher levels of beta amyloid. Others have many other factors that weaken mitochondrial function and make them more susceptible to smaller amounts of beta amyloid.
The last thing the study looked at was adding a factor that improves mitochondrial function, CoQ10. This is used in the mitochondrial energy production and to reduce injurious free radicals. In brain cells pretreated with extra CoQ10 adding beta amyloid failed to cause the altered mitochondrial gene expression and cell injury.
A second new study also looked at the use of a specialized nutrient to improve mitochondrial energy production and cognition in an animal model of Alzheimer’s disease. (2) Brain cells convert niacin, or B3, into an important molecule used in mitochondrial energy production, NAD+. Several problems can happen to interfere with this important step. Dietary niacin can be inadequate, or an individual’s weak metabolism of niacin can impair NAD+ levels both resulting in mitochondrial energy production impairment. Several drugs such as acetaminophen, antibiotics, statins, NSAIDs and antidepressants impair mitochondrial energy production increasing the requirements of NAD+.
Another form of NAD+ precursor, nicotinamide riboside, has a much higher conversion rate to NAD+ than dietary niacin.
It can be supplemented to improve mitochondrial function. Researchers recently reported using nicotinamide riboside in a mouse that is highly susceptible to neurodegeneration identical to human Alzheimer’s. Treated mice had less mitochondrial damage and had higher rates of production of new neuronal stem cells and new neurons in the brains key memory area called the hippocampus. They also performed better on a water maze test, a standard test for memory.
Beta amyloid is an important factor in Alzheimer’s disease, but there are other factors fundamental to the process of brain cell and function loss. Mitochondrial energy production appears to be a key factor resulting in that outcome. Steps to support and restore mitochondrial energy production is an important step in treating the disease.
Another breakthrough in enhancing mitochondrial energy processing in neurodegenerative disease has been photobiomodulation, or PBM. This procedure involves using infrared diodes to target key brain areas affected by the disease. Infrared light penetrates into the brain about 35-40 millimeters, which is well into the “gray matter” (the brain neurons). The exposed neurons display a significant increase in mitochondrial energy production.
Early animal studies of PBM in Alzheimer’s disease found that in addition to increasing mitochondrial energy production it stimulated immune cells in the brain that are responsible for removing any formed beta amyloid causing them to reduce this protein in the stimulated areas. This is a double benefit in that it is beta amyloid that causes some of the impaired energy production in the beginning.
A case series treating Alzheimer’s patients with PBM produced favorable results. A major clinical trial is now underway at 8 institutions with the first location, St. Michael’s Hospital in Toronto, Canada, already in progress. PBM appears to be an emerging breakthrough in the treatment of this disease previously characterized as progressive and unresponsive to all drug treatments.
A key takeaway from all of this is that factors involved in helping mitochondrial energy production such as diet, the nutrients CoQ10, B vitamins and antioxidants, and PBM treatment offer protection against brain cell energy failure and death. These mitochondrial supplements are useful in prevention, and they are an integral part of the Bredesen Protocol™.