Diffusion- and Perfusion-weighted Magnetic Resonance (MR) Imaging and MR Angiography in Apolipoprotein E Polymorpism and Stroke

Diffusion- and Perfusion-weighted Magnetic Resonance (MR) Imaging and MR Angiography in Apolipoprotein E Polymorpism and Stroke

Hartikainen Päivi, Liu Yawu, Vanninen Ritva L

European Neurological Review, 2009;4(2):48-50

download article

| More
dots

Abstract
Apolipoprotein E (ApoE) allele ε4 may have both adverse and beneficial effects in patients with acute stroke. ApoE allele ε4 is associated with increased vulnerability of the brain, which is reflected in relatively greater lesion growth and low threshold for the brain tissue to survive stroke and in the lack of correlation between the imaging findings and clinical outcome in ε4 carriers. Conversely, ε4 has at least a seemingly beneficial effect on the cerebral blood flow, i.e. collateral blood flow is better in ε4 carriers compared with non-carriers. In the clinical studies that focus on the relationship between harbouring ε4 and clinical outcomes in ischaemic stroke patients, the adverse and beneficial effects may be compromised. In any case, when possible, ApoE allele ε4 should be classified as a confounding factor when studying stroke either by imaging methods or clinically.

Keywords
Apolipoprotein E, genetics, imaging, magnetic resonance, diffusion, perfusion, acute, stroke, outcome

Disclosure: The authors have no conflicts of interest to declare.
Received: 4 January 2009 Accepted: 21 April 2009
Correspondence: Ritva L Vanninen, Professor, Department of Clinical Radiology, Kuopio University Hospital, PO Box 1777, 70211 Kuopio, Finland. E: ritva.vanninen@kuh.fi

Stroke is the leading cause of long-term disability and the second leading cause of death worldwide. According to World Health Organization (WHO) estimates, 15 million people each year suffer from strokes and five million are left permanently disabled.1 Ischaemic stroke is the most common type of stroke, accounting for 65–80% of all strokes. Accumulated data strongly suggest genetic influences in the pathogenesis of ischaemic stroke. Genetic factors could act by modulating the effects of conventional risk factors on the end organs or by a direct independent effect on stroke risk and on infarct evolution in acute phase and outcome.2,3

Apolipoprotein E (ApoE) is a polymorphic glycoprotein associated with the transport of cholesterol and other lipids. In the central nervous system, ApoE is involved in the growth, maintenance and regeneration of both peripheral and central nervous tissue both during development and following an injury.4 Three major isoforms arising from different amino acid substitutions and encoded by the different alleles, ε2, ε3 and ε4, have been identified. The range of ε4 allele frequency is about 5–35% depending on the population studied, and it is approximately 15% in the North American population of European descent.4 Individuals who carry ε4 are at increased risk of various dementias,5 and are also more likely to have impaired recovery of a less specific brain insult following closed head injury,6 intracerebral haemorrhage and subarachnoid haemorrhage.7,8 ε4 has been postulated as a genetic risk factor for human ischaemic stroke in case–control studies9–12 and meta-analyses.13–16 Experimental studies on stroke in ApoE knockout17,18 and transgenic animals19 have shown that the ApoE genotype may affect the infarct volume and outcome. This article provides a review of the literature for magnetic resonance imaging (MRI) evidence of the influence of ApoE on acute stroke and its outcome.

123next ›last »
Keywords:
Apolipoprotein E, genetics, imaging, magnetic resonance, diffusion, perfusion, acute, stroke, outcome

References:
  1. American Heart Association, International Cardiovascular Disease Statistics, 2008.
  2. Hassan A, Markus HS, Brain, 2000;123:1784–1812.
  3. Rubattu S, Giliberti R, Volpe M, Am J Hypertens, 2000;13:1139–48.
  4. Mahley RW, Rall SC, Jr, Annu Rev Genomics Hum Genet, 2000;1:507–37.
  5. Helisalmi S, Linnaranta K, Lehtovirta M, et al., Neurosci Lett, 1996;205:61–4.
  6. Teasdale GM, Nicoll JA, Murray G, Fiddes M, Lancet, 1997;350:1069–71.
  7. Martinez-Gonzalez NA, Sudlow CL, J Neurol Neurosurg Psychiatry, 2006;77:1329–35.
  8. Lanterna LA, Ruigrok Y, Alexander S, et al., Neurology, 2007;69:766–75.
  9. Chowdhury AH, Yokoyama T, Kokubo Y, et al., J Epidemiol, 2001;11:131–8.
  10. Szolnoki Z, Somogyvari F, Kondacs A, et al., J Neurol, 2002;249:1391–7.
  11. Pezzini A, Grassi M, Del Zotto E et al., Stroke, 2004;35:438–42.
  12. Baum L, Ng HK, Wong KS et al., Clin Chem Lab Med, 2006;44:274–81.
  13. McCarron MO, Delong D, Alberts MJ, Neurology, 1999;53:1308–11.
  14. Sudlow C, Martinez Gonzalez NA, Kim J, Clark C, Stroke, 2006;37:364–70.
  15. Ariyaratnam R, Casas JP, Whittaker J, et al., PLoS Med, 2007;4:e131.
  16. Banerjee I, Gupta V, Ganesh S, J Hum Genet, 2007;52:205–19.
  17. Laskowitz DT, Sheng H, Bart RD, et al., J Cereb Blood Flow Metab, 1997;17:753–8.
  18. Horsburgh K, Kelly S, McCulloch J, et al., Neuroreport, 1999;10:837–41.
  19. Sheng H, Laskowitz DT, Bennett E, et al., J Cereb Blood Flow Metab, 1998;18:361–6.
  20. Liu Y, Laakso MP, Karonen JO, et al., J Cereb Blood Flow Metab, 2002;22:1336–42.
  21. McCarron M, Muir KW, Weir CJ, et al., Stroke, 1998;29:1882–7.
  22. McCarron MO, Muir KW, Nicoll JA et al., Arch Neurol, 2000;57:1480–84.
  23. Yonas H, Pindzola RR, Cerebrovasc Brain Metab Rev, 1994;6:325–40.
  24. Karonen JO, Liu Y, Vanninen RL et al., Radiology, 2000;217:886–94.
  25. Sorensen AG, Copen WA, Østergaard L et al., Radiology, 1999;210:519–27.
  26. Liu Y, Nuutinen J, Laakso MP et al., Acta Neurol Scand, 2006;114:323–8.
  27. Plump AS, Smith JD, Hayek T et al., Cell, 1992;71:343–53.
  28. Reddick RL, Zhang SH, Maeda N, Arterioscler Thromb, 1994;14:141–7.
  29. Zhang SH, Reddick RL, Piedrahita JA, Maeda N, Science, 1992;258:468–71.
  30. Weir CJ, McCarron MO, Muir KW, et al., Neurology, 2001;57:1097–1100.
  31. McCarron MO, Nicoll JA, Neurosci Lett, 1998;247:45–8.
  32. Lemmens R, Gorner A, Schrooten M, Stroke, 2007;38:1185–8.
  33. Vernooij MW, van der Lugt A, Ikram MA et al., Neurology, 2008;70:1208–14.
  34. Lövblad KO, Baird AE, Schlaug G et al., Ann Neurol, 1997;42:164–70.
  35. Beaulieu C, de Crespigny A, Tong DC, et al., Ann Neurol, 1999;46:568–78.
  36. Kluytmans M, van Everdingen KJ, Kappelle LJ, et al., Eur Radiol, 2000;10: 1434–41.
  37. Warach S, Pettigrew LC, Dashe JF, et al., Ann Neurol, 2000;48:713–22.
  38. Baird AE, Dambrosia J, Janket S, et al., Lancet, 2001;357:2095–9.

Copyright® 2012 Touch Group PLC. All rights reserved.
Touch Neurology is for informational purposes and should not be considered medical advice, diagnosis or treatment recommendations.