Here is some information
on Alzheimer’s disease.
Article #1: “Alzheimer's Brain Change Measured in Humans” from Science Daily.
Researchers and
physicians at Washington University School of Medicine in St. Louis have been
able to identify amyloid beta 42 as the most probable primary cause of
Alzheimer’s disease.
It has long been
speculated that amyloid beta 42, a type of protein fragment, was the
primary cause of amyloid plaque buildup in the brain, in addition to its
counterparts amyloid beta 38 and 40, during the onset of Alzheimer’s disease.
Autopsies of Alzheimer’s patients have shown overwhelmingly larger volumes of amyloid
beta 42 in comparison to other amyloids, but medical professionals were unable
to determine if the amyloid beta 42 was synthesized before the onset of
Alzheimer’s disease thus causing the disease itself, or if it was a byproduct
amyloid synthesized during the the later stages of the disease.
The production of
amyloid beta 42 had never been properly observed in living Alzheimer’s patients
until recently. Researchers at the University of Washington in St. Louise have
been able to confirm that amyloid beta 42 synthesizes before the onset of
Alzheimer’s disease, and is likely to be the primary contributor in the
development of the amyloid plaques that cause the disease.
This recent breakthrough
is key to understanding how Alzheimer’s develops, as well as how it advances.
Now that researchers have been able to pinpoint a primary contributor of
Alzheimer’s disease, they can potentially develop preventative treatments, as
well as various medications that could directly halt the progression of the
disease altogether.
A cure is still a long
ways away, and damage that has already been inflicted is going to be near
impossible to heal, but researchers are heading in the right direction when
attempting to understand Alzheimer’s.
Article #2: “Stress Hormone Could Trigger Mechanism for the Onset of Alzheimer's”
from Science Daily.
Researchers at Temple
University have been able to connect the stress hormone Corticosteroid with the
rapid degeneration of neurons, during Alzheimer’s Disease.
Corticosteroid is a
hormone that is released into the bloodstream as a stress response. It is a
relatively common hormone, but to the surprise of researchers, the hormone was
found at levels that are two to three times higher in Alzheimer’s patients, as
opposed to non-Alzheimer’s patients. Upon conducting a series of experiments,
Temple University Researchers were able to discover that Corticosteroid caused
the brain enzyme 5-lipoxygenase to overexpress, therefore resulting in
increased levels of the enzyme.
This is significant due
to the fact that the brain enzyme 5-lipoxygenase has been linked to the
production of tau protein. Tau protein and amyloid beta plaques have been
identified as the two primary contributors to the onset and progression of
neurodegeneration and neuron death in Alzheimer’s patients. The fact that
Corticosteroid causes the enzyme 5-lipoxygenase to increase in presence and
activity directly links the hormone to the production of tau protein. This in
turn links the hormone to the progression of Alzheimer’s as a whole.
In addition to this, the
experiments showed that Corticosteroid caused the brain enzyme 5-lipoxygenase
to release tau protein in the areas of the brain responsible for memory,
learning, and cognition. Researchers now have strong reason to believe that
Corticosteroid elevation results in the onset of early memory problems
associated with Alzheimer’s patients.
Now that there is a
definitive relationship between Corticosteroid and the progression of
Alzheimer’s disease, scientists and researchers alike can start experimenting
with drug that effectively limits or controls Corticosteroid levels. This may
result in the development of a treatment that is capable of suppressing or
halting the memory loss associated with Alzheimer’s disease. Regardless of what
is brought about by this researcher, we are one step closer to understanding
Alzheimer’s.
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