xt78gt5ffp7w https://exploreuk.uky.edu/dips/xt78gt5ffp7w/data/mets.xml University of Kentucky. Office of the Vice President for Research and Graduate Studies Kentucky University of Kentucky. Office of the Vice President for Research and Graduate Studies 1994 volumes. Call Number: LD2762.9 .K38c. Accession Number: 2018ua049 journals LD2762.9 .K38c English Office of the Vice President for Research and Graduate Studies  Contact the Special Collections Research Center for information regarding rights and use of this collection University of Kentucky Odyssey Magazine Research -- Kentucky -- Periodicals Education -- Research -- Periodicals Research -- Kentucky Odyssey: The Magazine of University of Kentucky Research, Summer/Falll 1994 text images Odyssey: The Magazine of University of Kentucky Research, Summer/Falll 1994 1994 1994 2026 true xt78gt5ffp7w section xt78gt5ffp7w  

    

 

/./THEMAGAZIN'I;I: UNIVERSITY OF KENTUCKY RESEARCH 0 SUMMER/FALL 1994 o

 

 

 Cover Illustration
Once again we feature the topic of
Alzheimer's disease in ()rb'sset'. it is a
natural area for us to cover. since we have
one of the premier centers in the nation for
the study of aging. The Alzheimer’s research
featured in tltis isstte may be among the most
significant work on this disease in recent
years, A inultidisciplinary team of lil’x’ re
searchers will take you through some of the
complex processes that led to a significant
new discovery that focuses on cell death in
Alzheimer‘s. The bottom line of this rev
search, though. is people—that this
deadly disease can and will affect many
of us. That is what our cover, full of
people like you and me, indicates,
This disease makes us all vulnerable.

  
 
  
 
 
  

 

he l'niversity ofKentuckv, tlte com—
monwealth‘s gradttate education
and research institution, exists to pro
vide opportunities for the education,
personal growth and development of
indhiduals and to contribute to the

improvement ofsocietv.

With this mission as its premise. one
goal of the universit) is to condtict
prt igramsofbasic and applied research
which support graduate and profes-
sional education, provide for the ad-
vaucetnent of knowledge, and seek
soltttions for the acttte problems of
societ}.

The university's research mission
also acts as a magnet for attracting top
graduate students who want to partici-
pate in nationallv competitive research
projects.'I‘hisresearchexperience can
offer them a significant advantage in
their edttcation while laving tlte foun-
dation for future research and devel—
optnent. ODYSSEY. through articles
about various research projects and
graduate education programs, reflects
the breadth of the universitv s searclt
for new knowledge and the myriad of
research endeavors underwav The
progress that the university has made
toward achieving its research mission
and securing the extramural funds
required to support these types ofen—
deavors would have been impossible
without the talents and dedication of
our researchers.

The goal of ODYSSI'Jl'is to offer the
reader the opportunitv to share in
sortie of the excitement. curiosity and
creatitiu evident in the research un-
detwav at the l'ni\ ersitv of Kentucky.

 

 

  

 

Bug Love?
we Kiosk, [)2 7

Volume XII, No.1

(”MKS/{l is published by the
Office ol’ the Vice President for
Research and Graduate Studies
Each issue ()1’ ()[))'.\'.S'Iil‘describes
(with a ten olthe many L'niyersity
of Kentucky research projects un-
derway in a Variety of areas.

Requests for permission to re-
print material and readers. com-
ments regarding ()l))l\l\'[§l'are \vel-
come and should he sent to the
Editor. (1t)rnnnmieationsan(l.\(l-
\aneenient. L'niyersity of Keir
lucky. Lexington 40506-0057
(phone (306 '257-8297).

The publication of ()[))'.S'Slfl'is
not linaneed bythe State (‘weneral
Fund.

Editor: Susan Hodgeus Slempel
Assoc. Editorrletl Worley
Designer: Shear & Shear
Publications Asst.: Lisa D. Irizer
Staff Writer: (lraharn Shelby
Contributing Writers: Sharon
Reynolds. Ruthie leisliri. Kathy
lrarkin, Barbara (Lreider
Photography: Alix Roughen, Lee
Thomas

Printing: Merrick Printing Inc,
(oner Photo by lee Thomas
@1991 L'niyersity of Kentucky.
All rights reserved.

 

    

 

Science Boom, [1. 8

 

Working toward (1 Flt/1117’
with A/Iemory, /’~ 2

Contents
Alzheimer’s Breakthrough:

 

 

 

 

 

 

Working toward a Future with Memory 2
Science Boom 8
College Degree and Flexibility

Keys to American Job Future 12
Launching Capsules into Inner Space 14
Honorable Mention 30
Kiosk: Bug LoyeP, Defining Mental Disorder,

Improving Farm Safety and Health, and More... 27

 

Update:
Snuffing Out Tobacco Use among Adolescents

Us}
Jr

 

autumn Archlves
“mm. l. Kérag Library - North
Ural/(wry o? Knack)»:

Lexingon, K ”tricky ’5?

 

  

Alzheimer’s Breakthrough:
Working toward a
Future with Memory

lat/elfubrlo

 

UK Researchers Develop
“Shrapnel Model” to Explain
Plaque Formation and Cell
Death in Alzheimer’s Disease

S c [emf/1c Brett/em rough.

This phrase is almost surely gttaranteed to
make a scientist cringe under its weightiness.
its unequivocal claim. And Allan Butterfield.
a professor of chemistry and head of the
Center for Membrane Sciences at the Uniyer-
sity of Kentucky. knows this isn't a phrase to
he tossed off lightly.

“A group of us here in the last few months

have made some yery exciting dis:
“This dehumanizing (125de lcoveriesahouthowhraincells
are killed in the piocess of
[Alzheimer’s disease] 2's byfd?" Alzheimer's disease." says
Butterfield. "This is a hreak—
the most threatening gpzdgmzc through in the understanding
, _ ” of this disease." This dehu-
we have m OUT nation. manizing disorder is. accord
NIH Director T. Franklin Williams ing to NIH Director T. Franklin
Williams, “by far the most
threatening epidemic we have

in our nation."

The result of a team effort at UK. the
“molecular shrapnel model” of brain cell

 

 

ODYSSEY 2

 

 

‘ [0/112 (Hartley. [)1](l)‘)ll([('()/()g:\', has been working/m

I 5 years 1‘0 riisnmer 110w oxidalive mrlimls damage
neurons.

death in .~\l‘/.heimer's disease \\ ill for the first
time. liutterlield says. permit a rational ap~
proach to therapy in this disorder. This model.
he emphasizes. was dm eloped through a
multidisciplinary approach. The I ‘K research—
ers inyolyed include ‘lolm Carney. an associe
ate professor of pharmacology. Mark .\lattson.
a neurohiologist and associate professor at
the Sanders—Brown Center on Aging. and two
graduate students whose PhD. dissertations
are focused on this research—KennethI iensley
and Marni Harris.

T be Challenges of Alzheimer’s

The {K group‘s findings. which were puh-
lished last April in the Proceedings off/ye
.Vclz‘l'o/m/ Academy of Sciences. hold signifi-
cance for the millions of Americans projected
to he stricken with Alzheimer's in the decades
to come. By the turn of the century. it is
estimated that fiye million Americans will he
diagnosed with the disease; hy the year 2050.
the numher of older Americans with
Alzheimer‘s is expected to he hetween 7.3
million and 1+3 million. depending on the
rate of population growth. There are now
approximately four million Americans with
the disorder. Alzheimer‘s is the nation‘s fourth
leading cause of death. accounting for some
100.000 deaths annually. Only heart disease.

.‘l/l‘.\‘l\’(11((Q/)(‘II

 

 

  

Allan Buller/ield, (lirerlorof L’K’s (lemma/Mem—
brane Sciences, says that [he Iherapeulic implica—
tions ofthe group is discovery are potentially
sight/[can]: “l/Lyou can interfere with this free
radical damage, or pnmml it, you could, in prin—
ciple. modulate this disease tremendously. ”

cancer and stroke claim more lives.

Although the cause. or. more likely. causes
of Alzheimer‘s haven't yet been pinpointed.
the disease has two unique physical features.
always found together abnormalities in the
brain called plaques (clumps ofbeta—amyloid
protein outside brain cells) and neurofibril—
lary tangles (shriveled strands resembling
bundles of straw inside damaged neurons).
These two features have constituted a nag—
ging mystery that has impeded the search for
what triggers Alzheimer's. because research-
ers haven‘t been able to determine whether
the plaques and tangles cause the disease or
are simply its byproducts. In recent years.
Butterfield says. much Alzheimer‘s research
has focused on the beta—amyloid protein. a
peptide (a series of amino acids) that is the
core block of the plaques.

“The odd thing about this peptide." says
Butterfield in explaining his thinking process
that led to the group‘s shrapnel model. "is that
no matter what you try to do to dissolve it. you
can‘t do it. As a chemist and a membrane
scientist. I asked myself. ‘How can you ac
count for this?‘ The only answer I could come
up with is that the peptide was forming
covalent bonds—very strong chemical asso—

 

 

xl/IZV Rang/Jen

 

ciations. ‘And how are covalent bonds formed?
I asked. The answer that occurred to me is by
peptide free radical reactions."

Free radicals, Butterfield explains. are mol-
ecules with one or more unpaired electrons.
an imbalance that causes them to be extremely
unstable. "Nature abhors haying unpaired
electrons." says Butterfield. "So free radicals
are very reactive because they are always
trying to either give up or accept an electron."

Butterfield made this intellectual connec—
tion while walking one day from the chemistry
building to his "third or fourth" meeting ofthe
day. “I couldn‘t wait to talk with ~lohn lCarneyl
and to Mark [Mattson]." Butterfield says. "And
to Kenneth Hensley, a grad student from
Ashland who ended up contributing a lot to
the project."

"I was immediately excited about this."
Carney says. "We were over in the chemistry
lab the next day to see if the beta peptide
formed a free radical. and we found that it
did." Carney explains that free radicals can be
determined in solution by use of electron
paramagnetic resonance spectroscopy. or EPR.
equipment purchased a few years ago as a
result of the states 820 million bond issue.
Though you can't literally see free radicals.
they do give off signals that can be read like
a fingerprint. Each free radical can be seen as
a unique graphic representation. so Butterfield
and Carney knew, after checking their library
of “fingerprints." that what they were detect-
ing had to come from the beta peptide.

"It turned out." Manson says, after the three
researchers did more control experiments.
“that other peptides also form free radicals.
But they don‘t damage cell proteins the way
the beta amyloid peptide does. Only amino
acids in the sequence of the beta peptide
damaged enzymes and inactivated them. I‘ve
never seen Allan quite so exuberant. and at
this point. I got pretty excited too."

For Mattson. who has spent the past seven
years studying the mechanisms involved in
the death of nerve cells in the brain. the
fragmentation of the beta peptide into free
radicals was a missing piece ofthe neurotoxic
puzzle he had put together. In a paper authored
by Mattson and several co—researchers which
appeared in 'l’rencls in .VezIroscl'ences last ()ce

t'UH/lHl/(‘l/ on page 71

 

Alzheimer’s is the
nation ’5 fourth
leading cause of
death, accounting
for some 100, 000
deaths annually.
Only heart dis—
ease, cancer and
stroke claim more
lives.

fl ODYSSEY

 

  

“Call it brain
rust. In many
ways the process
of protein aging
involves iron
inside the cell
promoting oxida-
tion. So the iron
is actually rust-
ing the protein. ”

John Carney,
UK Department of
Pharmacology

ODYSSEY 4

 

tober. he shows how the amyloid beta pep—
tides break off from the larger protein. collect
outside the cell. and stick together. This
"aggregate” of the peptide is extremely toxic
to nerve cells. His research shows that it then
attaches to the cell. which needs relatively
little calcium to function. damaging proteins
that are involved in keeping calcium out. The
barrage of calcium into the cell kills it.
"The new thing we found.“ says Manson.
“is that this peptide—after it breaks off—
fragments into smaller reactive pieces, or free
radicals. Because the nature ofthese radicals
is to pair up. we think now that they specifi—
cally attack the cell membranes. substantially
damaging them." Butterfield‘s discovery of
free radical formation and the ability ofthese
radicals to damage the cell membrane. thereby
allowing calcium to leak in. explains how the
beta peptide works to kill cells. This discov—
ery was the missing piece of the puzzle.

Combining Years of Expertise

This leap forward in understanding how
brain cells are undermined was possible
because of a lot of preliminary groundwork
and the combined expertise of the researclr
ers. “What coalesced at UK." says Carney. "is
a synergy of expertise. We‘re lucky to have
people here in different but related disci—
plines. people with a lot of experience under
their belts to help enlarge findings from
another area."

Butterfield's experience includes the use
of EPR to study membrane abnormalities in
degenerative neurological disorders, includ‘
ing Alzheimer‘s disease. Carney has been
examining protein oxidation in stroke for
many years. “We knew from previous studies
of Alzheimer‘s brains that there was an age—
related increase in protein oxidation and loss
of critical enzymes." Carney explains. “The
central question was, How did the cell be—
come oxidized?" Manson has been working
for the past seven years—sometimes in col—
laboration with Carney—on how brain pro—
teins protect nerve cells against stroke in
animal models. “What we‘ve learned from
this research," Mattson says, “is that certain
proteins prevent elevation in calcium levels
by sort of scavenging up free radicals. The

 

 

Mark .\ Iattson, who works al ('K’s Sariders-Brown

(Jen/er on Aging, was one oft/1 tee researchers in the
l S. to reeeirte [he I 992 illetmpolilan 14/2» Foam/av
tion Ii’esearrh Award. and the $5100, 000 grant that
goes along with it.

proteins are able to do this by increasing
production of antioxidant enzymes."

“Anti—oxidants." Butterfield explains. are
molecules that can destroy these damaging
free radicals. "How do you explain why an
old person gets Alzheimer‘s and young people
don‘t?" Butterfield asks. “The answer is. in all
likelihood. that as young people we have a
tremendous amount of anti—oxidant strength
within our system. But as we get older our
genetic machinery winds downw—the ability
to reproduce these beneficial chemicals weak—
ens and free radicals more easily subvert the
brain‘s cells."

The analogy of the brain as a machine that
wears down seems to be a recurring analogy
in their talk. Hensley. whose l’hl). disserta—
tion deals in part with the role of oxygen
radicals. explains the importance of the
body‘s ability to control oxygen levels. "For
a good many years.” Hensley says. "there has
been a hypothesis that aging and Alzheimer‘s
disease have one commonality—the body
loses its ability to defend against oxidated
stress. We obviously need oxygen to live.
but the reactions that oxygen undergoes in
the body have to be carefully controlled or

 

 

 

  

else your body begins to produce oxygen
radicals which escape and can then damage
cells."

"Call it brain rust." says Carney. "Ifthe brain
gets too much oxygen that's essentially what
happens," Carney adds that this comparison
is particularly apt because rust is iron oxide.
or oxidized metal. "In many ways the process
of protein aging involves iron inside the cell
promoting oxidation." Carney says. "So the
iron is actually rusting the protein,”

What Causes Alzheimer’s?

Researchers investigating possible causes
for Alzheimer‘s have from the beginning
looked for common traits in the various
explanations of why people get the disease.
even while acknowledging that Alzheimer‘s
is almost surely multicausal. Perhaps the most
important result of the Hi group‘s research.
Butterfield says. is that their work for the first
time puts Alzheimer's disease into a single
theoretical framework. accounting for what
other scientists have observed in making
various suppositions about what causes the
disease.

Some researchers believe. forexample. that
at least some cases of Alzheimer‘s disease
may result from an inherited defect in mito~
chondria. the oxygenrdependent energy fac—
tories in cells. Other scientists have put forth
the idea that membrane defects may be the
main cause of Alzheimer's (in fact. the first
researchers to do so [in 1980] were Butterfield
and William Markesbery. director ofthe Sandi
ersrBrown Center on Aging at ITK), Still other
researchers point an accusing finger at disoi>
ders of the immune system or at trace metals
such as aluminum or mercury—found by
some scientists in high concentrations in
amyloid plaques during autopsy ofAlzheimer’s
victims.

One other leading theory has been that
Alzheimer‘s is genetic. Allen I). Roses. a
neurology professor at Duke I'niversity. be—
lieves that late—onset Alzheimer's is of genetic
origin. His research indicates that the gene
responsible is located on chromosome 19.
and that it is some sort of ”housekeeping gene
that is supposed to keep cells tidy and opera—

 

tional but burns out with age." Roses adds
that. "We could all potentially develop the
disease by 120 years of age." but that "since
none of us live that long what we see is the
beginning of the curve—patients who begin
to display symptoms in their ()Os. 70s and
80s."

Roses. in a study reported last November.
showed that a rare form of a gene called
apoEZ appears to protect people from devel—
oping Alzheimer's disease. But people with
another form of the gene. apoF/i. were at
substantially greater risk of developing the
disease. This discovery. for the first time.
offers the possibility ofdeveloping a drug that
would copy the natural protective action
against Alzheimer‘s that may be provided by
the apoIZZ gene. The Duke research. which
has been verified by others. shows that people
with two copies of the E4 gene had 11 to 17
times greater risk of developing Alzheimer‘s.

"I hope it doesn‘t sound too grandiose to
say this." states Butterfield. “but a real strength
of our shrapnel model is that it accounts for
various abnormalities of Alzheimer‘s disease

 

Incidence Expected to Increase

The («limo/Ml number o/‘lmzs‘ons 65 and older i n [be I'niml States will]
Alzlzwinzt’rk~ disease (AD) zoos 2.88 million in 1980. T/iw numbm‘ 11ml rismz lo
about 4 million by l 990. By llwymr 2050. the number ofolzlwAmericans
toil/1A1) is (’X/N’fll’fl (0 b1) bletwn 7.5 million and 14.3 million, (lopomling on
the mic ofpo/mlalion growl/z.

   

20
Census projection of population growth
Low
1 .
Middle
E
.g
g 10
3
'§
.E
%
E
E
a
7
0
Year 1980 1990 2000 2010 2020 2030 2040 2050

  
  

rtm'vllamx» to Hi» l mtul Vol/i."
\\.. \.- 3. l"“‘l‘

iX/rlttu‘. llNlH \. lemma/1;. " i '

llic \l: .

S ODYSSEY

 

  

Ally [toughen

 

 

Ken nelh Hensley, from
Ashlanrl, Kentucky,
plans to complete his
PILI). work in chemistry
in the/all of I 995.
Marni H(1nis,_/i"oni
Irvine, California, hopes
to receive her doctorate
in pharmacology next
spring. Both were in—
strumental in helping to
develop the group ”s
molecular shrapnel
model of cell death asso—
riaterl with Alzheimm‘is
disease.

ODYSSEY ()

 

that have been obseiyed for years
in the literature. Eveiything fits.
It accounts for various enzymes
that have been reported to be
abnormal. various transport pro—
cesses that have been seen to be
aberrant. particular proteins that
have been compromised because
ofattack by a free radical peptide

Our model puts all of these
observances under a solid um—
brella."

Defensive Strategies
and Implications for
the Future

If the shrapnel model proves
to be accurate, then what? What
can people do to protect them
selves against the onslaught of
Alzheimer's?

“The therapeutic implications of our re—
search are that if one could interfere with this
free radical damage. if you could prevent it.
then you could significantly modulate the
disorder." Butterfield says. “Eventually. it might
be possible to give people anti—oxidant pills
that protect them—that may not be all that far
in the future." Hensley adds. “In fact right
now, there are a number of people who
believe taking lots of vitamin (I and vitamin E
can help protect brain cell membranes."
Hensley goes on to say that in separate studies
done at [K it was shown that vitamin F.
protects cell membranes by inserting itself into
the membrane and preventing damaging over-
oxidation.

“1 think of it as a preventative measure." says
Mattson. “Vitamins F and A absorb free radi—
cals and prevent them from damaging cells.
We‘ve found that vitamin F. in HCI'VC cell
cultures. for example. can protect against
amyloid beta peptide toxicity." Butterfield.
Hensley. and an undergraduate chemistry
major, Beverly Howard. have found that vita—
min E protects brain membranes from the
damaging effects of beta peptide free radicals
Hensley. Mattson and Butterfield admit to

 

“I am absolutely convinced that
within 10 years we will have a pill

that prevents Alzheimer’s disease.”

Allen D. Roses.
Duke University

taking "more than the normal recommended
daily dosage” of vitamin E. “There‘s abso-
lutely no evidence that these vitamins are bad
for you, and there‘s some strong evidence that
they‘re good for you.” says Mattson.

Now that the researchers have gotten this
far. what‘s next?

“We’ve, recently filed patents on several
compounds that we find. at least in cultured
nerve cells. can protect against beta peptide
toxicity." Mattson says. “On one hand. we're
trying to understand more and more about
how the free radical kills cells. and were also
trying to identify compounds that interfere in
this process. So that's the strategy now."

“How significant is this research?" Farl
Stadtman asks rhetorically from his office at
the National Heart. Blood and Lung Institute.
Stadtman. the chiefofthe laboratory of chem—
istry in Bethesda. pauses only briefly. “This
work is highly significant. It's becoming in—
creasingly apparent that free radical damage
to proteins is important in a numberof disease
processes. The l‘niversity of Kentucky group
has shown that the beta peptide is converted
into a form which has the ability to spontane—
ously generate free radicals. They've taken a
very novel approach to understanding the
part free radicals play." he continues. "I know
thatjohn Carney. in collaboration with Robert
Floyd in the Oklahoma Medical Research
Foundation. has been looking directly for
such an event for some time. This is unquesi
tionably a breakthrough in the understanding
of the pathology of Alzheimer‘s disease."

For the millions of Americans who will
develop Alzheimer‘s disease in the next few
years. any maior discovery that may lead to
the control or cure of the disease is welA
comed. And indications that the Alzheimer‘s
puzzle may be solved and effective therapies
developed have never been stronger "I am
absolutely convinced that within 10 years we
will have a pill that prevents Alzheimer's
disease." says Roses of Duke.

“Within the next five years." says [K‘s
Markesbery. "we're probably going to have a
drug that will enhance memoiy. There are too
many drug companies working on this and
too many ingenious pharmacologists for this
not to happen." 9

 

 

 

  

 

Studies Show Mental Activity
Helps Ward OffAlzhez‘mer’s Disease

The Friedrich Nietzsche 3004
page workout?

It may be more beneficial than
you think. in addition to satisfy-
ing the intellect. mental aerobics
just might help to keep you from
developing Alzheimer‘s disease.

A recent study in Shanghai.
one of seven such inquiries being
conducted worldwide. has shown that
levels of education have a profound
effect on the ravages of Alzheimer's
disease and other forms of dementia
that chiefly affect older people. Nae
Chicago 'l'rilmne reported After
studying more than 5.000 Shanghai
residents ages 33 to 73. researchers
found that. all other factors being
equal. the uneducated subjects of the
study had twice the risk of dementia
as those with elementary or middle—
school education.

Robert Katzman of the University
of California at San Diego wrote in
the journal .\'e11rolog}' that the find!
ings of this and other such studies
have profound social. biological. and
medical implications. Harvard
neuropsychologist Marilyn Albert.
who conducted a study of elderly
Bostonians. says "having more edu-
cation means not only that you de—
velop your brain when you‘re young
but that you use it more through your
life. and that produces some sort of
protective mechanism that helps keep
the brain from developing Alzheimer‘s
disease.“

A unique study by L'niversity of
Kentucky res Jarcher David Snowdon
is also focusing on the connection
between early education and later—
life mental functioning. For the past
seven years. Snowdon has been study—
ing the School Sisters of Notre Dame
congregation. comparing disease and
death rates of the more educated
sisters to those of the less educated.
[See “Aging with Grace: The School
Sisters of Notre Dame Study." in the

 

Sisters Columbine Kumba and Gad/nit
Huber, both/miner teachers now in their
mid—905, are participating in, an ongoing
UK aging study being conducted by David
Snowdon.

Winter/Spring 1995 Odyssey]

Initial studies focused on sisters of
similar age who represented a broad
range of function and health—from
those who were confused and bedrid
den to those still holding full—time jobs
in the community. The more highly
educated sisters lived approximately
four years longer. with a good level of
mental and physical functioning. than
those who had less than a bachelor’s
degree. At every age, between 20 and
95. the less-educated sisters had twice
the mortality rates of the more edu—
cared.

"One explanation for this might be
that higher cognitive function is due in
part to higherseducated people having
jobs—as well as recreational activi—
ties—that keep them mentally alive.“
says Snowdon, who is working with a
team of other scientists at UK's Sanderse
Brown Center on this study. "Another
line of evidence is that people who
have a rich vocabulary early in life end
up having high mental function later in
life." These results have been deter—
mined. Snowdon explains. from exam
ining words used in autobiographies
written at age 21 and mental function
assessed ()0 years later.

"We also looked at what the sisters
were writing at age 21. then looked

again at what they were writing 23
years later, at age 40." says Snowdon.
"Those sisters who improved their
vocabulary between ages 21 and 46
had better mental function at age
80.

“My suspicion is he says. "that
education has nothing to do with
the pathology of Alzheimer‘s. It isn‘t
that lower—educated people have more
plaques and tangles; rather. it may be
that more highly educated people have
better connected brain cells.“ Snowdon
goes on to say that one explanation for
these stronger connections in the brain
is that more highly educated people
might exercise their brains more and
thus end up with an agile brain in old
age.

Snowdon cites evidence for this theory
from a study by Katzman. who discov—
ered in his work that the brains of more
highly educated people are literally better
connected than those of less—educated
people. "Katzman found that the syn—
apses in the brains of higher-educated
people were much denser." Snowdon
says. According to Katzman. higher—
educated people develop "brain re‘
serves.” which become useful if the
person develops the lesions of
Alzheimer's or has a small stroke. “if
other parts of the brain are well con-
nected." Snowdon says. “the healthy
parts of the brain may have a better
chance of taking over the functions of
the parts of the brain damaged by
Alzheimer‘s."

In discussing the nature of brain cells
and the ongoing Nun Study. Snowdon
says there is no reason to believe that
brain cells are any different than muscle
cells. “There‘s a lot of good evidence to
back up the idea of 'use it or lose it.“‘ he
says. “The women in our study keep
very intellectually active, whether it‘s
reading. playing scrabble or watching
Wheel of Fortune. They refuse to resign
themselves to downward mental dev
cline. One sister told me. "fhere‘s only
one time we retire at night"

 

 

 

T ODYSSEY

 

  

 

ODYSSEY 8

V Biology professor Gracejones, third from [if/l,

 

    

says that undergraduates play an important
role in her lab. Paul Taylor, from Springfield,
Kentucky, Mona Saidi, originalivfrom Iran
and now living in Houston, and Enrique Tze
Leuk Pang, from Hong Kong, are currently
working on research projects with/ones.

 

.i/iy [mug/ten

 

Student Interest
in Science Classes Increasing

by Graham Shel/{y

Call it a major migration.

Over the last fiye years. umlergraduates
haye been swarming to the sciences at the
l‘niyersity of Kentucky. Since 1989. enrolk
ment in chemistry classes has increased by ()1
percent. Biology is up ‘3 percent. The (jol-
lege of Allied Health has experienced a stuv
dent population explosion of 130 percent.

Many students. faculty and administrators
say the decision by undergraduates to select
science as their field of study results from a
combination of genuine interest and basic.
pragmatic concerns. Students \\‘ant jobs. good
jobs. and they’re \\illing to work hard to get
them.

Bill l\'orn. a spokesman for the Higher
Education Research Institute in l.os Angeles.
says the trend at 1'1\' is part of a national
phenomenon. In terms ofthe stated academic
preferences of students. he says. "There‘s
been a substantial increase oyer the last se\ en
or eight years in the biological sciences.” The
institute compiles suryeys taken of 200.000
entering freshmen.

From 198“ to 1993’). the number of students
nationwide reporting an interest in pursuing
biological sciences (defined as biology. bit»
chemistry and microbiology) increased from
3.8 to 5.6 percent. The institute's research
found that during this time period substatr
tially more freshmen became health profes-
sions majors. That classification. which in~
eludes pre-medical. nursing. pie—pharmacy
and physical therapy. leapt from 72 percent
in 198"" to 13.8 percent in 1995’».

Rhonda Smith. a [K piepharmacy senior
from St. Louis. says students“ reasons for
shifting to science are largely pragmatic. That
doesn‘t mean. she says. that eyeryone can
succeed in science courses. "You haye to
have a general interest in science. first of all."
she says. If so. she adds. a student can follow
a path that hopefully will lead to job and
economic security. "The outlook in science
fields is very good financially." she says. "If
you have a science degree. there‘s always

 

 

 

 “I see more peeple being interested in science because 9f the
job market; they) don. ’t want to get a degree they) can, ’t go
out andfind ajobfor. ”

 

something you can do." The money and
stability many students belieye awaits them
once they'ye finished school is enough of an
incentiye to lure them into sometimes diffictilt
and lengthy degree programs. "It is expen—
siye. there's no doubt abotit it." Smith says, "I
figttre after it‘s all oyer. I‘ll be happy."

(Ihuck Staben teaches Principles of Genet—
ics. a i()()rleyel class for biology majors. The
School of Biological Sciences capped the
enrollment at ‘3. Before Staben had prepared
his first transparency. St) names sat on the
courses waiting list. He says more students
asked to be admitted. btit he stopped taking
names at St).

Asked why more students are now intei>
ested in pursuing careers in science. Staben
says that while their interest may be genuine.
most students aren‘t interested in becoming
scientists. "It‘s not about science. it‘s about
health professional careers.” he says, “They‘re
preparing for a profession." ()fthe students in
his genetics class. Staben estimates that about
St) percent haye some pre—health professional
orientation. "They want to be a physician. a
dentist. a physicians assistant." he says.

Staben adds that he understands the ltire of
healthrcare professions. particularly medical
school. liyen if students haye to borrow
Slt).()()l) a year for four years of med school.
they can be drawing sixefigure paychecks
within it) years of finishing their undergradu—
ate work. he explains. "Anybody who doesn‘t
see that as a cheap imestment needs to go
back to Business 101."

.\Iona Saidi. a junior biology major from
Houston. says. "I see more people being
interested in science because of the job mar—
ket: they dont want to get a degree they can‘t
go out and find a job for." Saidi. who plans to
go on to medical school. says that students are
attracted to science also because they see
technology becoming an increasing part of
eyery aspect of modern life, "A lot of our
pr