Biological Predictors of Alzheimer's Disease Treatment

알츠하이머병 치료의 생물학적 예측인자

  • Joo, Soo-Hyun (Department of Psychiatry, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea) ;
  • Im, Jeejin (Catholic Argo-Medical Center, Seoul St. Mary's Hospital, The Catholic University of Korea) ;
  • Lee, Chang-Uk (Department of Psychiatry, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea)
  • 주수현 (가톨릭대학교 의과대학 서울성모병원 정신과학교실) ;
  • 임제진 (가톨릭대학교 서울성모병원 농의학연구센터) ;
  • 이창욱 (가톨릭대학교 의과대학 서울성모병원 정신과학교실)
  • Received : 2014.11.12
  • Accepted : 2014.11.14
  • Published : 2014.11.30

Abstract

Variety of biomarkers that are related to the Alzheimer's disease and its diagnosis and progress have been found. However, research lacks in predicting the reaction of the treatment. In addition, there is no definite treatment reaction to the disease but rather it is varied. The purpose of this review article is to study the research of the biomarkers that are able to predict the treatment reaction. There was a research that illustrated a relationship between plasma amyloid ${\beta}$ peptide, cerebrospinal fluid tau, neuroanatomical biomarkers and acetylcholinesterase inhibitors. Polymorphisms in genes of the cholinergic markers AChE, BuChE, ChAT and PON-1 were found to be associated with better clinical response to acetylcholinesterase inhibitors. Many pharmacogenetic studies have been conducted to evaluate the impact of the lipoprotein apolipoprotein E (APOE) genotype on treatment response to acetylcholinesterase inhibitor. However, there is no significant influence of the APOE genotypes on treatment response. Further research is needed to find other predictors of treatment with acetylcholinesterase inhibitors in patients with Alzheimer's disease.

Keywords

References

  1. Miller BL, Boeve BF. The behavioral neurology of dementia. Cambridge: Cambridge University Press;2009.
  2. Jack CR Jr, Knopman DS, Jagust WJ, Shaw LM, Aisen PS, Weiner MW, et al. Hypothetical model of dynamic biomarkers of the Alzheimer's pathological cascade. Lancet Neurol 2010;9:119-128. https://doi.org/10.1016/S1474-4422(09)70299-6
  3. Albert MS, DeKosky ST, Dickson D, Dubois B, Feldman HH, Fox NC, et al. The diagnosis of mild cognitive impairment due to Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. Alzheimers Dement 2011;7:270-279. https://doi.org/10.1016/j.jalz.2011.03.008
  4. Sobow T, Flirski M, Liberski P, Kloszewska I. Plasma Abeta levels as predictors of response to rivastigmine treatment in Alzheimer's disease. Acta Neurobiol Exp (Wars) 2007;67:131-139.
  5. Wallin AK, Hansson O, Blennow K, Londos E, Minthon L. Can CSF biomarkers or pre-treatment progression rate predict response to cholinesterase inhibitor treatment in Alzheimer's disease? Int J Geriatr Psychiatry 2009;24:638-647. https://doi.org/10.1002/gps.2195
  6. Wilquet V, De Strooper B. Amyloid-beta precursor protein processing in neurodegeneration. Curr Opin Neurobiol 2004;14:582-588. https://doi.org/10.1016/j.conb.2004.08.001
  7. Tanzi RE, Bertram L. Twenty years of the Alzheimer's disease amyloid hypothesis: a genetic perspective. Cell 2005;120:545-555. https://doi.org/10.1016/j.cell.2005.02.008
  8. Basun H, Nilsberth C, Eckman C, Lannfelt L, Younkin S. Plasma levels of Abeta42 and Abeta40 in Alzheimer patients during treatment with the acetylcholinesterase inhibitor tacrine. Dement Geriatr Cogn Disord 2002;14:156-160. https://doi.org/10.1159/000063605
  9. Sobow T, Flirski M, Kloszewska I, Liberski PP. Plasma levels of alpha beta peptides are altered in amnestic mild cognitive impairment but not in sporadic Alzheimer's disease. Acta Neurobiol Exp (Wars) 2005; 65:117-124.
  10. Zimmermann M, Borroni B, Cattabeni F, Padovani A, Di Luca M. Cholinesterase inhibitors influence APP metabolism in Alzheimer disease patients. Neurobiol Dis 2005;19:237-242. https://doi.org/10.1016/j.nbd.2005.01.002
  11. Moriearty PL, Seubert P, Galasko D, Markwell S, Unni L, Vicari S, et al. Effects of time and cholinesterase inhibitor treatment on multiple cerebrospinal fluid parameters in Alzheimer's disease. Methods Find Exp Clin Pharmacol 1999;21:549-554. https://doi.org/10.1358/mf.1999.21.8.794837
  12. Stefanova E, Blennow K, Almkvist O, Hellstrom-Lindahl E, Nordberg A. Cerebral glucose metabolism, cerebrospinal fluid-beta-amyloid1-42 (CSF-Abeta42), tau and apolipoprotein E genotype in longterm rivastigmine and tacrine treated Alzheimer disease (AD) patients. Neurosci Lett 2003;338:159-163. https://doi.org/10.1016/S0304-3940(02)01384-8
  13. Wallin AK, Blennow K, Zetterberg H, Londos E, Minthon L, Hansson O. CSF biomarkers predict a more malignant outcome in Alzheimer disease. Neurology 2010;74:1531-1537. https://doi.org/10.1212/WNL.0b013e3181dd4dd8
  14. Csernansky JG, Wang L, Miller JP, Galvin JE, Morris JC. Neuroanatomical predictors of response to donepezil therapy in patients with dementia. Arch Neurol 2005;62:1718-1722. https://doi.org/10.1001/archneur.62.11.1718
  15. Hongo J, Nakaaki S, Shinagawa Y, Murata Y, Sato J, Tatsumi H, et al. SPECT-identified neuroanatomical predictor of the cognitive effects of donepezil treatment in patients with Alzheimer's disease. Dement Geriatr Cogn Disord 2008;26:556-566. https://doi.org/10.1159/000181148
  16. Modrego PJ, Rios C, Perez Trullen JM, Garcia-Gomara MJ, Errea JM. Carotid intima-media thickness as a predictor of response to cholinesterase inhibitors in Alzheimer's disease: an open-label trial. CNS Drugs 2009;23:253-260. https://doi.org/10.2165/00023210-200923030-00006
  17. Noetzli M, Eap CB. Pharmacodynamic, pharmacokinetic and pharmacogenetic aspects of drugs used in the treatment of Alzheimer's disease. Clin Pharmacokinet 2013;52:225-241. https://doi.org/10.1007/s40262-013-0038-9