Brain Power Repair for Alzheimer's

A Brain Fried in Cortisol


So what happens in the brain of an Alzheimer’s patient? On a physical level, it appears that nerves in the Alzheimer’s brain die, severing important links between two sections of the brain (the forebrain and hippocampus) responsible for thinking and memory. These nerves become encrusted with protein deposits which turn them into dysfunctional tangled masses of abnormal fibers. These “neurofibrillary tangles” occur most often in the hippocampus, the brain’s memory center.

Brain autopsies of Alzheimer’s patients also show strange plaques and lesions, which are clots of dead cellular material. Innumerable brain cells wither and die in the Alzheimer’s brain as their dendrites (the multiple branching connections between nerve cells) disappear. There also can be up to a 90% decline in the levels of an important brain chemical called acetylcholine, considered to be the prime molecular carrier of memory.

Scientists have a somewhat better idea as to what causes Alzheimer’s than they do about its treatment. For one, there might be a genetic factor. It appears that individuals with two particular genes (called ApoE-4) are eight times more likely to develop Alzheimer’s than those who don’t have them.

For another, there is a heart factor. A newly identified high-risk population group is people who have some degree of pre-existing vascular disease. A lack of oxygen to the brain is strongly linked with the typical Alzheimer’s symptoms. Brain autopsies of people with Alzheimer’s have shown they tend to have had a much higher incidence of strokes, says Dr. Khalsa.

Another consideration is this: does the patient really have Alzheimer’s? Several other clinical and treatable conditions can mimic the primary symptoms of Alzheimer’s and must be ruled out before the diagnosis is valid, Dr. Khalsa explains.

For example, it’s estimated that 20% of suspected Alzheimer’s patients actually are suffering the effects of multiple minor strokes; another 20% are reaping the negative results of “lifestyle errors” (substandard nutrition, excessive alcohol intake, recreational drug use), and another 10% have clinical depression. Symptoms of cognitive impairment can also be produced by chronic food allergies, exposure to environmental chemicals (lead, arsenic, aluminum), and mercury toxicity (from dental amalgams).

Of the suspected causes of Alzheimer’s and its precursor, age-associated memory impairment, one factor is gaining ever stronger emphasis: “a lifetime of chronic, unrelenting stress,” says Dr. Khalsa. Stress is blamed for so many medical conditions, it sounds almost trivial to link it with Alzheimer’s, but there is a demonstrable hormonal basis.

This stress excess releases inordinate amounts of cortisol, a hormone produced by the adrenal glands. Cortisol is naturally released by the adrenal glands in response to stress. In moderate amounts, it’s not harmful. But the brain’s chronic exposure to toxic levels of cortisol, due to daily stress, injures, even kills, brain cells “by the billions,” says Dr. Khalsa. “I believe that cortisol toxicity is one of the primary causes of Alzheimer’s.”

Clinical studies show that cortisol damages the nerve cells of the hippocampus and blocks their ability to absorb blood sugar (glucose), the brain’s sole nutrient. Brain scans of Alzheimer’s patients show that their temporal lobe (site of the hippocampus) and frontal lobe both have a decreased capacity to absorb glucose. Cortisol blocks the delivery of glucose to the mitochondria, the “energy factories” of all cells.

Cortisol also impedes the smooth functioning of the brain’s messenger chemicals called neurotransmitters. Information that is supposed to jump from one nerve cell to the next doesn’t, and you start forgetting names, faces, and contexts. These chemical abnormalities lead to the brain being flooded with calcium and free radicals (toxic substances that damage cells) and the free radicals further damage the mitochondria.

Eventually, nerve cells swell, then shrink, then often die, especially in the hippocampus and amygdala (part of the temporal lobe). “Because these are the primary ‘sorting and shipping’ areas for memories, memory is particularly damaged by cortisol during the aging process,” Dr. Khalsa says.

The net result is a serious decline in one’s ability to lay down new memory, to effectively remember things, and to remain emotionally calm and even. A recent Canadian study showed that those patients with the highest level of cortisol elevation after a four-year period had a marked deficit in memory function, such as remembering previously learned information, Dr. Khalsa reports. Put differently, “increases in these patients’ cortisol levels accurately predicted decreases in memory and cognitive function,” he says.