Research Paper Topics On Alzheimers

1. United Nations. World population prospects: the 1996 revision. Washington, DC: Population division of the Department of Economic and Social Affairs of the United Nations Secretariat, 1998.

2. Evans DA, Funkenstein HH, Albert MS, et al. Prevalence of Alzheimer's disease in a community population of older persons. JAMA 1989;262:2551-2556. [PubMed]

3. Katzman R, Fox P. The world-wide impact of dementia. Projections of prevalence and costs. In: Mayeaux R, Christen Y, eds. Epidemiology of Alzheimer's disease: from gene to prevention. New York: Springer-Verlag, 1999:1-17.

4. McKhann G, Drachman D, Folstein M, et al. Clinical diagnosis of Alzheimer's disease: a report of the NINCDS-ADRDA work-group under the auspices of the Department of Health and Human Services Task Force on Alzheimer's disease. Neurology 1984;34:939-944. [PubMed]

5. Mayeaux R. Predicting who will develop Alzheimer's disease. In: Mayeaux R, Christen Y, eds. Epidemiology of Alzheimer's disease: from gene to prevention. New York: Springer-Verlag, 1999:19-31.

6. Peterson RC, Smith GE, Waring SC, et al. Mild cognitive impairment: clinical characterization and outcome. Arch Neurol 1999;56:303-308. [PubMed]

7. Cummings JL, Vinters H, Cole G, et al. Alzheimer's disease: etiologies, pathophysiology, cognitive reserve and treatment opportunities. Neurology 1998;51(suppl 1):2-17S. [PubMed]

8. Lendon C, Ashall F, Goate, AM. Exploring the etiology of Alzheimer disease using molecular genetics. JAMA 1997;277:825-831. [PubMed]

9. Strittmatter WJ, Roses AD. Apolipoprotein E and Alzheimer's disease. Annu Rev Neurosci 1996;19:53-57. [PubMed]

10. Slooter AJC, Cruts M, Kalmijn S, et al. Apolipoprotein E and dementia. Risk estimates from a population-based incidence study: the Rotterdam study. Arch Neurol 1998;55:964-968. [PubMed]

11. Murphy GM, Taylor J, Tinklenberg JR, et al. The apolipoprotein E epsilon 4 allele is associated with increased behavioral disturbance in Alzheimer's disease [letter]. Am J Geriatr Psychiatry 1997;5:88-89. [PubMed]

12. O'Hara R, Yesavage JA, Kraemer HC, et al. The APOE ε4 allele is associated with decline on delayed recall performance in community-dwelling older adults. J Am Geriatr Soc 1998;46:1493-1498. [PubMed]

13. Relkin NR, Younga JK, Tsai J, et al. The National Institute on Aging/Alzheimer's Association recommendations on the application of apolipoprotein E genotyping to Alzheimer's disease. Ann N Y Acad Sci 1996;802:149-171. [PubMed]

14. Katzman R. Education and the prevalence of dementia and Alzheimer's disease. Neurology 1993;43:13-20. [PubMed]

15. Haan M, Shemanski L, Jagust WJ, et al. The role of APOE e4 in modulating effects of other risk factors for cognitive decline in elderly persons. JAMA 1999; 282:40-46. [PubMed]

16. Small GW. Treatment of Alzheimer's disease: current approaches and promising developments. Am J Med 1998;104(suppl):32-38S. [PubMed]

17. Bassuk SS, Glass TA, Berkman LF. Social disengagement and incident cognitive decline in community-dwelling elderly persons. Ann Intern Med 1999;131:165-73. [PubMed]

18. Duara R, Lopez-Alberola R, Barker WW, et al. Age at onset of Alzheimer's disease (AD): interaction of gender, family history, and apolipoprotein E genotype. Neurology 1995;45(suppl 4):A470.

19. Sirvio J. Strategies that support declining cholinergic neurotransmission in Alzheimer's disease patients. Gerontology 1999;45:3-14. [PubMed]

20. Nordberg A, Svensson AL. Cholinesterase inhibitors in the treatment of Alzheimer's disease: a comparison of tolerability and pharmacology [published correction appears in Drug Saf 1999 Feb;20:146]. Drug Saf 1998;19:465-480. [PubMed]

21. Qizilbash N, Birks J, Lopez Arrieta J, et al. Tacrine for Alzheimer's disease. Cochrane Library. Issue 4. Oxford: Update Software, 1999.

22. Schneider LS. New therapeutic approaches to cognitive impairment. J Clin Psychiatry 1998;59:8-13. [PubMed]

23. Burns A, Rossor M, Hecker J, et al. The effects of donepezil in Alzheimer's disease—results from a multinational trial. Dement Geriatr Cogn Disord 1999;10:237-244. [PubMed]

24. Rogers SL, Doody RS, Mohs RC, et al. Donepezil improves cognition and global function in Alzheimer disease: a 15-week, double-blind, placebo-controlled study. Arch Intern Med 1998;158:1021-1031. [PubMed]

25. Birks JS, Melzer D. Donepezil for mild and moderate Alzheimer's disease. Cochrane Library. Issue 4. Oxford: Update Software, 1999.

26. Birks J, Iakovidou V, Tsolaki M. Rivastigmine for Alzheimer's disease. Cochrane Library. Issue 4. Oxford: Update Software, 1999.

27. Krall WJ, Sramek JJ, Cutler NR. Cholinesterase inhibitors: a therapeutic strategy for Alzheimer disease. Ann Pharmacother 1999;33:441-450. [PubMed]

28. Kawas C, Resnick S, Morrison A, et al. A prospective study of estrogen replacement therapy and the risk of developing Alzheimer's disease: the Baltimore longitudinal study of aging. Neurology 1997;48:1517-1521. [PubMed]

29. Henderson VW. The epidemiology of Alzheimer's disease: the role of estrogen in reducing risk. In: Mayeaux R, Christen Y, eds. Epidemiology of Alzheimer's disease: from gene to prevention. New York: Springer-Verlag; 1999:49-63.

30. Honjo H, Ogino Y, Tanaka K, et al. An effect of conjugated estrogen to cognitive impairment in women with senile dementia-Alzheimer's type: a placebo-controlled, double-blind study. J Jpn Menopause Soc 1993;1:167-171.

31. Asthana S, Craft S, Baker LD, et al. Cognitive and neuroendocrine response to transdermal estrogen in postmenopausal women with Alzheimer's disease: results of a placebo-controlled, double-blind pilot study. Psychoneuroendocrinology 1999;24:657-677. [PubMed]

32. Schneider LS, Farlow MR, Henderson VW, et al. Effects of estrogen replacement therapy on response to tacrine in patients with Alzheimer's disease. Neurology 1996;46:1580-1584. [PubMed]

33. Behl C, Skutella T, Lezoualch F, et al. Neuroprotection against oxidative stress by estrogens: structure-activity relationship. Mol Pharmacol 1997;51:535-541. [PubMed]

34. Nathan L, Chaubhuri G. Antioxidant and prooxidant actions of estrogens: potential physiological and clinical implications. Semin Reprod Endocrinol 1998;16:309-314. [PubMed]

35. Yaffe K, Sawaya G, Lieberburg I, et al. Estrogen therapy in postmenopausal women: effects on cognitive function and dementia. JAMA 1998;279:688-695. [PubMed]

36. Wickelgren I. Estrogen stakes claim to cognition. Science 1997;276:675-678. [PubMed]

37. Jaffe AB, Toran-Allerand CD, Greengard P, et al. Estrogen regulates metabolism of Alzheimer amyloid beta precursor protein. J Biol Chem 1994;269:13065-13068. [PubMed]

38. Kawas CH. Inflammation, anti-inflammatory drugs and Alzheimer's disease. In: Mayeaux R, Christen Y, eds. Epidemiology of Alzheimer's disease: from gene to prevention. New York: Springer-Verlag; 1999:65-72.

39. Aisen PS, Marin D, Altstiel L, et al. A pilot study of prednisone in Alzheimer's disease. Dementia 1996;7:201-206. [PubMed]

40. Rogers J, Kirby LC, Hempelman SR, et al. Clinical trial of indomethacin in Alzheimer's disease. Neurology 1993;43:1609-1611. [PubMed]

41. Sayre LM, Zagorski MG, Surewicz WK, et al. Mechanisms of neurotoxicity associated with amyloid beta deposition and the role of free radicals in the pathogenesis of Alzheimer's disease: a critical appraisal. Chem Res Toxicol 1997;10:518-526. [PubMed]

42. Le Bars PL, Katz MM, Berman N, et al. A placebo-controlled, double-blind, randomized trial of an extract of Ginkgo biloba for dementia. JAMA 1997;278:1327-1332. [PubMed]

43. Kanowski S, Hermann WM, Stephan K, et al. Proof of efficacy of the ginkgo biloba special extract EGb 761 in outpatients suffering from mild to moderate primary degenerative dementia of the Alzheimer type or multi-infarct dementia. Pharmacopsychiatry 1996;29:47-56. [PubMed]

44. Oken BS, Storzbach DM, Kaye JA. The efficacy of Ginkgo biloba on cognitive function in Alzheimer disease. Arch Neurol 1998;55:1409-1415. [PubMed]

45. Sano M, Ernesto C, Thomas RG, et al. A controlled trial of selegiline, alpha-tocopherol, or both as treatment for Alzheimer's disease. N Engl J Med 1997;336:1216-1222. [PubMed]

46. Birks J, Flicker L. Selegiline for Alzheimer's disease. Cochrane Library. Issue 4. Oxford: Update Software, 1999.

47. Consensus on diagnosis and treatment of dementia: summary of recommendations. American Geriatric Society Symposia May 1998:13-14.

48. Poirier J. Apolipoprotein E4, cholinergic integrity and the pharmacogenetics of Alzheimer's disease. J Psychiatry Neurosci 1999;24:147-153. [PMC free article][PubMed]

49. De Deyn PP, Rabheru K, Rasmussen A, et al. A randomized trial of risperidone, placebo, and haloperidol for behavioral symptoms of dementia. Neurology 1999;53:946-955. [PubMed]

50. Katz IR, Jeste DV, Mintzer JE, et al. Comparison of risperidone and placebo for psychosis and behavioral disturbances associated with dementia: a randomized, double-blind trial. J Clin Psychiatry 1999;60:107-115. [PubMed]

51. Teri L, Logsdon RG, Uomoto J, et al. Behavioral treatment of depression in dementia patients: a controlled clinical trial. J Gerontol B Psychol Sci Soc Sci 1997;52:P159-P166. [PubMed]

52. Thompson C, Thompson G. Support for carers of people with Alzheimer's type dementia. Cochrane Library. Issue 4. Oxford: Update Software, 1999.

53. Toide K, Iwamoto Y, Fujiwara T, et al. JTP-4819: a novel prolyl endopeptidase inhibitor with potential as a cognitive enhancer. J Pharmacol Exp Ther 1995;274:1370-1378. [PubMed]

54. Schenk D, Barbour R, Dunn W, et al. Immunization with amyloid-beta attenuates Alzheimer-disease-like pathology in the PDAPP mouse. Nature 1999;400:173-177. [PubMed]

The Biology and Psychology of Alzheimer’s

Alzheimer’s is a well-known medical condition in the elderly with no known cause.The psychological impact is well documented and includes memory loss as the major noticeable symptom but is also includes confusion, loss of language cognition and eventually loss of motor skills. While the cause is unknown there are certain biologic sequences common to all Alzheimer’s patients such as physical shrinking of the brain and hardened brain tissue.

Memory loss is the largest and most alarming psychological symptom of Alzheimer’s. Often it starts with forgetting recently learned information, such as dates and appointments or directions. Solving problems or paying bills becomes more difficult requiring much greater concentration than previously required to perform the same task. Confusion is also common as the disease progresses. Patients often find themselves lost and not remembering how they arrived where they are. Changes in mood and personality also occur in the later stages as fear, depression and anxiety take over their lives.

Eventually the patient loses long term memory. They are no longer able to recognize family and become dependent on others for physical care. The final stages of Alzheimer’s leaves the patient with the inability to communicate, loss of bodily functions, weight loss, seizures and death.

Research into the biological cause of Alzheimer’s continues. Tangles, misfolds of the protein tau, are found in the brains cells of Alzheimer’s patients. The tangles resemble fibers that clump together in areas of the brain, causing the tau protein to fail. It is not known why the tau protein fails to fold properly and lose function only that the misfolds cause the tangles. The misfiring tau’s spread from one brain region to another in a recognizable pattern that causes the progressive degeneration of the brain as seen by the psychological symptoms.

Another major biologic change in an Alzheimer’s affected brain is Amyloid plaques, protein fragments accumulated outside of the brain cells. These plaques are uniquely different from the tau proteins found within the brain cell. Normal brain function allows for the absorption and processing of the protein fragments without damage while the Alzheimer’s affected brain loses this ability causing the proteins to build hard plaques further causing the psychological changes associated with the disease.

The combination of the tau protein damage inside the cell and the Amyloid plaque buildup outside the brain cell creates a loss of connectivity between cells leading to diminished function, cell death, the psychological changes and the eventual death of the patient. While the biological and psychological role of Alzheimer’s is more understood the cause of these protein failures is still unknown and still being researched.


Leave a Reply

Your email address will not be published. Required fields are marked *