Dr. Sturgill graduated from Omaha with an undergraduate and masters degree in experimental psychology. He then obtained his doctorate in cognitive psychology in California. Dr. Sturgill has been teaching at Rockhurst University for about 24 years. He currently teaches cognitive neuroscience, cognition, sensation and perception, psych of language, history of psych, stats, experimental methods, and a course at KCUMB. Dr. Sturgill has done no previous research with Alzheimer’s or other types of dementia.
When research of the brain occurs, there are three classes of subjects: lesion patients, paralogically intact, and animal models. Lesion patients are individuals who already have damage to the brain. The paralogically intact is the group of individuals with healthy, normal brains. Animal models, such as primates or rats, are used as a third group.
Alzheimer’s begins in the temporal lobe, causing problems forming new memories. Individuals with Alzheimer’s typically are fine as long as they’re in familiar surrounds because they can rely on older memories. However, problems arise when they go on vacation or visit new places. Alzheimer’s then progresses along the temporal lobe and then into the the parietal lobe, causing some spacial and motor problems. From the parietal lobe, it progresses into the frontal lobe. However, the occipital lobe seems to be unaffected.
The main differences between the early stages of Alzheimer’s disease and aging is the speed of progression and occurrence of cell death. In normal aging, Dr. Sturgill said the “processing speed of an old brain slows down, but there’s not a loss of intelligence or cognitive abilities.... The extent of cell degeneration in Alzheimer’s doesn’t occur within old ages. A scan of an old brain that is 70 or 80 years old will look healthy.” The progression of alzheimer’s is much faster than normal aging and usually occurs at a younger age than age related memory losses. The early-set Alzheimer’s occurs in the late 40’s or early 50’s, which Dr. Sturgill said is “way too early for normal age related kinds of losses.” The second kind of Alzheimer’s, late on-set, tends to present after age 65 “which is approximately the same time age related memory loss begins,” according to Dr. Sturgill. In a brain with Alzheimer’s there is lots of cell death and the guri are thin. Tau and amaloid proteins, which are related to Alzheimer’s disease, are present in all individuals. Some build up of protein occurs in old age, but not to the extent of those individuals with Alzheimer’s.
When explaining the
structure of the brain and it’s relation to Alzheimer’s Dr. Sturgill says, “You
know there are … difference in the microstructure, for instance, between the
left hemisphere and the right hemisphere in certain areas just the cell sizes
are different, their dendritic arbors
are different… so there could be something about those particular kinds of
cells that are in the entorhinal cortex and those cells that are in the
hippocampus, which are different kinds of cells… that are particularly…
producing these filament problems in the cells in generating tau.” From here we
went on to a discussion about how tau works, it has been recently been found
that tau spreads from cell to cell, which Dr. Sturgill compare to an infection.
Dr. Sturgill insisted that there had to be some role for tau and that the difference
between individuals with Alzheimer’s and people without Alzheimer’s was that those
with Alzheimer’s patients had large amounts of the tau protein. In
understanding the new evidence and knowing the pathways of the spread Dr.
Sturgill says, “they’ve known for a while that Alzheimer’s along that kind of pathway
from the entorhinal, to the hippocampus, to the medial temporal area and that’s
just where these neurons are connected one to the next. So finding that they
know how it spreads now may actually help generate some sort of a treatment to
stop it, if they can stop the spread of tau then they can stop Alzheimer’s.” In understanding this and
earlier highlighting that the occipital lobe doesn’t seem to be affected by the
disease, it easy to question why this is. Dr. Sturgill clears this up by
explaining that though there are pathways that do go from the occipital lobe to
the temporal lobe, but there are different types of cell structures that are in
the occipital cortex so proteins produced may play a role in why tau doesn’t
seem to affect this area of the brain.
When talking
about grid computing, which he knew as parallel processing, he agreed that is certainly
possible for a cure to come about as a result of a grid.
In talking about
evolution and its relation to Alzheimer’s Dr. Sturgill says, “It [Alzheimer’s] is
some kind of a mutation and if one of those mutations turned out to have some
kind of benefit in the long run,
overtime it showed up then that might be a evolutionary kind of change.” It seems
as though animals should be just as susceptible to have a neurodegenerative disease,
like that of Alzheimer’s, but we were all unsure if that is the case.
When looking at
a few possible solutions he states that the precursors of the production of the
beta-amyloid, which creates plaque in the brain, could be found that could lead
to stopping the production or overproduction of the beat-amyloid. It had been
found that a vaccine was something in the works for stopping or slowing down
Alzheimer’s. According to Dr. Sturgill “… the treatments have been aimed
primarily at neurotransmitters particularly at acetylcholine because it affects
the acetyl cholinergic system. This entorhinal cortex is very near the basil
forebrain, where the temporal lobe and the frontal cortex all come together.
The very center base of the fore brain and that’s where these neurons are the
generate acetylcholine in the basal forebrain. So right away you have this
cholinergic problem and they spread out throughout the cortex, that cholinergic
system and so then there is this loss of that acetylcholine. So trying to up
that has been one effort and what it’s done
primarily is slow down or sort of retard the time it takes for people to
be admitted to a home where they have to spend the rest of their time. That in
itself, that slowdown, saves billions of dollars in medical costs, but that’s
been primarily the effort to aim at neurotransmitters at this point.”
Dr. Strugill had
read earlier in experiment dealing with Parkinson’s disease how fetal cells
were used to combat tau proteins, but it was found that the tau proteins even
overtook the fetal proteins, which was unexpected.
We would like
that to thank Dr. Sturgill for taking his time to do this interview and for
furthering our knowledge of Alzheimer’s and how the brain works.
