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Grant Proposal – Proposed Study,
Budget
, and Draft Grant Proposal
This week you will write the Proposed Study and Budget sections of your Grant Proposal. The Proposed Study section will resemble a typical methods section like the one you would write in an empirical paper (except that the data have not yet been
collected
). In this section you will describe the study that you are proposing to conduct to test your hypothesis.
You will also write the Budget Justification section and the Budget for your grant proposal. The Budget Justification section will contain a description of your proposed budget including how grant funds will be used and justifying costs. Proposed costs must be reasonable, necessary and allocable to carry out the project’s goals and objectives.
The Budget, which will be Appendix A of your grant proposal, will follow the format of the budget in the
Sample Grant Proposal Template (Links to an external site.)Links to an external site.
, Appendix A . There is also a
Budget Calculation spreadsheet (Links to an external site.)Links to an external site.
that you can use to determine the direct and indirect costs for your proposed study.
After writing the Proposed Study, Budget Justification and Budget sections, combine them with the completed sections you have done in Weeks Two and Three (with feedback incorporated), and create the first draft of your grant proposal. Submit your draft grant proposal this week for the Week Five Grant Proposal – Peer Review assignment.
See the
Grant Proposal Guidelines (Links to an external site.)Links to an external site.
for detailed instructions on writing your grant proposal. See the Sample Grant Proposal Template (Links to an external site.)Links to an external site. as an example of an actual proposal and use it as a template for your grant proposal.
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
Budget
| Principal Investigator: Instructor B. Jones, PhD | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Grant Title: | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Period of Performance: 9/1/15 – 8/31/16 | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Funds Requested | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Salaries | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Full Time Faculty Annual Salary | $ 90,000 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Percentage of effort | 1 | 0% | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Number of months | 12 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Full Time A/P (10% time 12 Mo) | $ 9,000 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Full Time Graduate Assistant Annual | $ 50,000 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| 50% | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Graduate Assistant (50% time, 12 months) | $ 25,000 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Total Salaries | $ 34,000 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Equipment | $ | – 0 | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Travel | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Travel for PI to one meeting to present results | $ 1,500 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Travel for research assistant to particpants homes | $ 1,000 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Total Travel Costs | $ 2,500 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Participants | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| number of subjects: | 40 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| payment per subject: | $50 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Total Participant Cost | $ 2,000 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Supplies | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Computer | $ 3,247 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Quality of Life Scale | $ 1,200 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Office supplies (postage, paper, etc) | $ 689 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Total Supplies | $ 5,136 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Total Direct Costs | $ 43,636 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| 37.5% | Indirect Costs* | 16,364 | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Total Funds Requested | $ 60,000 |
Inflation Factor
– emp 1
| Employee Name: | |||||||||||||||||||||||||||||||
| Contract Term: | |||||||||||||||||||||||||||||||
| Health Insurance Type | |||||||||||||||||||||||||||||||
| Health Insurance $: | (Yearly Total) | ||||||||||||||||||||||||||||||
| ORP (1) or VRS (2) | |||||||||||||||||||||||||||||||
| Fill in red cells only | |||||||||||||||||||||||||||||||
| 3.00% | 10.00% | ||||||||||||||||||||||||||||||
| Time Period | Salary + inflation Increase | Fringe Benefits (not incl health care) | Health Care | Total Fringe | Calculated Benefit Rate for this salary | FICA Salary Caps | |||||||||||||||||||||||||
| 7/1/2009 – 6/30/2010 | $ – 0 | FICA 6.2% of $109,300, Medicare @ 1.45% | |||||||||||||||||||||||||||||
| 7/1/2010 – 6/30/2011 | FICA 6.2% of $114,417, Medicare @ 1.45% | ||||||||||||||||||||||||||||||
| 7/1/2011 – 6/30/2012 | FICA 6.2% of $119,774, Medicare @ 1.45% | ||||||||||||||||||||||||||||||
| 7/1/2012 – 6/30/2013 | FICA 6.2% of $125,382, Medicare @ 1.45% | ||||||||||||||||||||||||||||||
| 7/1/2013 – 6/30/2014 | FICA 6.2% of $131,252, Medicare @ 1.45% | ||||||||||||||||||||||||||||||
| 7/1/2014 – 6/30/2015 | FICA 6.2% of $137,397, Medicare @ 1.45% | ||||||||||||||||||||||||||||||
| 7/1/2015 – 6/30/2016 | FICA 6.2% of $143,830, Medicare @ 1.45% | ||||||||||||||||||||||||||||||
| 7/1/2016 – 6/30/2017 | FICA 6.2% of $150,564, Medicare @ 1.45% | ||||||||||||||||||||||||||||||
| 7/1/2017 – 6/30/2018 | FICA 6.2% of $157,613, Medicare @ 1.45% |
Inflation – emp 2
Inflation – emp 3
Sheet4
Sheet5
Running Head: Stress-induced cognitive impairment 1
Stress-induced cognitive impairment
Lana Eliot
Psychology 625
Professor Beharie
January 29, 2018
Stress-induced cognitive impairment
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.
RunningHead: STRESS-INDUCED COGNITIVE IMPAIRMENT 1
STRESS INDUCED COGNITIVE IMOAIRMENT 6
Stress-induced cognitive impairment
Lana Eliot
Psychology 625
Professor Beharie
January 24, 2018
Stress-induced cognitive impairment
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.
