Recently
we were visited by Dr. Roberto Fernandez-Romero who presented his research on
Alzheimer’s Disease which effects an estimated 5.7 million people in the United
states alone. Which is quite the infamous disease as of late. Dr.
Fernandez-Romero detailed the progressive pathology of Alzheimer’s disease. He
explained this is a neurodegenerative disease, that usually occurs once someone
reaches their older life, generally around the age of 65, and dementia is one
of the signs of the emergence of the disease.
He
explained how the proteins Beta Amyloid and Tau are proteins that maintain microtubule
structure and transport. When these proteins begin to malfunction, they form
plaque within the brain, which then ends up blocking transmission at the
synapses resulting in the inhibition of brain activity. This plaque often starts
in the medial temporal lobes and progress toward the parietal and temporal,
which is the memory center of the brain. Which is why dementia occurring.
Something of note that Dr. Fernandez explained was the visuospatial symptoms
that are prevalent in over a third of the patients with Alzheimer’s disease. He
explains the relevance of the visuospatial symptoms in terms of Alzheimer’s
since it is used to help identify faces, while the dorsal region is used for
attaching meaning to locations of objects. When posterior cortical and the
parietal lobes begin to atrophy the degeneration of these networks occur. Dr.
Fernandez-Romero wanted to find markers of network degradation by age and stage
by correlation them to errors in the simulator.
He
tested this Dr. Fernandez-Romero had subjects perform simulated driving tests
where they would have to remember how to get to and from certain locations in
the simulation. He observed many memory errors and accidents that occurred
within the simulator to tests the participants to create and retain a temporary
visuospatial memory map. The participants varied in age and had different
stages of Alzheimer’s disease. The whole point of this was to mimic how some
Alzheimer’s patients would be driving and then suddenly forget where they are
going or were they are at while driving. Even if they have done so before.
One
thing that Dr. Fernandez-Romero made note of was that the reason for Alzheimer’s
is due to the amyloid buildup. In a study conducted last month by the National
Institute on Alcohol Abuse and Alcoholism they saw that one night of sleep
resulted in an immediate increase in beta-amyloid, which is one of the protein’s
that Dr. Fernandez-Romero stated causes a plaque buildup in the brain which is
thought to be the source of Alzheimer’s. The researchers used PET scans on 20 healthy
subjects. They saw a 5% increase in of beta-amyloid after the participants have
been awake for 31 hours straight. This could help shed some light as to why so
many people have this disease, especially scary for college students. Who tend
to essentially put off sleep in favor of studying for class.
On a
sadder note, a drug that showed promised has failed in a large scale clinical trial
that was conducted by Eil Lilly. The drug, solanezumab was used to treat
patients with mild dementia. It failed detailing how by that time it might to
extensive of a damage. The drug worked by attacking amyloid plaques. Although,
it was thought this type of buildup is what causes Alzheimer’s disease, it
seems that no drug that that removes or prevents the plaque build has shown any
promise as a real treatment. Apparently, some experts in Alzheimer’s weren’t too
surprised that it wasn’t effective. They believe that this reflects that the
disease is due to “multipronged cascade of causes, including amyloid buildup.”
This could also be since that Alzheimer’s pathology begins damaging the brain
long before the symptoms emerge. Detailing how complex this disease truly is; there
might be other factors besides that amyloid buildup and how it could be too
late to actually treat once it appears.
Fernandez, Roberto, and Charles J. Duffy. “Early
Alzheimer's Disease Blocks Responses to Accelerating Self-Movement.”
Neurobiology of Aging, vol. 33, no. 11, 2012, pp. 2551–2560.,
doi:10.1016/j.neurobiolaging.2011.12.031.
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