Alzheimer’s
Disease (AD) is still quite a mystery in the neuroscience and medical
fields. While knowledge of the cause is
still incomplete, awareness and technology for the disease are starting to
develop. Specifically, a gene connected
to familial AD, ApoE4, has been found and is detectable through genetic
testing. Therefore, people with family
members affected by the disease are able to know if it is genetic and has been passed
on to them. There is a lot of debate
about whether or not this knowledge is a good thing. Coping with the fact that your brain is sure
to fail is not easy. Many people
struggle immensely with that information.
However, others become motivated and are able to turn their lives
around. They work to lower every other
risk factor that could increase the severity and speed up the process. Healthier living can help with those things,
but unfortunately genetic effects will eventually take their toll. There has recently been a push for an
affordable diagnostic test. Bill Gates
is even donating to research in order for this to happen. Researchers are specifically looking for a
blood test that would be able to detect and diagnose early signs of AD.
Beth
Stutzmann is also studying Alzheimer’s Disease in her lab. Although only around five percent of AD cases
are familial, that is the form that can most easily be studied in a research
setting. Dr. Stutzmann and her team give
mice a gene similar to ApoE4. They are
then able to analyze AD neurons and directly compare them to unaffected neurons. Her team is specifically looking for
therapeutic targets for AD. The only
option that has worked is to target the synaptic loss that then leads to memory
loss. Targeting amyloid plaques,
neurofibrillary tangles, and cholinergic cell loss has led to failed trials and
masking of symptoms but no treatment. In
addition, plaques and tangles are such late mechanisms in AD, that it would
make more sense to target earlier mechanisms.
Synaptic change and loss show up before tangles and plaques. In their
quest for variables of synaptic change, Dr. Stutzmann and her team have found
that calcium signaling differs in AD neurons.
An unaffected neuron has a normal influx of calcium in the presynaptic
terminal when an action potential reaches it.
They found that an AD neuron has a much higher influx of calcium in the
presynaptic terminal when the action potential reaches it. They then noticed that the number of synaptic
vesicles is much lower in AD neurons.
Therefore, those neurons cannot send as many signals as unaffected
neurons. Plasticity and the ability to
change and grow is essential to neuronal development, but AD neurons are less
able to do this. Dr. Stutzmann and her
team are, thus, looking at developing medications that normalize the calcium
response in early AD neurons.
These two approaches
work well together in their future-oriented research for technology and
treatment of AD. Genetic and blood
testing will be a great early detection system for AD. Then, Dr. Stutzmann’s research will eventually
provide a medication to slow or halt the progression of AD on neurons early
enough in the process of the disease to catch it before the life-altering
symptoms begin.
Article:
Kennedy, Pagan. “What If You Knew Alzheimer’s Was Coming for
You?” The New York Times,
The New York Times, 17 Nov. 2017,
Dr. Stutzmann’s Research:
Chakroborty, Shreaya, et al. "Early Presynaptic and
Postsynaptic Calcium Signaling
Abnormalities Mask Underlying
Synaptic Depression in Presymptomatic Alzheimer's
Disease Mice." The Journal
of Neuroscience, vol. 32, no. 24, 13 June 2012, pp. 8341
8353. EBSCOhost,
doi:10.1523/JNEUROSCI.0936-12.2012.
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