“One in every eight individuals above
the age of sixty-five have Alzheimer’s disease.” (Stutzmann) For the most part,
95% of the affected people contract the sporadic
type of Alzheimer’s disease (AD), where the symptoms become apparent in late
adulthood. The current therapeutic targets that exist for this condition
include: amyloid plaques, neurofibrillary tangles, cholinergic cell loss, as
well as memory and synaptic loss. Specifically, the two treatments available in
the pharmaceutical market today (known as cholinesterase inhibitors and
Memantine) address the symptoms of AD in decreasing their progression only after they have already become present
within the subjects' life. These remedies give emphasis on the late-onset
features of AD. For this reason, Dr. Beth Stutzmann sought out to develop a
treatment that avoids the rise of synaptic loss before it becomes
apparent. Synaptic loss is the only feature of Alzheimer’s disease that
directly correlates with cognitive impairment and limits the formation of new
memories.
New memories are created when
neurons, the nerve cells that transmit information throughout our bodies, are
able to receive electric stimuli and communicate among themselves to pass these
along to our brain. They are able to do so when calcium rushes into their ion
channels and thus ensues a response within them to pass along the information to
the neuron closest to it. Furthermore, the process is repeated again in the
next neuron and a cycle is formed until the stimuli reaches the brain and the
information is decoded. In AD patients, however, this communication is
disrupted, resulting in memory loss of recently acquired facts. To study how she
could stop this from occurring, Dr. Stutzmann measured calcium responses in
mice that had Alzheimer’s disease. She saw that calcium signals are much larger
in AD neurons and that this dysfunction was causing them to use up the vesicles
they utilize to transmit the stimuli in. Moreover, she discovered that they
lost vesicles in a rate that they could later not catch up with. Therefore, the
neurons are unable to replenish themselves and end up depleted of their
pre-synaptic vesicles. This leads to a decrease in neurological activity.
Consequently, a drug that restores calcium levels back to normal could help AD
individuals from suffering synaptic loss.
Membrane Potential, Ion Transport and Nerve Impulse. (n.d.). Retrieved December 9, 2017, from https://wikispaces.psu.edu/display/230/Membrane Potential%2C Ion Transport and Nerve Impulse
After various trials and errors,
she found the drug Dantrolene could serve this purpose. Not only did it restore synaptic
plasticity and calcium levels, but it also reduced the AD neurons' amyloid
levels. Presently, Dr. Stutzmann and her team are working on creating a Dantrolene-derived medicine that targets the Central Nervous System—the system within our bodies that is most affected by Alzheimer’s disease. For now, her discovery is promising and has worked in both AD mice neurons, as well as the human ones she has
cultivated in her lab.
Another encouraging discovery has
been that of the Betabloc, a vaccine
that “attacks the build-up of a protein called beta-amyloid, which forms a
damaging waxy plaque on brain cells” (Chapman, James). Just like Dr. Stutzmann's treatment, this vaccine also tackles the early-onset aspect of AD symptoms. Although it is still
being tested, they have also had positive outcomes in AD mice neurons. Additionally, they have also seen the removal of such proteins and the restoration of mental function in their second
set of safety trials with eighty Alzheimer’s disease patients. “It
would not be unrealistic to say that [they] might see a treatment within five
years.” (Cayton, Harry)
These alternatives might not cure
Alzheimer’s disease just yet, but they do promise a step in the right direction towards
achieving that purpose!
Works Cited
Chapman, J. (2014, December 21). Cure for Alzheimer's Closer. Retrieved December 9, 2017, from http://www.dailymail.co.uk/news/article-10539/Cure-Alzheimers-closer.html
No comments:
Post a Comment