PL EN


Preferences help
enabled [disable] Abstract
Number of results
2006 | 6 | 2 | 95-107
Article title

Leczenie choroby Alzheimera: czy istnieją możliwości przewidywania klinicznej odpowiedzi na inhibitory cholinesterazy?

Content
Title variants
EN
Predictors of clinical response to cholinesterase inhibitors in dementia of Alzheimer’s type
Languages of publication
EN PL
Abstracts
EN
Acetylcholinesterase inhibitors are the mainstay of treatment of Alzheimer’s disease. However, in the majority of studies the proportion of patients demonstrating a significant clinical improvement under treatment does not exceed 40%. A routine method of identifying responders in clinical practice is the assessment of change in their cognitive functions during treatment. This review presents the available data on predictors of response to acetylcholinesterase inhibitor therapy in Alzheimer’s disease – factors allowing the prognosis of a patient’s reaction to treatment (in terms of target symptoms and tolerance) at its very beginning or even before therapy has been initiated. A variety of predictors will be discussed: genetic factors (apolipoprotein E, butyrylcholinesterase, choline acetyltransferase), demographic factors (age, gender), clinical factors (severity and rate of progression of dementia, comorbid neuropsychiatric symptoms, vascular risk factors, response to the test dose of the drug, results of neuropsychological testing, orthostatic hypotension), and work-up results (SPECT, MRI, EEG). The ability to predict patient’s response to treatment would allow a precise choice of szczególdrug for a given patient, taking into account its clinical efficacy in different subpopulations and potency for the generation of side effects, could also help cut down the global costs of prescribing those medications, and stimulate research on the biological mechanisms of Alzheimer’s disease. Altogether, the current level of knowledge on predictors of response to acetylcholinesterase inhibitors, with good tolerance and benign side-effect profile of this class of drugs, and lack of alternative, more effective methods of treatment of Alzheimer’s disease cannot entitle the physician to give up on the introduction of treatment in any single patient.
Discipline
Year
Volume
6
Issue
2
Pages
95-107
Physical description
References
  • 1. Francis P.T., Palmer A.M., Snape M. i wsp.: The cholinergic hypothesis of Alzheimer’s disease: a review of progress. J. Neurol. Neurosurg. Psychiatry 1999; 66: 137-147.
  • 2. Birks J.: Cholinesterase inhibitors for Alzheimer’s disease. Cochrane Database Syst. Rev. 2006; 1: CD005593.
  • 3. Bianchetti A., Ranieri P., Margiotta A. i wsp.: Pharmacological treatment of Alzheimer’s Disease. Aging Clin. Exp. Res. 2006; 18: 158-162.
  • 4. Giacobini E.: Cholinesterase inhibitor therapy stabilizes symptoms of Alzheimer disease. Alzheimer Dis. Assoc. Disord. 2000; 14 (S1): S3-10.
  • 5. Foster R.H., Plosker G.L.: Donepezil. Pharmacoeconomic implications of therapy. Pharmacoeconomics 1999; 16:99-114.
  • 6. Mega M.S., Masterman D.M., O’Connor S.M. i wsp.: The spectrum of behavioral responses to cholinesterase inhibitor therapy in Alzheimer disease. Arch. Neurol. 1999; 56: 1388-1393.
  • 7. Lanctot K.L., Herrmann N., Yau K.K. i wsp.: Efficacy and safety of cholinesterase inhibitors in Alzheimer’s disease: a meta-analysis. CMAJ 2003; 169: 557-564.
  • 8. Corder E.H., Saunders A.M., Strittmatter W.J. i wsp.: Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer’s disease in late onset families. Science 1993: 261: 921-923.
  • 9. Rubinsztein D.C., Easton D.F.: Apolipoprotein E genetic variation and Alzheimer’s disease: a meta-analysis. Dement. Geriatr. Cogn. Disord. 1999; 10: 199-209.
  • 10. Hirono N., Hashimoto M., Yasuda M. i wsp.: Accelerated memory decline in Alzheimer’s disease with apolipoprotein epsilon4 allele. J. Neuropsychiatry Clin. Neurosci. 2003; 15: 354-358.
  • 11. Schmechel D.E., Saunders A.M., Strittmatter WJ. i wsp.: Increased amyloid beta-peptide deposition in cerebral cortex as a consequence of apolipoprotein E genotype in late-onset Alzheimer disease. Proc. Natl. Acad. Sci. U.S.A. 1993; 90: 9649-9653.
  • 12. Farlow M.R., Cyrus P.A., Nadel A. i wsp.: Metrifonate treatment of AD: influence of APOE genotype. Neurology 1999; 53: 2010-2016.
  • 13. Poirier J., Delisle M.C., Quirion R. i wsp.: Apolipoprotein E4 allele as a predictor of cholinergic deficits and treatment outcome in Alzheimer disease. Proc. Natl. Acad. Sci. U.S.A. 1995; 92: 12260-12264.
  • 14. Farlow M.R., Lahiri D.K., Poirier J. i wsp.: Treatment outcome of tacrine therapy depends on apolipoprotein genotype and gender of the subjects with Alzheimer’s disease. Neurology 1998; 50: 669-677.
  • 15. MacGowan S.H., Wilcock G.K., Scott M.: Effect of gender and apolipoprotein E genotype on response to anticholinesterase therapy in Alzheimer’s disease. Int. J. Geri-atr. Psychiatry 1998; 13: 625-630.
  • 16. Rigaud A.S., Traykov L., Caputo L. i wsp.: The apolipoprotein E epsilon4 allele and the response to tacrine therapy in Alzheimer’s disease. Eur. J. Neurol. 2000; 7:255-258.
  • 17. Almkvist O., Jelic V, Amberla K. i wsp.: Responder characteristics to a single oral dose of cholinesterase inhibitor: a double-blind placebo-controlled study with tacrine in Alzheimer patients. Dement. Geriatr. Cogn. Disord. 2001; 12: 22-32.
  • 18. Sjogren M., Hesse C., Basun H. i wsp.: Tacrine and rate of progression in Alzheimer’s disease - relation to ApoE allele genotype. J. Neural Transm. 2001; 108: 451-458.
  • 19. Wallin A.K., Gustafson L., Sjogren M. i wsp.: Five-year outcome of cholinergic treatment of Alzheimer’s disease: early response predicts prolonged time until nursing home placement, but does not alter life expectancy. Dement. Geriatr. Cogn. Disord. 2004; 18: 197-206.
  • 20. Raskind M.A., Peskind E.R., Wessel T. i wsp.: Galantamine in AD: A 6-month randomized, placebo-controlled trial with a 6-month extension. The Galantamine USA-1 Study Group. Neurology 2000; 54: 2261-2268.
  • 21. Wilcock G.K., Lilienfeld S., Gaens E.: Efficacy and safety of galantamine in patients with mild to moderate Alzheimer’s disease: multicentre randomised controlled trial. Galantamine International-1 Study Group. BMJ 2000; 321: 1445-1449.
  • 22. Aerssens J., Raeymaekers P., Lilienfeld S. i wsp.: APOE genotype: no influence on galantamine treatment efficacy nor on rate of decline in Alzheimer’s disease. Dement. Geriatr. Cogn. Disord. 2001; 12: 69-77.
  • 23. Suh G.H., Jung H.Y., Lee C.U. i wsp.; Korean Galantamine Study Group: Effect of the apolipoprotein E epsilon4 allele on the efficacy and tolerability of galantamine in the treatment of Alzheimer’s disease. Dement. Geriatr. Cogn. Disord. 2006; 21: 33-39.
  • 24. Greenberg S.M., Tennis M.K., Brown L.B. i wsp.: Donepezil therapy in clinical practice: a randomized crossover study. Arch. Neurol. 2000; 57: 94-99.
  • 25. Oddoze C., Michel B.F., Lucotte G.: Apolipoprotein: E ε4 allele predicts a better response to donepezil therapy in Alzheimer’s disease. Alzheimer Reports 2000; 3: 213-216.
  • 26. Winblad B., Engedal K., Soininen H. i wsp.; Donepezil Nordic Study Group: A 1-year, randomized, placebo-controlled study of donepezil in patients with mild to moderate AD. Neurology 2001; 57: 489-495.
  • 27. Rigaud A.S., Traykov L., Latour F. i wsp.: Presence or absence of at least one epsilon 4 allele and gender are not predictive for the response to donepezil treatment in Alzheimer’s disease. Pharmacogenetics 2002; 12: 415-420.
  • 28. Courtney C., Farrell D., Gray R. i wsp.; AD2000 Collaborative Group: Long-term donepezil treatment in 565 patients with Alzheimer’s disease (AD2000): randomised doubleblind trial. Lancet 2004; 363: 2105-2115.
  • 29. Bizzarro A., Marra C., Acciarri A. i wsp.: Apolipoprotein E epsilon4 allele differentiates the clinical response to donepezil in Alzheimer’s disease. Dement. Geriatr. Cogn. Disord. 2005; 20: 254-261.
  • 30. Almkvist O., Darreh-Shori T., Stefanova E. i wsp.: Preserved cognitive function after 12 months of treatment with rivastigmine in mild Alzheimer’s disease in comparison with untreated AD and MCI patients. Eur. J. Neurol. 2004; 11: 253-261.
  • 31. Farlow M., Lane R., Kudaravalli S. i wsp.: Differential qualitative responses to rivastigmine in APOE epsilon 4 carriers and noncarriers. Pharmacogenomics J. 2004; 4: 332-335.
  • 32. Visser P.J., Scheltens P., Pelgrim E. i wsp.; Dutch ENA-NL-01 Study Group: Medial temporal lobe atrophy and APOE genotype do not predict cognitive improvement upon treatment with rivastigmine in Alzheimer’s disease patients. Dement. Geriatr. Cogn. Disord. 2005; 19: 126-133.
  • 33. Bullock R., Touchon J., Bergman H. i wsp.: Rivastigmine and donepezil treatment in moderate to moderately-severe Alzheimer’s disease over a 2-year period. Curr. Med. Res. Opin. 2005;21:317-327.
  • 34. Perry E.K., Perry R.H., Blessed G. i wsp.: Changes in brain cholinesterases in senile dementia of Alzheimer type. Neuropathol. Appl. Neurobiol. 1978; 4: 273-277.
  • 35. Bartels C.F., Jensen F.S., Lockridge O. i wsp.: DNA mutation associated with the human butyrylcholinesterase K variant and its linkage to the atypical variant mutation and other polymorphic sites. Am. J. Hum. Genet. 1992: 50: 1086-1103.
  • 36. Ballard C., Morris C., Kalaria R. i wsp.: The k variant of the butyrylcholinesterase gene is associated with reduced phosphorylation of tau in dementia patients. Dement. Geriatr. Cogn. Disord. 2005; 19: 357-360.
  • 37. Holmes C., Ballard C., Lehmann D. i wsp.: Rate of progression of cognitive decline in Alzheimer’s disease: effect of butyrylcholinesterase K gene variation. J. Neurol. Neu-rosurg. Psychiatry 2005; 76: 640-643.
  • 38. Bertram L., McQueen M., Mullin K. i wsp.: The Alz-Gene Database. Alzheimer Research Forum. Available at: www.alzgene.org. Accessed 2006/08/03.
  • 39. Wilcock G.K., Esiri M.M., BowenD.M. i wsp.: Alzheimer’s disease. Correlation of cortical choline acetyltransferase activity with the severity of dementia and histological abnormalities. J. Neurol. Sci. 1982; 57: 407-417.
  • 40. Harold D., Macgregor S., Patterson C.E. i wsp.: A single nucleotide polymorphism in CHAT influences response to acetylcholinesterase inhibitors in Alzheimer’s disease. Pharmacogenet. Genomics 2006; 16: 75-77.
  • 41. Ho G.J., Hansen L.A., Alford M.F. i wsp.: Age at onset is associated with disease severity in Lewy body variant and Alzheimer’s disease. Neuroreport 2002; 13: 1825-1828.
  • 42. Bullock R., Bergman H., Touchon J. i wsp.: Effect of age on response to rivastigmine or donepezil in patients with Alzheimer’s disease. Curr. Med. Res. Opin. 2006; 22: 483-494.
  • 43. Kraemer H.C., Tinklenberg J., Yesavage J.A.: “How far” vs. “how fast” in Alzheimer’s disease. The question revisited. Arch. Neurol. 1994; 51: 275-279.
  • 44. Kaufer D., Cummings J.L., Christine D.: Differential neuropsychiatric symptom responses to tacrine in Alzheimer’s disease: relationship to dementia severity. J. Neuropsychiatry Clin. Neurosci. 1998; 10: 55-63.
  • 45. Farlow M.R., Brashear A., Hui S. i wsp.: The effects of tacrine in patients with mild versus moderate stage Alzheimer’s disease. W: Iqbal K., Mortimer J., Winblad B. i wsp.: Research Advances in Alzheimer’s Disease and Related Disorders. Chichester, England, John Wiley & Sons Inc. 1995: 2884-2892.
  • 46. Qizilbash N., Whitehead A., Higgins J. i wsp.: Choline-sterase inhibition for Alzheimer disease: a meta-analysis of the tacrine trials. Dementia Trialists Collaboration. JAMA 1998; 280: 1777-1782.
  • 47. Doraiswamy P.M., Krishnan K.R., Anand R. i wsp.: Long-term effects of rivastigmine in moderately severe Alzheimer’s disease: does early initiation of therapy offer sustained benefits? Prog. Neuropsychopharmacol. Biol. Psychiatry 2002; 26: 705-712.
  • 48. Potkin S.G., Anand R., Hartman R i wsp.: Impact of Alzheimer’s disease and rivastigmine treatment on activities of daily living over the course of mild to moderately severe disease. Prog. Neuropsychopharmacol. Biol. Psychiatry 2002;26:713-720.
  • 49. Galasko D., Kershaw P.R., Schneider L. i wsp.: Galantamine maintains ability to perform activities of daily living in patients with Alzheimer’s disease. J. Am. Geriatr. Soc. 2004; 52: 1070-1076.
  • 50. Sano M., Wilcock G.K., van Baelen B. i wsp.: The effects of galantamine treatment on caregiver time in Alzheimer’s disease. Int. J. Geriatr. Psychiatry 2003; 18: 942-950.
  • 51. Farlow M.R., Hake A., Messina J. i wsp.: Response of patients with Alzheimer disease to rivastigmine treatment is predicted by the rate of disease progression. Arch. Neurol 2001; 58: 417-422.
  • 52. Farlow M.R., Small G.W., Quarg P. i wsp.: Efficacy of rivastigmine in Alzheimer’s disease patients with rapid disease progression: results of a meta-analysis. Dement. Geriatr. Cogn. Disord. 2005; 20: 192-197.
  • 53. Stern R.G., Mohs R.C., Davidson M. i wsp.: A longitudinal study of Alzheimer’s disease: measurement, rate, and predictors of cognitive deterioration. Am. J. Psychiatry 1994; 151: 390-396.
  • 54. Barker W.W., Luis C.A., Kashuba A. i wsp.: Relative frequencies of Alzheimer disease, Lewy body, vascular and frontotemporal dementia, and hippocampal sclerosis in the State of Florida Brain Bank. Alzheimer Dis. Assoc. Disord. 2002; 16:203-212.
  • 55. Grossberg G.T.: The ABC of Alzheimer’s disease: behavioral symptoms and their treatment. Int. Psychogeriatr. 2002; 14 (Sl): 27-49.
  • 56. Liberini P, Valerio A., Memo M. i wsp.: Lewy-body dementia and responsiveness to cholinesterase inhibitors: a paradigm for heterogeneity of Alzheimer’s disease? Trends Pharmacol. Sci. 1996; 17: 155-160.
  • 57. Samuel W, Caligiuri M., Galasko D. i wsp.: Better cognitive and psychopathologic response to donepezil in patients prospectively diagnosed as dementia with Lewy bodies: a preliminary study. Int. J. Geriatr. Psychiatry 2000; 15: 794-802.
  • 58. Touchon J., Bergman H., Bullock R. i wsp.: Response to rivastigmine or donepezil in Alzheimer’s patients with symptoms suggestive of concomitant Lewy body pathology. Curr. Med. Res. Opin. 2006; 22: 49-59.
  • 59. McKeith I., Del Ser T., Spano P i wsp.: Efficacy of rivastigmine in dementia with Lewy bodies: a randomised, double-blind, placebo-controlled international study. Lancet 2000: 356:2031-2036.
  • 60. Kalaria R.N.: The role of cerebral ischemia in Alzheimer’s disease. Neurobiol. Aging 2000; 21: 321-330.
  • 61. Fukui T., Taguchi S.: Do vascular lesions and related risk factors influence responsiveness to donepezil chloride in patients with Alzheimer’s disease? Dement. Geriatr. Cogn. Disord. 2005; 20: 15-24.
  • 62. Erkinjuntti T, Kurz A., Gauthier S. i wsp.: Efficacy of galantamine in probable vascular dementia and Alzheimer’s disease combined with cerebrovascular disease: a randomised trial. Lancet 2002; 359: 1283-1290.
  • 63. Kurz A.F., Erkinjuntti T, Small G.W. i wsp.: Long-term safety and cognitive effects of galantamine in the treatment of probable vascular dementia or Alzheimer’s disease with cerebrovascular disease. Eur. J. Neurol. 2003: 10: 633-640.
  • 64. Bullock R., Erkinjuntti T, Lilienfeld S.; GAL-INT-6 Study Group: Management of patients with Alzheimer’s disease plus cerebrovascular disease: 12-month treatment with galantamine. Dement. Geriatr. Cogn. Disord. 2004; 17: 29-34.
  • 65. Kumar V, Anand R., Messina J. i wsp.: An efficacy and safety analysis of Exelon in Alzheimer’s disease patients with concurrent vascular risk factors. Eur. J. Neurol. 2000; 7: 159-169.
  • 66. Erkinjuntti T, Skoog I., Lane R. i wsp.: Rivastigmine in patients with Alzheimer’s disease and concurrent hypertension. Int. J. Clin. Pract. 2002; 56: 791-796.
  • 67. Erkinjuntti T, Skoog I., Lane R. i wsp.: Potential longterm effects of rivastigmine on disease progression may be linked to drug effects on vascular changes in Alzheimer brains. Int. J. Clin. Pract. 2003; 57: 756-760.
  • 68. Connelly P.J., Prentice N.P., Fowler K.G.: Hypertension, white matter change and response to cholinesterase inhibitors in Alzheimer’s disease. Int. J. Geriatr. Psychiatry 2005; 20: 623-628.
  • 69. Connelly PJ., Prentice N.P.: Current smoking and response to cholinesterase inhibitor therapy in Alzheimer’s disease. Dement. Geriatr. Cogn. Disord. 2005; 19: 11-14.
  • 70. Connelly P.J., Prentice N.P., Fowler K.G.: Predicting the outcome of cholinesterase inhibitor treatment in Alzheimer’s disease. J. Neurol. Neurosurg. Psychiatry 2005; 76: 320-324.
  • 71. Alhainen K., Helkala E.L., Riekkinen P: Psychometric discrimination of tetrahydroaminoacridine responders in Alzheimer patients. Dementia 1993; 4: 54-58.
  • 72. Di Lazzaro V, Oliviero A., Pilato F. i wsp.: Neurophysiological predictors of long term response to AChE inhibitors in AD patients. J. Neurol. Neurosurg. Psychiatry 2005; 76: 1064-1069.
  • 73. Schneider L.S., Lyness S.A., Pawluczyk S. i wsp.: Do blood pressure and age predict response to tacrine (THA) in Alzheimer’s disease? A preliminary report. Psychopharmacol Bull 1991; 27: 309-314.
  • 74. Pomara N., Deptula D., Singh R.: Pretreatment postural blood pressure drop as a possible predictor of response to the cholinesterase inhibitor velnacrine (HP 029) in Alzheimer’s disease. Psychopharmacol Bull 1991; 27: 301-307.
  • 75. Holman B.L., Johnson K.A., Gerada B. i wsp.: The scintigraphic appearance of Alzheimer’s disease: a prospective study using technetium-99m-HMPAO SPECt. J. Nucl. Med. 1992; 33: 181-185.
  • 76. Hanyu H., Shimizu T., Tanaka Y. i wsp.: Regional cerebral blood flow patterns and response to donepezil treatment in patients with Alzheimer’s disease. Dement. Geriatr. Cogn. Disord. 2003; 15: 177-182.
  • 77. Mega M.S., Dinov I.D., Lee L. i wsp.: Orbital and dorsolateral frontal perfusion defect associated with behavioral response to cholinesterase inhibitor therapy in Alzheimer’s disease. J. Neuropsychiatry Clin. Neurosci. 2000; 12: 209-218.
  • 78. Tanaka M., Namiki C., Thuy D.H. i wsp.: Prediction of psychiatric response to donepezil in patients with mild to moderate Alzheimer’s disease. J. Neurol. Sci. 2004; 225: 135-141.
  • 79. Shimizu S., Hanyu H., Iwamoto T i wsp.: SPECT follow-up study of cerebral blood flow changes during Donepezil therapy in patients with Alzheimer’s disease. J. Neuroimaging 2006; 16: 16-23.
  • 80. Tanaka Y., Hanyu H., Sakurai H. i wsp.: Atrophy of the substantia innominata on magnetic resonance imaging predicts response to donepezil treatment in Alzheimer’s disease patients. Dement. Geriatr. Cogn. Disord. 2003; 16:119-125.
  • 81. Csernansky J.G., Wang L., Miller J.P i wsp.: Neuroanatom-ical predictors of response to donepezil therapy in patients with dementia. Arch. Neurol. 2005; 62: 1718-1722.
  • 82. Riekkinen P. Jr., Soininen H., Helkala E.L. i wsp.: Hippocampal atrophy, acute THA treatment and memory in Alzheimer’s disease. Neuroreport 1995; 6: 1297-1300.
  • 83. Visser PJ., Scheltens P., Pelgrim E. i wsp.; Dutch ENA-NL-01 Study Group: Medial temporal lobe atrophy and APOE genotype do not predict cognitive improvement upon treatment with rivastigmine in Alzheimer’s disease patients. Dement. Geriatr. Cogn. Disord. 2005; 19: 126-133.
  • 84. Rosen I.: Electroencephalography as a diagnostic tool in dementia. Dement. Geriatr. Cogn. Disord. 1997; 8:110-116.
  • 85. Brassen S., Adler G.: Short-term effects of acetylcholinesterase inhibitor treatment on EEG and memory performance in Alzheimer patients: an open, controlled trial. Pharmacopsychiatry 2003; 36: 304-308.
  • 86. Alhainen K., Partanen J., Reinikainen K. i wsp.: Discrimination of tetrahydroaminoacridine responders by a single dose pharmaco-EEG in patients with Alzheimer’s disease. Neurosci. Lett. 1991; 127: 113-116.
  • 87. Alhainen K., Riekkinen PJ. Sr.: Discrimination of Alzheimer patients responding to cholinesterase inhibitor therapy. Acta Neurol. Scand. Suppl. 1993; 149: 16-21.
  • 88. Knott V, Mohr E., Mahoney C. i wsp.: Pharmaco-EEG test dose response predicts cholinesterase inhibitor treatment outcome in Alzheimer’s disease. Methods Find Exp. Clin. Pharmacol. 2000; 22: 115-122.
  • 89. Adler G., Brassen S., Chwalek K. i wsp.: Prediction of treatment response to rivastigmine in Alzheimer’s dementia. J. Neurol. Neurosurg. Psychiatry 2004; 75: 292-294.
Document Type
article
Publication order reference
YADDA identifier
bwmeta1.element.psjd-a8fbd210-dddb-4e29-a767-e95f52acdcbc
Identifiers
JavaScript is turned off in your web browser. Turn it on to take full advantage of this site, then refresh the page.