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Alzheimer's Brain: Degenerative Changes Page #2
 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.
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.
Information from
DSM-IV-TR Mental Disorders : Diagnosis,
Etiology & Treatment by Michael B. First and Allan Tasman
Additional information and webpage by
Paul
Susic M.A. Licensed Psychologist Ph.D Candidate (Geriatric
Psychologist)
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