Alzheimer’s disease is known to affect the brain, cells, and nerves, nervous and psychic-emotional system. Alzheimer’s is the progressive disorder which results in the loss of cognitive abilities. It is the most concerned structure of dementia. As of today, there is still no clue to why or what causes this disorder, but there are ample ideas and suggestions for this disorder.
One of the most relevant symptoms of Alzheimer’s disease is the reduction of the ability to interpret your sensory perceptions and to understand the meaning of things. There is no current treatment, but there are drugs that are been used to slow down its progression.
In 1906, Alexander Alois described this disorder as a pathological presenile of dementia. It is believed that by the 2015, there will be a diagnosis of 5.3 million with Alzheimer’s disease which will eventually cause death.
Alzheimer’s disease is a progressive neurodegenerative disorder leading to sever cognitive, memory and behavioral impairment.
Significance
This proposal is to show how and why there are research done on Alzheimer’s disease. This disease affects 500 million people in the U.S. This is known as the aging disease.
The testing of Alzheimer’s is important because it is a way to find the cause of it and ways to prevent it or either slows down the progression rate in AD.
The diagnosis of Alzheimer’s disease is an important research because it contributes to helping our aging America and onset of Dementia. Alzheimer’s could be cause by other significant disease that may be at bay in our mind and body.
The significance of this proposal is to give insight on ways to prevent AD. It may also be a cure for it as well as what causes it. It also details where in the brain Alzheimer’s may begin in its early stages.
Literature Review
Alzheimer’s is the most common form of dementia. It is assumed to grow as the population of the aging grows. So far there is no treatment to stop the growth of AD. The growth of AD gets worsen due to the cognitive ability, functional ability and behavioral and mood changes. Alzheimer’s has signs of mood changes, depression, anger and confusion when changes happen. Someone of normal aging process will exhibit decrease in coordinator and movement whereas AD recipient will exhibit halting in movement or coordination and loss of balance.
The criterion for diagnosis of AD is definite, probable, and possible. Definite syndrome is histopathological confirmed. Probable has two cognitive deficits and severity of deficits. Possible has atypical awareness. There will be more updates to include brain imaging and peripheral biomarkers. These interventions may have some evidence to reduce or delay the onset of Alzheimer disease and dementia. It could possibly change the effect of normal aging on the brain activity. Physical exercise has been suggested to reduce the risk of dementia by lessen deterioration and cognitive deficit by reversal. It is suggested that keeping the brain healthy can have a major effect on cognitive changes in the aging process and may even lower the risk of Alzheimer’s disease.
Cognitive training for the treatment of AD has shown some promising effects. This has shown effects in the sizes for learning, memory, functioning, and daily living which is associated with general cognitive problems such as depression, and self-rated general funding. There have been strategies for restoring the main effect on this function. There are some limitations to this which are:
(1) Individuals with AD may have some cognitive and functional benefits from the cognitive training.
(2) Strategies in cognitive training may have a bigger effect than strategies in compensatory.
(3) The greatest effects are in the domains of learning memory, executive functioning of daily activities, depression, and general and cognitive functions.
Consideration for the effect ways that samples weighed in by each results of the sample size. Performance based measures were limited. Multiple treatment strategies where not easy to evaluate through individual strategies. Cognitive deficits of Alzheimer’s disease can produce significant functional impairment. Memory deficits are the more prone impairments in behavioral disturbances as well as executive functioning. Cognitive training is associated with any non-pharmacological intervention made to make cognitive functioning better.
There are reviews that will show that CT strategies have at least minimal effect on the memory and behavioral problems in connection to AD. There are even suggestions that CT may have some relations in the treatment of AD. There have been studies of reminisce therapy which was not supported because there were lack of evidence to support its given. CT may be improved domains function but it lacks support of CT for treatment of AD or early onset dementia.
These findings must be used with caution because of lack of methodological limitations of studies in review. The effects of CT on AD exists in treatments before and after because of variations of sizes in the individual study and domains of functions.
Women are considered to be at a higher risk for Alzheimer’s disease. This is believed because ovarian hormones and early stage of Alzheimer’s disease may be in connection. There have been many conflicts of this study because some shows that here is no difference in women and men for AD since estrogen biosynthesis is the main source in cognitive reduction in both.
Memory is not a unitary function. There has been a strategy on memory dysfunction by getting cognitive impaired individuals and regular people to memory altering procedures. Individuals who had AD were unable to contribute to recall performance because of responsive memory impairment. Memory impairment has been founded to be attributes to many kinds of elements of cognitively impaired individuals.
Alzheimer’s disease has given more fear in the last centuries than cancer, heart disease or strokes. One of the beginning diagnoses of AD was that the brain changes and this still exist today as a description of it. Depression and apathy are symptoms of Alzheimer’s disease in the mid stages of the behavioral process. In the moderate stage of AD, there are showings of delusion, agitation, aggressiveness, and hallucinations. In the severe stage of AD, individuals will show signs of agitation, anxiety, abnormal motor behavior, and can’t distinguish between day and night. Within an 80% rate, most people with AD will show signs of disturbance behavior.
If there are signs of neuropsychiatric symptoms, they may be administered an antipsychotic and antidepressant drug. The treatments used are haloperidol or melperone, but yet the treatments for neuropsychiatric symptoms are not satisfactory. But most individuals with AD will get a treatment that has cholinesterase inhibitors. Cholinesterase has moderate effect on behavior disturbances in AD whereas further study is needed in the effects and risks associated with the drug.
One model that has been constructed is an economic model. This model is used to represent the disease and its course. There is still a lot to be done when it comes to modeling AD for therapeutic developmental options for AD.
References
Grimmer, Timo; Kunz, Alexander. (Dec. 2006). Effects of cholinesterase inhibition on
behavioral disturbances in Alzheimer’s disease: A systematic review. In: Drugs and
Aging. Vol 23. Issue 12. P597, 11p. Walters Kluver Health. Language: English,
Database: Expanded Academic ASAP.
Green, Colin (2007). Modeling Disease Progression in Alzheimer’s disease. Pharmaco
Economics. Vol 25 Issue 9 p. 735-750 16p. 2 Charts.
Sitzer, D.I; Twamley, E.W.; Jeste, D.V. (Aug. 2006). Cognitive training in Alzheimer’s disease;
A meta-analysis of the literature. Acta Psychiatricia Scandinavica. Vol. 114 Issue 2, p75-
90, 16p. Publisher: Wiley-Blackwell.
Roos, P. (Oct 2012). Memory, menopause, and cognition. Obstertrics and Gynaeclolgy Forum. \
Vol 22 issue 4. P19-23 5p. 1 chart
Weingatner, Herbert; Eckardt, Michael; Grafman, Jordan; Molchan, Susan; Putnam, Karen;
Rawlings, Robert; Sunderland, Trey. (Jul 1993). The effects of repetition on memory
Performance in cognitively impaired patients. Neuropsychology, Vol 7(3) pp 385-395.
Publisher: American Psychological Association. (Journal Article) Database:
PsycARTICLES.
Mendiola-Precoma J.; Beruman, L.C.; Padilla, K; Garcia-Alcocer, G.; 7/28/2016. Therapies for
Prevention and Treatment of Alzheimer ’s disease. BioMed Research International. 1-17.
17p. (Article). ISSN
Bohn, Linzy, Kwong See, Sheree T., Fung, Helene H., 09/01/2016. Time Perspective and
Positivity Effects in Alzheimer’s Disease. Psychology and Aging. 08827974. Vol.
31, Issue 6.
Duke, James. Spring 2016. Still No Cure for Alzheimer ’s disease. Journal of the American
Herbalist Guild. 14(1); 65-75. 11p (Article) ISSN: 1538-7496. Database: CINAHL with
Full Text.
Oltra-Cucarella, Javier, Perez-Elvira, Rueben; Espert, Raul; Sohn McCormick, Anita. July 2016.
Are cognitive interventions effective in Alzheimer’s disease? A controlled meta-analysis
of the effects of bias. Special Issue; Cognitive Aging pp. 631-652. Publisher: American
Psychological Association; Corrected by: Corretion to Oltra-Cucarella et al. (Journal
Article). Database: PsycARTICLES
Lesourd, Mathieu, Baumand, Josselin; Jarry, Christophe; Etcharry-Bouyx, Frederique; Belliard,
Serge; Moreaud, Olivier; Croisile, Bernard; Chauvire; Valerie, Granjon, Marine; LeGall,
Didier, Osiurak, Francios. July 2016.Mechanical problem-solving strategies in
Alzheimer’s disease an semantic dementia. Neuropsychology. Vol 30(5). Special Issue.
Cognitive Aging. Pp. 612-623. Publisher: American Psychological Association. (Journal
Article) Database: PsycARTICLES
Magi, Simona; Castaldo, Pasqualing; Marci, Maria Loredana; Maiolino, Marta; Matteucci,
Alessandra, Bastioli, Guendalina; Gratteri, Santo; Amonoso, Salvatore;Laricora,
Vincenzo. 6/2/2016.Intracellular Calcuim Dysregulation: Implications for Alzheimer’s
Disease. BioMed Research International. 1-14. 14p. (Article) ISSN:2314-6133. Database
CINAHL with Full Text.
Ganske, Steffi, Haussmann, Robert, Gruschwitx, Antonia, Werner, Annett; Osterrah, Antje;
Baumgaertel, Johanna; Lange, Jan; Donix Katharina L.; Linn, Jennifer; Donix, Markus.
August 2016. American Journal of Alzheimer’s Disease and other Dementias. Family
History of Alzheimer’s disease and cortical thickness in patients with dementia. Pp.450-
456. Publisher: Sage Publications (Journal Article). Database: PsycINFO.
Cummings, Jeffery, Aisen, Paul S; Dubosi, Bruno; Frolich, Lutz; Jack Jr. Clifford R.; Jones, Roy
W.; Morris, John C.; Raskin, Joel; Dowsett, Sherie A.; Scheltens, Phillip. 9/20/2016
Drug Development in Alzheimer’s disease: The path to 2025. Alzheimer’s Research and
Therapy. Vol 8. P1-12. 12p. DOI:10. 1186/s 13195-016-0207-9.
Chen, Peiqing; Zhao, Wenjuan; Guo, Yanjie; XU, Juan; Yin, Ming. 6/27/2016. CX3CL1/CX3
CR1 in Alzheimer’s Disease: Target of Neuroprotection.BioMed Research International.
1-9. 9p (Article) ISSN: 2314-6133. Database: CINAHL with FullText.
Colangeli, Stefano; Boccia, Maddalena; Verde, Paola; Guariglia, Paola; Bianchini, Filippo;
Piccardi, Laura. Cognitive Reserve in healthy aging and Alzheimer;s disease: A meta-
Analysis of MRI. August 2016. American Journal of Alzheimer’s Disease and Other
Dementias. Vol 3(5). Pp.443-449. Publisher: Sage Publications. (Journal Article)
Database: PsycINFO.
mrsseetnacyexander
proposal_13.docx
0
