Running Head STRESS-INDUCED COGNITIVE IMPAIRMENT1STRESS INDUC.docx

Running Head: STRESS-INDUCED COGNITIVE
IMPAIRMENT 1
STRESS INDUCED COGNITIVE IMOAIRMENT 6
Stress-induced cognitive impairment
Lana Eliot
Psychology 625
Professor Beharie
January 24, 2018
Bondi, Corina O., Gustavo Rodriguez, Georgianna G. Gould,
Alan Frazer, and David A. Morilak, (2008). Chronic
unpredictable stress induces a cognitive deficit and anxiety-like
behavior in rats that is prevented by chronic antidepressant drug
treatment. Neuropsychopharmacology, 33 (2), 320-331.
Bondi Cornia, Gustavo Rodriguez, Georgianna G. Gould and
their fellows have published an article named Chronic
unpredictable stress induces a cognitive deficit and anxiety-like
behavior in rats that is prevented by chronic antidepressant drug
treatment in the year 2008. Journal of
Neuropsychopharmacology is the source where this article is
submitted. In this article, the authors have mainly given several

dimensions that are associated with stress which associates
primarily with the cognitive deficit, in this concern an
experiment was done on rats. This research would be helpful for
us for our medical projects related to stress and its correlation
with cognitive abilities of human beings.
Joëls, Marian, Zhenwei Pu, Olof Wiegert, Melly S. Oitzl, and
Harm J. Krugers (2006). Learning under stress: how does it
work? Trends in cognitive sciences, 10 (4), 152-158.Joëls,
Marian, Zhenwei Pu, Olof Wiegert, Melly S. Oitzl, and Harm J.
Krugers have published this research-based article in the year
2006 in the journal of trends in cognitive sciences. The central
theme of this article moves around the concept of the
consequence of stress on the learning ability of the individuals.
In this article, it is also evaluated that the hormones of stress
when released develops the transmitters in response to stress.
This is an authentic article as is reviewed by expert authors so it
could consider for a more profound study on the topic of Stress-
induced cognitive dysfunction.
Luine, Victoria, Miriam Villegas, Carlos Martinez, and Bruce S.
McEwen (1994). Repeated stress causes reversible impairments
of spatial memory performance. Brain research, 639 (1), 167-
170.
Line, Victoria, Miriam Villegas, Bruce S. McEwen and Carlos
Martinez have published this article in the year 1994. The main
ideology considered in this article is that the repeated stress has
the impairments that are reversible and these could directly
affect the spatial memory as the hormones inside the brain are
released that negatively affects the cognitive ability of the
individual. This article is authentic as the proper sources are
given with the theory along with that it is reviewed by the
scholars so it could be considered while working on the project
related to stress-induced cognitive impairment.
Mizoguchi, K. Y. (2000). Chronic stress induces impairment of
spatial working memory because of prefrontal dopaminergic
dysfunction. Journal of Neuroscience, 20 (4), 1568-1574.

Mizoguchi, K., Yuzurihara, M., Ishige, A., Sasaki, H., Chui,
D.H. and Tabira, T have published this article in the year 2000
and kept in Journal of Neuroscience. The central theme of this
article is about chronic stress that directly affects the working
memory as several chemical reactions occur inside the brain.
This article is credible as the authors have broader experience
in the field and they have provided detailed analysis on the
topic along with the supporting evidence so it could be
considered for the future project as well.
Sandi, Carmen (2004). Stress, cognitive impairment and cell
adhesion molecules. Nature Reviews Neuroscience, 5 (12), 917.
Sandi, Carmen has published this article during the year 2004
naming it as cognitive impairment, Stress, and cell bond
molecules in the Nature Reviews Neuroscience. In this article,
the author has mainly demonstrated the inside brain chemical
reaction that occurs when stress occurs it eventually affect the
brain thinking process. This article is credible as the author has
excellent experience also this report is reviewed by experts so it
could be considered for the future project as well.
Shansky, R. M., & Jennifer, L. (2013). Stress-induced cognitive
dysfunction: hormone-neurotransmitter interactions in the
prefrontal cortex. Frontiers in human neuroscience, 4 (1), 7.
In the year 2013 Shansky, R. M., & Jennifer, L has published an
article in Frontiers in human neuroscience. The primary focus
of this article is on Stress prompted cognitive dysfunction in
which the neurotransmitter of hormone interacts with prefrontal
cortex which directly affects the memory. This topic is wide,
and the resource is credible due to reviews of experts on this
source so that this article could be helpful for us in our future
projects on the same topic.
Song, Li, Wang Che, Wang Min-Wei, Yukihisa Murakami, and
Kinzo Matsumoto. (2006). Impairment of the spatial learning
and memory induced by learned helplessness and chronic mild
stress. Pharmacology Biochemistry and Behavior, 83 (2), 186-
193.
Song, Li, Wang Che, Wang Min-Wei, Yukihisa Murakami, and

Kinzo Matsumoto have published this article in the year 2006.
This article mainly is based on the Impairment of the three-
dimensional learning and reminiscence persuaded by learned
powerlessness and chronic mild stress. This article is published
in the Pharmacology Biochemistry and Behavior to help the
medical individuals. It is a credible source so we can use it in
our future projects as well.
Arnsten, A. F. (2009). Stress signaling pathways that impair
prefrontal cortex structure and function. PMCID, 410–422.
Arnsten in his article on “Stress signaling pathways that impair
prefrontal cortex structure and function” states prefrontal cortex
is the most important region of the brain that plays a vital role
in cognition. The cognitive abilities of the person highly depend
on this PFC. When our brain is exposed to even little stress that
it faces architectural changes. These changes take place in
prefrontal dent tries. This research paper present that how
intercellular signaling pathways help in mediating the
consequences of stress on prefrontal cortex. Furthermore, this
research paper demonstrates that how environmental or genetic
insults disinhibit signals of stress that leads to the development
of signals. These signals provide indicators of reflective
prefrontal cortical dysfunction that drives a man to mental
illness (Arnsten, 2009).
Andrew Holmes, a. C. (2010 ). Stress-induced prefrontal
reorganization and executive dysfunction in rodents. PMCID,
773–783.
Andrew Holmes along with his coworker performed research on
“Stress-induced prefrontal reorganization and executive
dysfunction in rodents.” In his study, he states that prefrontal
cortex shows an executive part in selecting and processing
information that controls the behavior of a person in response to
this environment. Deficiency of these functions leads a man to
mood swings, schizophrenia and anxiety disorder as well as
addiction. That induces stress and trauma. Intense stress leads
to a significant change in the remodeling of PFC. Due to
deficiency of neuronal morphology deficit in executive

functions have been recorded for example loss of working
memory, set fluctuating, cognitive tractability along with
emotive dysregulation (Andrew Holmesa, 2010). The research
paper suggests that development in stress induces changes can
help in regulating the changes in rodent’s dysfunction
Maroun, I. A. (2008). The Role of the Medial Prefrontal Cortex-
Amygdala Circuit in Stress Effects on the Extinction of Fear.
PMCID, 30873.
Maroun along with his followers in their research on “The role
of the medial prefrontal cortex-amygdala circuit in stress effects
on the extinction of fear. Neural Plast” states that exposure to
stress depends on its intensity and duration that results in
effecting the learning and cognition behavior of human.
Gamma-aminobutyric acid plays a vital role in the transmission
of signals with the prefrontal cortex and amygdala (Maroun,
2008). The results of this study explain that dysfunction of
medial prefrontal cortex-amygdala circuit is due to the stressful
experience that is induced by impaired extinction to a stressor.
Specific Aims:
The effect of stress on human beings is terrible that leads them
to different diseases. The stress comes from environment and
change in human behavior. Stress profoundly impacts or minds
that leads to damages of prefrontal cortex which plays a
prominent role in cognition (Andrew Holmesa, 2010 ). The
cognitive abilities of a human being the effect a lot in the
presences of stress. That leads to mood swings, schizophrenia
and anxiety disorder. Hence, numerous studies are carried out
on the stress-induced cognitive abilities (Joëls, 2006).
Intense stress and even the minor stress is responsible for
changes in cognition impairment. It is responsible for
significant changes in the remodeling of neurons. It also brings
changes in neuronal morphology and effects the working
memory of human beings (Luine, 1994). This study
demonstrates that how stress-induced cognitive impairment
affects the different areas of the brain (Maroun, 2008). The
impact of stress on the human brain is studied under molecular

basis induced changes. There is numerous significance of this
study that includes how the brain is affected by stress and what
stress causes cognition problems. It will further demonstrate
how molecular basis changes the prefrontal cortex. It also gives
details about pathophysiology and its association with
dysfunction in neuropsychiatric diseases. Further strategies will
also have introduced for its treatment that helps in overcoming
stress-induced cognitive impairments.
Running Head: Stress-induced cognitive impairment
1
Lana Eliot
Psychology 625
Professor Beharie
January 29, 2018
Background of study:
Stress have destructive effects on human. These results are
related to all internal and external development of human body

and mind. Humans are exposed to multiple stressors in their
daily routine that leads to severe problems. When the human
body is exposed to stress at that time that time, they did notice
that how this stress affects them. But later on, when they are
more frequently exposed to stress they feel changes in their
behavior and brain as well. Mood swings and unpredicted
behavior of humans are the results of this stress. As well as the
brain is concerned, stress disturbs the chemical balance that
restricts brains from performing their ordinary functions. Most
importantly it affects the cognition problems in humans. They
more frequently started to forget about different things that they
did not realize initially. But with the passage of time when
these things get severe, they know that how this stress
negatively affect this stress. Furthermore, stress is the only
factors that induce cognition and learning problems in humans.
Bondi et al. (2007) conducted a study on chronic unpredictable
stress that induces cognitive deficit as well as anxiety problems.
Keeping in view the aim of this study, he experiments on rats
where he injected the chronic antidepressant drug to analyze its
effects. Stress-induced frontal lobe dysfunction, increase
depression and anxiety and psychiatric illness. To find the
relationship between stress-induced impairment and how it can
be recovered by using the antidepressant.
He experimented with rates where he induced desipramine and
escitalopram per day. These two chemicals are induced because
these are the one who produces in human brain as a result of
stress. After infecting this chemical daily, he notices that
desipramine induced effect on the brain of rats that is shown by
their behavior but escitalopram has no effect. He further treated
these rates with antidepressants (Bondi, 2008). From his
studies, it is proved that treatment of stress is present with the
use of antidepressants as it is also proved by clinical evidence.
Joels et al. (2006) along with his coworkers, performed research
on how stress affects the process of learning and how does it
work when an individual is frequently exposed to stress. In his
study, he stated that the relationship between stress and learning

is not always clear. Stress has to influence and impairing effects
on the human brain. But its results are varied from person to
person. In his study, he proposed unifying research, under this
theory, he states that stress is having an influencing impact on
memory process and learning (Joëls, 2006).
The stress hormone corticosteroids are responsible for stress
influenced behavior. This hormone increases the attention of
human being even in the stressed situation and improves his
learning. When an individual is more focused than he was more
likely to remember all the events due to transmitters and
hormones that are released in response to stress. From the
findings of this article, it is analyzed that it is not necessary
that stress have destructive functions but it has an important
function as well.
A line along with his fellow team conduct a study on repeated
stress reversible impairments that effects spatial memory
performance. His research states that if the human mind is
exposed to 6 hours per day and it continues for 21 days. It
results in impairments that occur due to the acquisition of
spatial memory task. These stress-induced impairments are
reversible that caused temporary blockage of phenytoin that acts
as a blocker for excitatory amino acid (Luine, 1994). In such
situation when an individual is frequently exposed to stress than
tianeptine which is an antidepressant is given to him which
lowers the extracellular serotonin. With the use of this drug,
dendrites of CA 3 neurons are temporarily blocked.
Mizoguchi, along with a team of experts, research chronic stress
that induces impairment in the spatial memory because of
dysfunction of prefrontal dopaminergic. From this research, it is
analyzed that chronic stress induces many impairments whether
it is in temporary memory or spatial working memory
(Mizoguchi, 2000). Its effect is in the long run that damages the
prefrontal cortical dopaminergic dysfunctions. The findings of
this research suggest that these can be controlled by using drugs
that control this dysfunction.
Sandi presented his findings on cognitive impairment effects on

cell adhesion molecules. The findings of his research suggest
that how stress changes the chemical reaction in the brain that
leads to sudden changes in the mood of an individual (Sandi,
2004). These chemical reactions are temporary but later on if
chronic stress increased than these chemicals would never come
back in their original foam. Thus it leads to severe diseases.
Shansky in his research on the stress-induced cognitive
dysfunction that effects hormone neurotransmitter interaction
that happens in the prefrontal cortex. The findings of this
research suggest that stress-induced cognitive dysfunction
(Shansky & Jennifer, 2013). Due to this dysfunction
neurotransmitter-induced hormones in prefrontal cortex which
have a direct impact on memory. Song revealed in his research
on impairment of memory and spatial learning that is induced
by chronic mild stress and helplessness. Under this study, three-
dimensional modal that is known as 3D modal is used to detail
analysis of impairment that is induced by chronic mild stress
(Song, 2006).
Arnstein in his research on stress signaling that induces
impairment of PFC (prefrontal cortex structure) and its
function. His research revealed that how the architecture of our
brain effects when it is exposed to even little stress. Moreover,
he further demonstrates that how genetics and environmental
factors induce stress signals that lead to dysfunction of PFC
dysfunction (Arnstein, 2009). In 2010, Andrew presented his
research on the dysfunction of rodents and prefrontal
reorganization due to induced stress. He states in research that
dysfunction of rodents leads to difficulties in information
processing. It most likely induces mood swings, anxiety
disorder, and schizophrenia. In some persons, it leads to
addiction (Andrew Holmesa, 2010).
Maroon in 2008 represents his findings on medial PFC
amygdala circuit that induce stress on the elimination of fear.
The intensity of stress induces that how much a person is
affected by it. The intensity of stress determines how much
cognition and learning of human being is affected. Due to an

imbalance in Gamma-aminobutyric acid, the cognitive abilities
of man become pretentious (Maroun, 2008).
Bisaz along with his fellow team present a study on the role of
neural cell hold molecule NCAM and its effect on learning that
is done under stress. The findings of this papers suggest that
stress occurs due to the combination of intrinsic and extrinsic
factors. When a human body is exposed to these factors, it
induces stress, under the NCAM molecule that helps in inducing
stress in brains it is analyzed that this molecule induces stress
and disturbs the learning behavior of human being (Bisaz R1,
2009).
Cheryl presents a study in 2017 that is conducted on
hippocampal dendritic complexity that leads to chronic stress
along with its functional and methodological considerations.
His study suggests that dendritic morphology framework acts as
a stress field. Where chronic stress leads to loss of spatial
memory. His study further elaborates that CA3 atrophied
dendrites are the molecules that help in post-stress recovery (M.
Judd, 2017). Gerard in his research on chronic social stress that
is conducted under the Curt Richter revealed that there are
many individuals in society that are more exposed to social
stress. The constant social stress related to food intake,
disturbed metabolism and body composition (J. Schwartzbc,
2017). Due to excess of food intake, it leads to obesity. The
incipient metabolic syndrome is responsible for it.
Resi, along with his coworkers presented research on neuron
transmitter of the central nervous system along with its
implication in memory and learning process. In his research, he
demonstrates that neurotransmitters are the one who is
responsible for action and reaction of a person that he did in
response to internal and external factors (Reis HJ, 2009). When
the person is exposed to stress, then the chemical balance of
these neurotransmitter is disturbed that leads to chronic stress.
Eva F. G (Eva F. G. Naninck, 2016) reflects his findings on
early micronutrients supplementations that help in protecting
individual form cognitive impairments. The findings of this

research evaluate that if micronutrients supplements are given
to individual than they are exposed to less stress. This help in
recovering the human being from deficiency.
The significance of study:
Stress-induced cognitive impairment is a problem due to which
everyone is suffered at different stages of their life. This
problem is most likely to occur with any individual even the
child is most often exposed to it due to the stress of studies and
environmental problems as well. As far as young people are
concerned, this stress-induced cognitive impairment affects
because a young person is more exposed to intrinsic and
extrinsic factors. These factors are responsible for creating
cognition problems in humans. The results of these problems are
in short and long run because it affects the memory of an
individual. This field of study id researched from multiple
perspectives but the findings are not used in a contractive way
that helps in solving these problems.
This project proposed that how the scientific knowledge of this
study help in exploring other factors which are associated with
this study. From the clinical practices, the issues that arise are
further tested in the laboratory to find its roots from where it
associates and how it can be researched that results in finding a
proposed solution to solve this stress-induced cognitive
problem.
If the proposed aim of this study has been achieved that it will
in solving cognition problems that are associated with stress.
Because in this study it is evaluated that how we can reduce
these stress-induced cognitive impairments. If the level of
nutrition in individual have been maintained from childhood
than it will help in competing with stress and they will gain
power competing with this problem.

References
Andrew Holmesa, a. C. (2010 ). Stress-induced prefrontal
reorganization and executive dysfunction in rodents. PMCID,
773–783.
Arnsten, A. F. (2009). Stress signalling pathways that impair
prefrontal cortex structure and function. PMCID, 410–422.
Bisaz R1, C. L. (2009). Learning under stress: a role for the
neural cell adhesion molecule NCAM. Neurobiol Learn Mem,
333-42.
Bondi, C. O. (2008). Chronic unpredictable stress induces a
cognitive deficit and anxiety-like behavior in rats that is
prevented by chronic antidepressant drug treatment.
Neuropsychopharmacology, 33(2), 320-331.
Eva F. G. Naninck, J. E.-Y.-N.-S. (2016). Early micronutrient
supplementation protects against early stress–induced cognitive
impairments. FASEB Journal , 1-10.
J.Schwartzbc, G. P. (2017). Randall Sakai, chronic social stress,
and the research tradition of Curt Richter. Physiology &
Behavior, 2 -6 .
Joëls, M. Z. (2006). Learning under stress: how does it work?
Trends in cognitive sciences , 10(4), 152-158.
Luine, V. M. (1994). Repeated stress causes reversible
impairments of spatial memory performance. Brain research ,
639(1), 167-170.
M.Judd, C. D. (2017). Chronic stress and hippocampal dendritic
complexity: Methodological and functional considerations.
Physiology & Behavior, 66-81.
Maroun, I. A. (2008). The Role of the Medial Prefrontal Cortex-
Amygdala Circuit in Stress Effects on the Extinction of Fear.
PMCID, 30873.
Mizoguchi, K. Y. (2000). Chronic stress induces impairment of
spatial working memory because of prefrontal dopaminergic

dysfunction. Journal of Neuroscience, 20(4), 1568-1574.
Reis HJ, G. C. (2009). Neuro-transmitters in the central nervous
system & their implication in learning and memory processes.
Curr Med Chem, 796-840.
Sandi, C. (2004). Stress, cognitive impairment and cell adhesion
molecules. Nature Reviews Neuroscience, 5(12), 917.
Shansky, R. M., & Jennifer, L. (2013). Stress-induced cognitive
dysfunction: hormone-neurotransmitter interactions in the
prefrontal cortex. Frontiers in human neuroscience, 4(1), 7.
Song, L. W.-W. (2006). Impairment of the spatial learning and
memory induced by learned helplessness and chronic mild
stress. Pharmacology Biochemistry and Behavior, 83(2), 186-
193.
BudgetPrincipal Investigator: Instructor B. Jones, PhDGrant
Title:Period of Performance: 9/1/15 - 8/31/16Funds
RequestedSalariesFull Time Faculty Annual Salary$
90,000Percentage of effort10%Number of months12Full Time
A/P (10% time 12 Mo)$ 9,000Full Time Graduate Assistant
Annual$ 50,000Percentage of effort50%Number of
months12Graduate Assistant (50% time, 12 months)$
25,000Total Salaries$ 34,000Equipment$ - 0TravelTravel for
PI to one meeting to present results$ 1,500Travel for research
assistant to particpants homes$ 1,000Total Travel Costs$
2,500Participantsnumber of subjects:40payment per
subject:$50Total Participant Cost$ 2,000SuppliesComputer$
3,247Quality of Life Scale$ 1,200Office supplies (postage,
paper, etc)$ 689Total Supplies$ 5,136Total Direct Costs$
43,63637.5%Indirect Costs*16,364Total Funds Requested$
60,000
Inflation Factor - emp 1Employee Name:Contract Term:Health
Insurance TypeHealth Insurance $:(Yearly Total)Retirement
Match $$:(Yearly Total)ORP (1) or VRS (2)Fill in red cells

onlyInflation FactorInflation Factor3.00%10.00%Time
PeriodSalary + inflation IncreaseFringe Benefits (not incl
health care)Health CareTotal FringeCalculated Benefit Rate for
this salaryFICA Salary Caps7/1/2009 - 6/30/2010$ - 0- 0-
00%FICA 6.2% of $109,300, Medicare @ 1.45%7/1/2010 -
6/30/2011- 0$ - 0- 0- 00%FICA 6.2% of $114,417, Medicare
@ 1.45%7/1/2011 - 6/30/2012- 0$ - 0- 0- 00%FICA 6.2% of
$119,774, Medicare @ 1.45%7/1/2012 - 6/30/2013- 0$ - 0- 0-
00%FICA 6.2% of $125,382, Medicare @ 1.45%7/1/2013 -
6/30/2014- 0$ - 0- 0- 00%FICA 6.2% of $131,252, Medicare
@ 1.45%7/1/2014 - 6/30/2015- 0$ - 0- 0- 00%FICA 6.2% of
$137,397, Medicare @ 1.45%7/1/2015 - 6/30/2016- 0$ - 0- 0-
00%FICA 6.2% of $143,830, Medicare @ 1.45%7/1/2016 -
6/30/2017- 0$ - 0- 0- 00%FICA 6.2% of $150,564, Medicare
@ 1.45%7/1/2017 - 6/30/2018- 0$ - 0- 0- 00%FICA 6.2% of
$157,613, Medicare @ 1.45%
Inflation - emp 2Employee Name:Contract Term:Health
00%FICA 6.2% of $109,300, Medicare @ 1.45%7/1/2010 -
6/30/2011- 0$ - 0- 0- 00%FICA 6.2% of $114,417, Medicare
@ 1.45%7/1/2011 - 6/30/2012- 0$ - 0- 0- 00%FICA 6.2% of
$119,774, Medicare @ 1.45%7/1/2012 - 6/30/2013- 0$ - 0- 0-
00%FICA 6.2% of $125,382, Medicare @ 1.45%7/1/2013 -
6/30/2014- 0$ - 0- 0- 00%FICA 6.2% of $131,252, Medicare
@ 1.45%7/1/2014 - 6/30/2015- 0$ - 0- 0- 00%FICA 6.2% of
$137,397, Medicare @ 1.45%7/1/2015 - 6/30/2016- 0$ - 0- 0-
00%FICA 6.2% of $143,830, Medicare @ 1.45%7/1/2016 -
6/30/2017- 0$ - 0- 0- 00%FICA 6.2% of $150,564, Medicare
@ 1.45%7/1/2017 - 6/30/2018- 0$ - 0- 0- 00%FICA 6.2% of
$157,613, Medicare @ 1.45%
Inflation - emp 3Employee Name:Contract Term:Health

00%FICA 6.2% of $109,300, Medicare @ 1.45%7/1/2010 -
6/30/2011- 0$ - 0- 0- 00%FICA 6.2% of $114,417, Medicare
@ 1.45%7/1/2011 - 6/30/2012- 0$ - 0- 0- 00%FICA 6.2% of
$119,774, Medicare @ 1.45%7/1/2012 - 6/30/2013- 0$ - 0- 0-
00%FICA 6.2% of $125,382, Medicare @ 1.45%7/1/2013 -
6/30/2014- 0$ - 0- 0- 00%FICA 6.2% of $131,252, Medicare
@ 1.45%7/1/2014 - 6/30/2015- 0$ - 0- 0- 00%FICA 6.2% of
$137,397, Medicare @ 1.45%7/1/2015 - 6/30/2016- 0$ - 0- 0-
00%FICA 6.2% of $143,830, Medicare @ 1.45%7/1/2016 -
6/30/2017- 0$ - 0- 0- 00%FICA 6.2% of $150,564, Medicare
@ 1.45%7/1/2017 - 6/30/2018- 0$ - 0- 0- 00%FICA 6.2% of
$157,613, Medicare @ 1.45%
Sheet4
Sheet5
Running Head: EFFECTS OF TRAINING ON COGNITION
12
EFFECTS OF TRAINING ON COGNITION
[Type over the sample text in this document to create your
Grant Proposal. Delete these instructions before submitting your
proposal.]

Effects of Internet Based Training on Cognition in Older Adults
Student A. Smith
PSY625: Biological Bases of Behavior
Instructor B. Jones, PhD.
September 19, 2014
Effects of Internet Based Training on Cognition in Older Adults
Specific Aims
The idea that maintaining high levels of cognitive activity
protects the brain from neurodegeneration is not new, and much
evidence has accumulated that people with high levels of
cognitive ability and activity tend to maintain cognitive
function well as they age (Hertzog et al. 2009). Beyond the idea
of maintaining cognitive function in healthy aging, studies such
as Verghese et al. (2003) found that higher levels of cognitive
activity were associated with lower rates of dementia in a 21-
year longitudinal study. While much of the data indicating
higher levels of cognitive activity leads to better long-term
function is necessarily correlational, a number of studies have
begun to systematically assess the effect of cognitive
interventions on cognitive function. The largest of these, the
Advanced Cognitive Training for Independent and Vital Elderly
(ACTIVE; Jobe et al. 2001) has found long lasting effects (5
years; Willis et al. 2006) of relatively short cognitive training
activities (10 hours).
The specific aim of this proposal is to assess the effectiveness
of A Fictitious Brain Training Program on research participants
followed longitudinally who may be experiencing the very
earliest signs of cognitive decline. Recent research tracking the
trajectory of age related cognitive decline (e.g., Mungas et al.
2010) has suggested that it may be possible to identify

cognitively healthy individuals at risk for significant imminent
cognitive decline by examining baseline cognitive assessments
or recent change, even though test scores do not reach the
abnormal range.
Background
Techniques for maintaining and enhancing cognitive function in
an increasingly aging population are of great potential benefit to
those who might suffer from Alzheimer’s disease and related
disorders and also to society as a whole. Higher cognitive
function leads to better maintenance of activities of daily life,
less need for chronic care, and direct improvements in quality
of life. Research examining effective methods for cognitive
enhancement is becoming increasingly prevalent and has led to
a number of recent review studies, e.g., Hertzog et al. (2009),
Lustig et al. (2009), Green & Bavalier (2008). These studies
review evidence from both longitudinal studies of increased
levels of mental activity on maintenance of cognitive function
and intervention studies aimed at directly improving cognition
with targeted cognitive training. For these cognitive
interventions to provide widespread benefit, it is critical to
identify who will gain from cognitive intervention studies and
to assess methods of administering effective cognitive training.
In a large scale cognitive intervention study (ACTIVE), Ball et
al. (2002) found that training increased cognitive function with
as little as 10 hours of task-specific training and these gains
were still evident 5 years later (Willis et al. 2006). However,
none of the three types of training used in that study were found
to generalize to the other types of cognitive function.
Participants were trained on either verbal episodic memory,
reasoning (pattern identification), or speed-of-processing
(visual search skills). Gains were observed in the domain of
training, but not on the other two domains. As noted by
Salthouse (2006), this result is inconsistent with the strongest
form of the “use it or lose it” hypothesis. However, it does hold
promise for cognitive training interventions that train broadly

across a wide variety of domains. The hypotheses implied by
the “use it or lose it” hypothesis is that cognitive training is
protective broadly against the cognitive decline associated with
aging. The more commonly observed specific areas of training
improvement suggest an analogy to physical fitness training: the
brain should not be thought of as a single “muscle” to be
strengthened but as a collection of individual abilities that
could each be improved through “exercise.” In addition, the
analogy could be extended to the idea that cognitive training
“exercise” should be thought of as an activity to be engaged in
on a regular basis, not as a single intervention.
The cognitive training that will be used in the proposed project
is based on an internet delivered set of activities designed by
the company BrainExercise. The training is based on practice
across a wide range of cognitive abilities, and by being highly
available via the internet, is also available for regular follow-up
re-training to maintain benefits. With this type of intervention,
even if a cognitive intervention training does not provide a
global benefit and delay decline across all types of cognition,
training can be used across many areas to increase overall
function. The ability to deliver cognitive training via the
internet becomes important logistically since the benefit of
training may depend on regular access to a broad array of
cognitive activities. In the successful ACTIVE study, training
was administered in face-to-face sessions requiring significant
personnel and logistical support.
The issue of identifying tasks suitable for cognitive training
with memory-impaired patients is an important one. In a follow-
up reanalysis of the ACTIVE study data, Unverzagt et al. (2007)
found that patients scoring >1.5 standard deviations low on
memory tests did not benefit from the verbal episodic memory
training in ACTIVE. In addition to seeing cognitive training as
a method for delaying or reducing the onset of memory
disorders such as MCI or AD (as in Verghese et al. 2003),
suitable interventions to try to rehabilitate memory function or
train compensatory strategies may provide an important benefit

to MCI and AD patients.
Numerous studies have suggested that elderly who are currently
cognitively within the normal range, but on the lower end of the
range are at risk for subsequent cognitive decline, including the
development of Alzheimer’s Disease (Rubin et al, 1998;
Sliwinski, Lipton, Buschke, & Stewart, 1996).
Older participants who score within normal cognitive ranges but
who exhibit personal cognitive decline within that normal range
are also at higher risk for the later development of Alzheimer’s
Disease (Villemagne et al, 2008; Collie et al, 2001). The most
at-risk group of currently healthy elderly may be those who
have shown some cognitive decline and are now at the bottom
of the healthy range. Since this proposal is to investigate at the
effectiveness of cognitive training in patients at risk for
Alzheimer’s Disease, the ideal comparison groups are healthy
older adults who are at increased risk relative to their age group
(cognitively normal, but lower scoring) and those who are
cognitively normal and exhibiting no current evidence of
memory impairment.
Significance
The proposed research will use an online-based software
company to administer a structured intervention of cognitive
skill training to patients experiencing some memory decline.
Prior intervention studies have typically provided cognitive
training in individual or small-group environments with the
patients physically present with a trainer. If interventions based
on training via the internet are shown to have similar benefits,
many more people can gain these benefits since the labor
involved in administering this type of training is much lower. In
addition, improvements in the type of training administered can
be made centrally and more quickly positively impact many
more patients. For the pilot intervention study proposed here,
we will be working with the Brain Science division at A
Fictitious Company. The Fictitious program is a home-based,
computerized, cognitive training program in which a customized

training plan is developed for each participant based on an
initial baseline cognitive assessment and ongoing training
progress. The training plan is based on 21 different tasks that
each focus on one or two of 14 different specific cognitive
abilities. To collaborate on examining the effectiveness of their
training plan, they are making available licenses for all study
participants to access the training program without cost. In
addition, all performance data on all compliance, cognitive
assessments and performance on training components will be
available for collaborative analysis to assess efficacy of specific
training elements in our study population.
The ability to deliver cognitive training via the internet holds
tremendous promise for making training benefits available
widely. Concerns about the task-specificity of benefits and the
need for consistent training to maintain cognitive function can
be met by making training easily available at home. The
proposed research will work with the cognitive science research
group of the A Fictitious company to assess the effectiveness of
their targeted, individually customized cognitive training
methods to improve cognitive functions in patients engaged in
long-term outcome research at the Brain Center at an Important
University.
Proposed Study
Participants:
Forty cognitively normal participants will be recruited,
including 20 participants scoring 1 SD below age and IQ-
adjusted norms on neuropsychological tests of memory (Rentz
et al. 2004), and 20 participants scoring no worse than .5 SD
below adjusted norms. Participants will be recruited from A
University. The patients will be randomly assigned to two
groups: intervention and waitlist (baseline) control. The
intervention group will receive cognitive training via Fictitious
Brain Training Program over a two month period. The waitlist
control will not initially receive training. However, since we
expect that the training will provide benefits to the patients,
participants in the waitlist control group will be given access to

the Fictitious Brain Training Program software at the end of the
protocol following the “post-training” assessment. This ensures
fair and ethical treatment of groups as well as providing
additional data about the effectiveness of the Fictitious Brain
Training Program.
There are no major risks to patients who participate in the
research. The training program is designed to be self-paced so
that patients can manage fatigue or frustration. Patients may
elect to stop participating in the study at any time. The potential
benefits of the proposed research are considerable. The study
protocol may provide a treatment to slow or reverse the
cognitive decline associated with MCI (and Alzheimer’s
Disease) using the internet, making this treatment broadly and
inexpensively accessible.
Procedures:
Once identified as a candidate for enrollment, patients will be
met with in person at their residence. Patients will have the
training protocol described and provide informed consent if
they wish to enroll. Availability of necessary internet access
will be assessed. Once enrolled, patients will be provided with a
license to access The Brain Training Program and a research
assistant will guide them through the initial setup process. The
intervention will follow the standard Brain Training Program
practice: initial assessment on a range of cognitive functions
followed by 24 20-minute training sessions over approximately
8 weeks. The rate of training sessions recommended is 3
sessions per week but is ultimately chosen by the patient.
These sessions are followed by a re-assessment within the Brain
Training Program of performance on their identified group of 14
cognitive functions.
Participants’ self-rating of quality of life will be assessed with a
Quality of Life-Alzheimer’s disease (QoL-AD) scale described
by Logson et al. (2002). While the current participants do not
require an assessment of quality of life appropriate for
cognitively impaired individuals, all cognitive training
improvement in these participants will also be compared with a

group of patients who have a diagnosis of MCI and who are
currently involved on an ongoing assessment of A Fictitious
Brain Training Program. The same set of performance
improvement instruments will be used in both studies to provide
maximum comparability across all groups.
Hypotheses & Analysis:
The intervention group is expected to exhibit reliably higher
scores on all post-training assessments than the waitlist control
group. Scores on the Fictitious Brain Training Program
cognitive assessments are very likely to improve reflecting the
training invested in those specific cognitive tasks.
Improvements on specific cognitive assessments will be
compared to estimates of improved domain-specific
performance available via the Brain Training Program.
For the current population of cognitively normal participants
who might be showing the first signs of memory impairment,
changes in self-rating of their quality of life (via the QoL-AD)
will be examined carefully. While improvements in activities of
daily life may not be significantly improved as these patients
are not generally impaired, increases in general cognitive
function may lead to better overall quality of life by improving
problem solving, language comprehension and general attention
skills. Improvements on this measure would be a key indicator
of the potential of cognitive training to provide significant
benefits to older adults.
Assessment of improvement will be made for only participants
who complete the training course of 24 sessions. Performance of
patients who do not complete the training will not indicate
whether the training is effective at improving cognitive
function. However, the drop-out rate is a key element to assess
for evaluating the overall effectiveness of internet-delivered
cognitive training. High rates of drop-out (e.g., >25%) may
indicate that the cognitive training needs to be adjusted in
difficulty to meet the needs of older adults or that additional
support (e.g., more patient contact) is needed to guide the
patients through the training. An important element of the

current project is the assessment of difficulty of completing the
training and obtaining feedback from participants about their
experiences with the online cognitive training.
Budget Justification
Funding is requested for a half-time graduate research assistant
to be responsible for all aspects of subject recruitment, training
and data collection. Addition funding of 10% is requested for
the principal investigator who will oversee the study and
conduct data analysis and publication of results.
Travel funding is requested for the PI to attend one national
meeting to present the preliminary results of the study.
Additional travel expenses are requested to pay for costs of
transportation by the research assistant to each subject’s home.
Subject payment of $50 for each subject (40 total) is requested
to reimburse subjects for their participation time.
Funding is requested for an Apple Laptop computer (15” with
retina display, 2.8 GHz processor, 1 TB hard drive) that will be
used for data collection and analysis. Additional funding will be
used to purchase the Quality of Life Scale and office supplies.
See Appendix A: Budget for detailed budget figures.
References
Ball, K., Berch, D. B., Helmers, K. F., Jobe, J. B., Leveck, M.
D., Marsiske, M., . . . Willis, S. L. (2002). Effects of cognitive
training interventions with older adults: a randomized
controlled trial. JAMA: Journal of the American Medical
Association, 288(18), 2271-2281.
Collie, A., Maruff, P., Shafiq-Antonacci, R., Smith, M., Hallup,
M., Schofield, P. R., . . . Currie, J. (2001). Memory decline in
healthy older people: implications for identifying mild cognitive
impairment. Neurology, 56(11), 1533-1538.
Green, C. S., & Bavelier, D. (2008). Exercising your brain: a
review of human brain plasticity and training-induced learning.
Psychology of Aging, 23(4), 692-701.

Hertzog, C., Kramer, A., Wilson, R., & Lindenberger, U.
(2008). Enrichment effects on adult cognitive development: Can
the functional capacity of older adults be preserved and
enhanced. Psychological Science in the Public Interest, 9(1), 1-
65.
Jobe, J. B., Smith, D. M., Ball, K., Tennstedt, S. L., Marsiske,
M., Willis, S. L., . . . Kleinman, K. (2001). ACTIVE: a
cognitive intervention trial to promote independence in older
adults. Controlled Clinical Trials, 22(4), 453-479.
Logsdon, R. G., Gibbons, L. E., McCurry, S. M., & Teri, L.
(2002). Assessing quality of life in older adults with cognitive
impairment. Psychosomatic Medicine, 64(3), 510-519.
Lustig, C., Shah, P., Seidler, R., & Reuter-Lorenz, P. A. (2009).
Aging, training, and the brain: a review and future directions.
Neuropsychology Review, 19(4), 504-522.
Mungas, D., Beckett, L., Harvey, D., Farias, S. T., Reed, B.,
Carmichael, O., . . . DeCarli, C. (2010). Heterogeneity of
cognitive trajectories in diverse older persons. Psychology of
Aging, 25(3), 606-619.
Rentz, D. M., Huh, T. J., Faust, R. R., Budson, A. E., Scinto, L.
F., Sperling, R. A., & Daffner, K. R. (2004). Use of IQ-adjusted
norms to predict progressive cognitive decline in highly
intelligent older individuals. Neuropsychology, 18(1), 38-49.
Rubin, E. H., Storandt, M., Miller, J. P., Kinscherf, D. A.,
Grant, E. A., Morris, J. C., & Berg, L. (1998). A prospective
study of cognitive function and onset of dementia in cognitively
healthy elders. Archives of Neurology, 55(3), 395-401.
Salthouse, T. (2006). Mental exercise and mental aging:
Evaluating the validity of the “use it or lose it” hypothesis.
Perspectives on Psychological Science, 1(1), 68-87.
Sliwinski, M., Lipton, R. B., Buschke, H., & Stewart, W.
(1996). The effects of preclinical dementia on estimates of
normal cognitive functioning in aging. Journal of Gerontology:
Series B Psychological Sciences and Social Sciences, 51(4),
P217-P225.
Unverzagt, F. W., Kasten, L., Johnson, K. E., Rebok, G. W.,

Marsiske, M., Koepke, K. M., . . . Tennstedt, S. L. (2007).
Effect of memory impairment on training outcomes in ACTIVE.
Journal of the International Neuropsychology Society, 13(6),
953-960.
Verghese, J., Lipton, R. B., Katz, M. J., Hall, C. B., Derby, C.
A., Kuslansky, G., . . . Buschke, H. (2003). Leisure activities
and the risk of dementia in the elderly. New England Journal of
Medicine, 348(25), 2508-2516
Villemagne, V. L., Pike, K. E., Darby, D., Maruff, P., Savage,
G., Ng, S., . . . Rowe, C. (2008). Aβ deposits in older non-
demented individuals with cognitive decline are indicative of
preclinical Alzheimer's disease. Neuropsychologia, 46(6), 1688-
1697.
Willis, S. L., Tennstedt, S. L., Marsiske, M., Ball, K., Elias, J.,
Koepke, K. M., . . . Wright, E. (2006). Long-term effects of
cognitive training on everyday functional outcomes in older
adults. JAMA: Journal of the American Medical Society,
296(23), 2805-2814
Appendix A: Budget
SUMMARY PROPOSAL BUDGET
FOR INSTITUTION USE ONLY
ORGANIZATION
PROPOSAL NO.
DURATION (MONTHS)
PRINCIPAL INVESTIGATOR (PI)/PROJECT DIRECTOR
Instructor B. Jones, PhD
AWARD NO.
A. PERSONNEL: PI/PD, Co-PIs, Faculty, Graduate Assistants,
etc.
Funds
List each separately with name and title.
Requested By
Proposer

1. Instructor B. Jones, PhD ($90,000/year) - 10% effort for
12 months
$9,000
2. Research Assistant (RA) - 50% effort for 12 months
$25,000
TOTAL SALARIES
$34,000
B. EQUIPMENT (LIST ITEM AND DOLLAR AMOUNT FOR
EACH ITEM EXCEEDING $5,000.)
None
TOTAL EQUIPMENT
$0
C. TRAVEL
1. DOMESTIC - PI attendance at national meeting
$1,500
2. OTHER - Travel for RA to participants home
$1,000
TOTALTRAVEL
$2,500
D. PARTICIPANT SUPPORT
$2,000
1. STIPENDS
$
50
2. TRAVEL

3. SUBSISTENCE
4. OTHER
TOTAL NUMBER OF PARTICIPANTS (40)
TOTAL PARTICIPANT COSTS
$2000
E. OTHER DIRECT COSTS
1. MATERIALS AND SUPPLIES- Computer for patient
training, data collection and analysis
$3200
2. OTHER Quality of Life scale
$1200
3 OTHER Office supplies
$736
4. OTHER
TOTAL OTHER DIRECT COSTS
$5,136
F. TOTAL DIRECT COSTS (A THROUGH E)
$43,636
G. TOTAL INDIRECT COSTS (F&A) (Rate = 37.5%)
$16,364
H. TOTAL DIRECT AND INDIRECT COSTS (F + G)

$60,000
PSY625: Biological Bases of Behavior Ashford
University

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