function. Research conducted over the past two decades has begun to elucidate processes associated with increased brain cell (brain neuron) damage and eventual widespread neuronal death, leading to changes in the function of specific areas of the brain and alterations in its overall architecture and appearance—the fundamental pathol- ogy, or disease process, of Alzheimer’s disease. Abnormal character- istics of the brain in AD include the accumulation in brain tissue and incorporation into plaques of a type of protein called amyloid beta (or beta amyloid protein [BAP]), the presence of tangled filament-like structures within the neurons (tau protein neurofibrillary tangles), and abnormalities in brain-cell membranes which disrupt their pro- tective function and make the cell within vulnerable to damage and destruction.
Mitochondrial Stress & Alzheimer’s Disease In recent years, a focus of AD research has been the mitochon-
dria, the tiny, complex oval compartments inside every cell in the body (except red blood cells) which are its energy-producing units. Commonly referred to as the powerhouses of the cell, they are like the energizing batteries which keep the little pink bunny going—in fact, they make more than 90% of the energy which keeps us run- ning. Mitochondria do much more than make energy, though; they have a hand in almost all of the processes that allow cells to live long, productive and healthy lives. They help the specialized cells of the liver, the heart, the kidney, and yes, the brain, to do what they are designed to do, for as long as they are supposed to do it. When mitochondria become damaged and wind down, the cell itself sick- ens, loses its ability to perform its specialized role in the body, and
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