Alzheimer’s brain: Changes do occur.
In the Alzheimer’s brain nerve cells stop functioning, lose connections with each other and ultimately die. The death of neurons in key parts of the Alzheimer’s brain causes those areas to shrink and results in substantial abnormalities in memory, thinking and behavior.
The Alzheimer’s early symptoms are derived from the destruction of neurons in particular parts of the Alzheimer’s brain controlling memory, especially the hippocampus (which is why the early signs of Alzheimer’s are related to memory impairment). As nerve cells in the hippocampus of the Alzheimer’s brain break down, short-term memory fails and the ability to do familiar tasks begin to decline as well.
The disease begins to attack the cerebral cortex which is responsible for some of the higher memory functions, such as language, reasoning, perception and judgment. Sometimes, unwarranted emotional outbursts (known as catastrophic reactions), and disturbing behaviors such as wandering and episodes of extreme agitation may appear after the early symptoms of Alzheimer’s appear.
Tangles and plaques in the Alzheimer’s brain:
Amyloid plaques and neurofibrillary tangles are some of the hallmarks of the changes that take place in the Alzheimer’s brain. Although, these changes may only be confirmed at autopsy, they are found in virtually every patient with Alzheimer’s disease. At the present time, it is not clear whether these abnormal deposits are the cause or byproduct of the disease process in the Alzheimer’s brain, although researchers have now come to understand how plaques and tangles are formed. The increasing knowledge in the area of Alzheimer’s disease has helped with new attempts to block the underlying disease process that may lead to their buildup. The eventual success of these strategies may ultimately provide the basis for prevention or treatment in the future, if these plaques and tangles are determined to be the cause of Alzheimer’s disease.
Amyloid plaques are known to develop in areas of the Alzheimer’s brain related to memory, and are believed to be a mixture of abnormal proteins and nerve cell fragments. They may develop from beta-amyloid, a protein that breaks off from a larger amyloid precursor protein. Beta-amyloid is formed when the amyloid precursor protein that is embedded in the cell membrane is broken down for disposal. Enzymes called secretases split the protein in two and form the beta-amyloid fragment in the Alzheimer’s brain.
Research into the Alzheimer’s brain has recently identified secretases as one of the “cleaving” enzymes. They are believed to cut amyloid precursor proteins in a place that cause beta-amyloid to become insoluble and form deposits in the brain of the Alzheimer’s patient. Investigators are now beginning to suspect that by blocking the activity of beta secretases you may prevent the production of undesirable forms of beta-amyloid. Current experiments are now underway to prove this hypothesis. It is still a mystery however of what happens to the beta-amyloid segment once it separates from the amyloid precursor protein, and why it may lead to these changes in the Alzheimer’s brain.
Neurofibrillary tangles are the other major pathological change characteristic of Alzheimer’s disease. These tangles are composed mostly of the protein tau, and are twisted, hair-like threads that remain after the collapse of the neuron’s internal support structure, which are referred to as microtubules. In healthy neurons, microtubules carry nutrients from one destination to another similar to railroad train tracks. Tau seems to serve as supporting “railroad ties”, but in the Alzheimer’s brain the protein becomes hopelessly twisted and disrupts the function of the microtubules. This defect is believed to clog communication within nerve cells, and eventually lead to cell death.
What is the deal with Pinl?
Alzheimer’s researchers are not sure why tau goes awry, but some of the more recent findings are beginning to state that Pin1 may play an important role in keeping the tau intact. When Pin1 binds to an altered tau in experiments, the protein begins to function as it should and microtubule assembly is restored. Also, researchers have began to find substantially lower levels of Pin1 in Alzheimer’s brains as contrasted to healthy subjects. While the significance of these findings is not certain, the presence of an enzyme such as Pin1 may help to maintain or restore the proper function of tau, and prevent the formation of neurofibrillary tangles. This possibility raises the hope that therapies might be developed in the future to keep tau functioning in the Alzheimer’s brain.
Neurotransmitters in the Alzheimer’s brain.
Another characteristic of the Alzheimer’s brain is a reduction in the level of certain neurotransmitters that are necessary for healthy brain functioning. Acetylcholine is produced in the brain by cholinergic neurons, which is a neurotransmitter that is believed to be crucial to memory and learning. These neurons are in abundance in the hippocampus and the cerebral cortex, which are two regions of the Alzheimer’s brain most ravaged by the disease. (As is true for the plaques and tangles, it is not known currently whether neuronal loss in these parts of the brain is a cause or an effect of Alzheimer’s disease.)
As the disease continues to progress in the Alzheimer’s brain, acetylcholine levels drop dramatically and dementia becomes more pronounced. The levels of serotonin, norepinephrine, somatostatin, and GABA, which are neurotransmitters involved in many aspects of brain functioning become diminished in at least half of the patients with Alzheimer’s disease. Such imbalances may lead to depression, aggression, insomnia and other mood and personality changes.
Some information from The Johns Hopkins Medical Guide to Health After 50
Additional information and webpage by Paul Susic Ph.D. Licensed Psychologist