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The Other Brain: From Dementia to Schizophrenia, How New Discoveries About the Brain Are Revolutionizing Medicine and Science
Our understanding of the brain is being profoundly challenged and changed by the discovery that cells other than neurons play an active role in brain functions. These cells, called glia, make up 85 percent of the brain and communicate without electrical impulses. They make up another brain, one that works independently, but cooperatively with the neuronal brain we are familiar with.
In The Other Brain: From Dementia to Schizophrenia, How New Discoveries About the Brain Are Revolutionizing Medicine and Science, R. Douglas Fields, Ph.D., a neuroscientist at the forefront of research on these long-overlooked cells, discusses how glia may cause and prevent disease as well as help the brain repair itself and the spinal cord after injury.
Glia had been viewed as merely housekeeping cells until the discovery that Albert Einstein's brain, examined thirty years after his death in an attempt to understand his genius, revealed that he had a typical number of neurons, but an extraordinary number of glia. Thus began a scientific adventure story that continues to this day. It is revolutionizing how we think about memory, emotions, drug and alcohol addiction, and consciousness.
The following excerpt is from Chapter 12, Aging: Glia Rage Against the Dying Light. In it Dr. Fields discusses how our new understanding of the four types of glial cells is expanding and shifting our understanding of the plaques and tangles known to build up in the brains of Alzheimer's patients.
Alzheimer’s: A Disease of Glia
Alzheimer’s disease destroys neurons and communication pathways in the brain. Certain parts of the brain are more vulnerable than others, notably those brain regions controlling thinking (cerebral cortex), memory (hippocampus), and fear, emotion, and aggression (amygdala). These are the main targets of Alzheimer’s disease. The disease afflicts 10 percent of us who reach the age of sixty-five. As average life spans increase through improved medicine, even more people will suffer from it. If you should reach the age of eighty-five, you will then have a fifty-fifty chance of acquiring Alzheimer’s disease. To put it another way, if both you and your spouse should survive to this ripe old age, one of you will probably suffer dementia or personality changes from Alzheimer’s disease. Age is the single greatest risk factor for this disease, which provides some intriguing biological insight into the disease mechanism.
The hallmark of Alzheimer’s disease is the senile plaques seen in brain tissue as first reported by Alzheimer in 1907 based on his examination of slices cut from Augustine Deter’s brain. These plaques are aggregates of material, beta-amyloid, that surround damaged neurons. But surrounding the plaques are large aggregates of microglia. Alzheimer himself saw and described these cells at these sites of brain damage. The plaques are also spots of intensive chronic inflammation of brain tissue. For this reason alone, it is to be expected that we should find these glial cells on the scene in abundance, but are they a part of the disease or just a response to it?
The plaques are not seen in the brains of elderly people who do not suffer dementia, so the plaques are the result of disease, not a natural process of the aging brain. The second diagnostic feature of Alzheimer’s disease is that neurons are choked with tangled bundles of protein filaments inside their cell body known as neurofibrillary tangles.
We are now beginning to realize that Alzheimer’s disease is a powerful example of what can happen to the brain and mind when the healthy interaction between neurons and glia goes awry. The neuronal damage in Alzheimer’s disease results from an attack on neurons by microglia and astrocytes that is linked to chronic, local brain inflammation. The excess beta-amyloid protein that forms the senile plaques in the brain of Alzheimer’s patients can be caused either by overproduction of the material or impaired clearance of beta-amyloid. Dysfunctional glia can contribute to the plaques in both ways. Microglia actively gorge themselves on the excess beta-amyloid, clearing it from the spaces between the neurons. This is the main reason why microglia are found in such abundance surrounding the senile plaques. However, under conditions of chronic inflammation, the ability of microglia to clear beta-amyloid from the brain is greatly diminished, so the toxic peptide accumulates more rapidly.
In addition, several neurotoxic factors are released from microglia when they are treated with beta-amyloid (the list includes reactive oxygen species, cytokines, chemokines, and others). Reactive astrocytes are also recruited to the amyloid deposits, and they probe their cellular fingers into the senile plaques to release enzymes that dissolve the beta-amyloid. Thus astrocytes aid microglia in clearing beta-amyloid from the brain.
But astrocytes also cause the death of neurons in Alzheimer’s disease. Astrocytes can generate the beta-amyloid peptide, which forms the senile plaques, by pathological processing of a precursor molecule, a protein called amyloid precursor protein (APP). This protein is cleaved by an enzyme in astrocytes to generate the toxic beta-amyloid peptide. Thus astrocytes make APP, as do neurons, and they also make the enzyme that generates the same neurotoxic beta-amyloid that is made by diseased neurons.
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