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The Pathophysiology and Clinical Presentation of Cerebral Amyloid Angiopathy

  • Cardiovascular Disease and Stroke (M Fink and J Safdieh, Section Editors)
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Abstract

Cerebral amyloid angiopathy (CAA) is defined as the deposition of amyloid ß peptide within leptomeningial and cortical vessels, likely reflecting an imbalance between Aβ production and clearance. Amyloid buildup triggers a series of destructive alterations in the cerebral vascular architecture, leading to a spectrum of neurological events including lobar intracerebral hemorrhage, brain ischemia and cognitive decline. Although traditionally diagnosed pathologically, neuroimaging has taken a central role in defining CAA. This review will discuss the pathological, clinical and radiological aspects of CAA.

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References

Papers of particular interest, published recently, have been highlighted as: • Of importance

  1. Vinters HV. Cerebral amyloid angiopathy. A critical review. Stroke. 1987;18:311–24.

    Article  PubMed  CAS  Google Scholar 

  2. Okazaki H, Reagan TJ, Campbell RJ. Clinicopathologic studies of primary cerebral amyloid angiopathy. Mayo Clin Proc. 1979;54(1):22–31.

    PubMed  CAS  Google Scholar 

  3. Pfeifer LA, White LR, Ross GW, et al. Cerebral amyloid angiopathy and cognitive function: the HAAS autopsy study. Neurology. 2002;58(11):1629–34.

    Article  PubMed  CAS  Google Scholar 

  4. Neuropathology Group. Medical Research Council Cognitive Function and Aging Study. Pathological correlates of late-onset dementia in a multicentre, community-based population in England and Wales. Neuropathology Group of the Medical Research Council Cognitive Function and Ageing Study (MRC CFAS). Lancet. 2001;357(9251):169–75.

    Article  Google Scholar 

  5. • Kimberly WT, Gilson A, Rost NS, et al. Silent ischemic infarcts are associated with hemorrhage burden in cerebral amyloid angiopathy. Neurology. 2009;72(14):1230–5. This recent study demonstrated that ICH, especially CAA related, predisposes to clinically silent cerebral microinfarction as well as intracerebral hemorrhage, suggesting that the lifetime burden of ischemic infarction in CAA could be substantial and might contribute to small vessel-related cognitive impairment.

    Article  PubMed  CAS  Google Scholar 

  6. • Gregoire SM, Charidimou A, Gadapa N, et al. Acute ischaemic brain lesions in intracerebral haemorrhage: multicentre cross-sectional magnetic resonance imaging study. Brain. 2011;134:2376–86. This recent study demonstrated that ICH, especially CAA related, predisposes to clinically silent cerebral microinfarction as well as intracerebral hemorrhage, suggesting that the lifetime burden of ischemic infarction in CAA could be substantial and might contribute to small vessel-related cognitive impairment.

    Article  PubMed  Google Scholar 

  7. • Prabhakaran S, Gupta R, Ouyang B, et al. Acute brain infarcts after spontaneous intracerebral hemorrhage: a diffusion-weighted imaging study. Stroke. 2010;41(1):89–94. This recent study demonstrated that ICH, especially CAA related, predisposes to clinically silent cerebral microinfarction as well as intracerebral hemorrhage, suggesting that the lifetime burden of ischemic infarction in CAA could be substantial and might contribute to small vessel-related cognitive impairment.

    Article  PubMed  Google Scholar 

  8. Jellinger KA. Alzheimer disease and cerebrovascular pathology: an update. J Neural Transm. 2002;109(5–6):813–36.

    Article  PubMed  CAS  Google Scholar 

  9. Herzig MC, Van Nostrand WE, Jucker M. Mechanism of cerebral beta-amyloid angiopathy: murine and cellular models. Brain Pathol. 2006;16(1):40–54.

    Article  PubMed  CAS  Google Scholar 

  10. Fukuchi K, Ho L, Younkin SG, et al. High levels of circulating beta-amyloid peptide do not cause cerebral beta-amyloidosis in transgenic mice. Am J Pathol. 1996;149(1):219–27.

    PubMed  CAS  Google Scholar 

  11. Burgermeister P, Calhoun ME, Winkler DT, Jucker M. Mechanisms of cerebrovascular amyloid deposition. Lessons from mouse models. Ann N Y Acad Sci. 2000;903:307–16.

    Article  PubMed  CAS  Google Scholar 

  12. Eisele YS, Obermüller U, Heilbronner G, et al. Peripherally applied Abeta-containing inoculates induce cerebral beta-amyloidosis. Science. 2010;330(6006):980–2.

    Article  PubMed  CAS  Google Scholar 

  13. Garcia-Alloza M, Gregory J, Kuchibhotla KV, et al. Cerebrovascular lesions induce transient β-amyloid deposition. Brain. 2011;134:3697–707.

    Article  PubMed  Google Scholar 

  14. Price DL, Tanzi RE, Borchelt DR, Sisodia SS. Alzheimer’s disease: genetic studies and transgenic models. Annu Rev Genet. 1998;32:461–93.

    Article  PubMed  CAS  Google Scholar 

  15. Greenberg SM, Nandigam RN, Delgado P, et al. Microbleeds versus macrobleeds: evidence for distinct entities. Stroke. 2009;40(7):2382–6.

    Article  PubMed  Google Scholar 

  16. Ishii K, Tamaoka A, Mizusawa H, et al. Abeta1-40 but not Abeta1-42 levels in cortex correlate with apolipoprotein E epsilon4 allele dosage in sporadic Alzheimer’s disease. Brain Res. 1997;748:250–2.

    Article  PubMed  CAS  Google Scholar 

  17. Love S, Miners S, Palmer J, et al. Insights into thepathogenesis and pathogenicity of cerebral amyloid angiopathy. Front Biosci. 2009;14:4778–92.

    Article  PubMed  CAS  Google Scholar 

  18. Masuda J, Tanaka K, Ueda K, Omae T. Autopsy study of incidence and distribution of cerebral amyloid angiopathy in Hisayama, Japan. Stroke. 1988;19(2):205–10.

    Article  PubMed  CAS  Google Scholar 

  19. Vinters HV, Gilbert JJ. Cerebral amyloid angiopathy: incidence and complications in the aging brain. II. The distribution of amyloid vascular changes. Stroke. 1983;14(6):924–8.

    Article  PubMed  CAS  Google Scholar 

  20. Van Broeck B, Van Broeckhoven C, Kumar-Singh S. Current insights into molecular mechanisms of Alzheimer disease and their implications for therapeutic approaches. Neurodegener Dis. 2007;4(5):349–65.

    Article  PubMed  Google Scholar 

  21. Mandybur TI. Cerebral amyloid angiopathy: the vascular pathology and complications. J Neuropathol Exp Neurol. 1986;45(1):79–90.

    Article  PubMed  CAS  Google Scholar 

  22. Vonsattel JP, Myers RH, Hedley-Whyte ET, et al. Cerebral amyloid angiopathy without and with cerebral hemorrhages: a comparative histological study. Ann Neurol. 1991;30:637–49.

    Article  PubMed  CAS  Google Scholar 

  23. Revesz T, Ghiso J, Lashley T, et al. Cerebral amyloid angiopathies: a pathologic, biochemical, and genetic view. J Neuropathol Exp Neurol. 2003;62:885–98.

    PubMed  CAS  Google Scholar 

  24. Hartz AM, Bauer B, Soldner EL, et al. Amyloid-β contributes to blood–brain barrier leakage in transgenic human amyloid precursor protein mice and in humans with cerebral amyloid angiopathy. Stroke. 2012;43:514–23.

    Article  PubMed  CAS  Google Scholar 

  25. Puchtler H, Waldrop FS, Meloan SN. A review of light, polarization and fluorescence microscopic methods for amyloid. Appl Pathol. 1985;3:5–17.

    PubMed  CAS  Google Scholar 

  26. Maia LF, Mackenzie IR, Feldman HH. Clinical phenotypes of cerebral amyloid angiopathy. J Neurol Sci. 2007;257:23–30.

    Article  PubMed  Google Scholar 

  27. Qureshi AI, Tuhrim S, Broderick JP, et al. Spontaneous intracerebral hemorrhage. N Engl J Med. 2001;344:1450–60.

    Article  PubMed  CAS  Google Scholar 

  28. Vinters HV, Wang ZZ, Secor DL. Brain parenchymal and microvascular amyloid in Alzheimer’s disease. Brain Pathol. 1996;6:179–95.

    Article  PubMed  CAS  Google Scholar 

  29. Winkler DT, Bondolfi L, Herzig MC, et al. Spontaneous hemorrhagic stroke in a mouse model of cerebral amyloid angiopathy. J Neurosci. 2001;21:1619–27.

    PubMed  CAS  Google Scholar 

  30. Greenberg SM, Vonsattel JP, Stakes JW, et al. The clinical spectrum of cerebral amyloid angiopathy: presentations without lobar hemorrhage. Neurology. 1993;43:2073–9.

    Article  PubMed  CAS  Google Scholar 

  31. Yamada M, Itoh Y, Otomo E, et al. Subarachnoid haemorrhage in the elderly: a necropsy study of the association with cerebral amyloid angiopathy. J Neurol Neurosurg Psychiatry. 1993;56:543–7.

    Article  PubMed  CAS  Google Scholar 

  32. Linn J, Herms J, Dichgans M, et al. Subarachnoid hemosiderosis and superficial cortical hemosiderosis in cerebral amyloid angiopathy. AJNR Am J Neuroradiol. 2008;29:184–6.

    Article  PubMed  CAS  Google Scholar 

  33. Finelli PF. Cerebral amyloid angiopathy as cause of convexity SAH in elderly. Neurologist. 2010;16:37–40.

    Article  PubMed  Google Scholar 

  34. Linn J, Halpin A, Demaerel P, et al. Prevalence of superficial siderosis in patients with cerebral amyloid angiopathy. Neurology. 2010;74:1346–50.

    Article  PubMed  CAS  Google Scholar 

  35. Raposo N, Viguier A, Cuvinciuc V, et al. Cortical subarachnoid haemorrhage in the elderly: a recurrent event probably related to cerebral amyloid angiopathy. Eur J Neurol. 2011;18:597–603.

    Article  PubMed  CAS  Google Scholar 

  36. Greenberg SM, Rebeck GW, Vonsattel JP, et al. Apolipoprotein E epsilon 4 and cerebral hemorrhage associated with amyloid angiopathy. Ann Neurol. 1995;38:254–9.

    Article  PubMed  CAS  Google Scholar 

  37. Premkumar DR, Cohen DL, Hedera P, et al. Apolipoprotein E-epsilon4 alleles in cerebral amyloid angiopathy and cerebrovascular pathology associated with Alzheimer’s disease. Am J Pathol. 1996;148:2083–95.

    PubMed  CAS  Google Scholar 

  38. McCarron MO, Nicoll JA, Ironside JW, et al. Cerebral amyloid angiopathy-related hemorrhage. Interaction of APOE epsilon2 with putative clinical risk factors. Stroke. 1999;30:1643–6.

    Article  PubMed  CAS  Google Scholar 

  39. Nicoll JA, Burnett C, Love S, et al. High frequency of apolipoprotein E epsilon 2 allele in hemorrhage due to cerebral amyloid angiopathy. Ann Neurol. 1997;41:716–21.

    Article  PubMed  CAS  Google Scholar 

  40. McCarron MO, Nicoll JA, Ironside JW, et al. Cerebral amyloid angiopathy-related hemorrhage. Interaction of APOE epsilon2 with putative clinical risk factors. Stroke. 1999;30:1643–6.

    Article  PubMed  CAS  Google Scholar 

  41. Holtzman DM. Role of apoe/Abeta interactions in the pathogenesis of Alzheimer’s disease and cerebral amyloid angiopathy. J Mol Neurosci. 2001;17:147–55.

    Article  PubMed  CAS  Google Scholar 

  42. Rosand J, Hylek EM, O’Donnell HC, Greenberg SM. Warfarin-associated hemorrhage and cerebral amyloid angiopathy: a genetic and pathologic study. Neurology. 2000;55:947–51.

    Article  PubMed  CAS  Google Scholar 

  43. Eckman MH, Wong LK, Soo YO, et al. Patient-specific decision-making for warfarin therapy in nonvalvular atrial fibrillation: how will screening with genetics and imaging help? Stroke. 2008;39:3308–15.

    Article  PubMed  Google Scholar 

  44. Biffi A, Shulman JM, Jagiella JM, et al. Genetic variation at CR1 increases risk of cerebral amyloid angiopathy. Neurology. 2012;78:334–41.

    Article  PubMed  CAS  Google Scholar 

  45. • Arima H, Tzourio C, Anderson C, PROGRESS Collaborative Group, et al. Effects of perindopril-based lowering of blood pressure on intracerebral hemorrhage related to amyloid angiopathy: the PROGRESS trial. Stroke. 2010;41:394–6. Currently there is no preventive strategy for CAA related ICH. In this subsidiary analysis of the PROGRESS trial routine blood pressure reduction was shown to protect patients with CAA from ICH.

    Article  PubMed  CAS  Google Scholar 

  46. Salloway S, Sperling R, Gilman S, et al. Bapineuzumab 201 Clinical Trial Investigators. A phase 2 multiple ascending dose trial of bapineuzumab in mild to moderate. Alzheimer disease. Neurology. 2009;73:2061–70.

    Article  PubMed  CAS  Google Scholar 

  47. Bayer AJ, Bullock R, Jones RW, et al. Evaluation of the safety and immunogenicity of synthetic Abeta42 (AN1792) in patients with AD. Neurology. 2005;64:94–101.

    Article  PubMed  CAS  Google Scholar 

  48. Biffi A, Greenberg SM. Cerebral amyloid angiopathy: a systematic review. J Clin Neurol. 2011;7:1–9.

    Article  PubMed  Google Scholar 

  49. Eckman MH, Rosand J, Knudsen KA, et al. Can patients be anticoagulated after intracerebral hemorrhage? A decision analysis. Stroke. 2003;34:1710–6.

    Article  PubMed  Google Scholar 

  50. Biffi A, Halpin A, Towfighi A, et al. Aspirin and recurrent intracerebral hemorrhage in cerebral amyloid angiopathy. Neurology. 2010;75:693–8.

    Article  PubMed  CAS  Google Scholar 

  51. Fisher M, Vasilevko V, Passos GF, et al. Therapeutic modulation of cerebral microhemorrhage in a mouse model of cerebral amyloid angiopathy. Stroke. 2011;42:3300–3.

    Article  PubMed  Google Scholar 

  52. Knudsen KA, Rosand J, Karluk D, Greenberg SM. Clinical diagnosis of cerebral amyloid angiopathy: validation of the Boston criteria. Neurology. 2001;56:537–9.

    Article  PubMed  CAS  Google Scholar 

  53. Greenberg SM, Vernooij MW, Cordonnier C, Microbleed Study Group, et al. Cerebral microbleeds: a guide to detection and interpretation. Lancet Neurol. 2009;8(2):165–74.

    Article  PubMed  Google Scholar 

  54. Greenberg SM, Eng JA, Ning M, et al. Hemorrhage burden predicts recurrent intracerebral hemorrhage after lobar hemorrhage. Stroke. 2004;35:1415–20.

    Article  PubMed  Google Scholar 

  55. Rosand J, Muzikansky A, Kumar A, et al. Spatial clustering of hemorrhages in probable cerebral amyloid angiopathy. Ann Neurol. 2005;58:459–62.

    Article  PubMed  Google Scholar 

  56. Mesker DJ, Poels MM, Ikram MA, et al. Lobar distribution of cerebral microbleeds: the Rotterdam Scan Study. Arch Neurol. 2011;68:656–9.

    Article  PubMed  Google Scholar 

  57. Smith EE, Greenberg SM. Clinical diagnosis of cerebral amyloid angiopathy: validation of the Boston criteria. Curr Atheroscler Rep. 2003;5:260–6.

    Article  PubMed  Google Scholar 

  58. Vernooij MW, Ikram MA, Hofman A, et al. Superficial siderosis in the general population. Neurology. 2009;73:202–5.

    Article  PubMed  CAS  Google Scholar 

  59. Klohs J, Deistung A, Schweser F, et al. Detection of cerebral microbleeds with quantitative susceptibility mapping in the ArcAbeta mouse model of cerebral amyloidosis. J Cereb Blood Flow Metab. 2011;31:2282–92.

    Article  PubMed  Google Scholar 

  60. Schrag M, McAuley G, Pomakian J, et al. Correlation of hypointensities in susceptibility-weighted images to tissue histology in dementia patients with cerebral amyloid angiopathy: a postmortem MRI study. Acta Neuropathol. 2010;119:291–302.

    Article  PubMed  Google Scholar 

  61. Johnson KA, Gregas M, Becker JA, et al. Imaging of amyloid burden and distribution in cerebral amyloidangiopathy. Ann Neurol. 2007;62:229–34.

    Article  PubMed  Google Scholar 

  62. Ly JV, Donnan GA, Villemagne VL, et al. 11C-PIB binding is increased in patients with cerebral amyloid angiopathy-related hemorrhage. Neurology. 2010;74(6):487–93.

    Article  PubMed  CAS  Google Scholar 

  63. Smith EE, Vijayappa M, Lima F, et al. Impaired visual evoked flow velocity response in cerebral amyloid angiopathy. Neurology. 2008;71:1424–30.

    Article  PubMed  CAS  Google Scholar 

  64. Thomas T, Thomas G, McLendon C, et al. beta-Amyloid-mediated vasoactivity and vascular endothelial damage. Nature. 1996;380:168–71.

    Article  PubMed  CAS  Google Scholar 

  65. Christie R, Yamada M, Moskowitz M, Hyman B. Structural and functional disruption of vascular smooth muscle cells in a transgenic mouse model of amyloid angiopathy. Am J Pathol. 2001;158:1065–71.

    Article  PubMed  CAS  Google Scholar 

  66. Smith EE, Gurol ME, Eng JA, et al. White matter lesions, cognition, and recurrent hemorrhage in lobar intracerebral hemorrhage. Neurology. 2004;63:1606–12.

    Article  PubMed  CAS  Google Scholar 

  67. Pantoni L. Cerebral small vessel disease: from pathogenesis and clinical characteristics to therapeutic challenges. Lancet Neurol. 2010;9:689–701.

    Article  PubMed  Google Scholar 

  68. Natté R, Maat-Schieman ML, Haan J, et al. Dementia in hereditary cerebral hemorrhage with amyloidosis-Dutch type is associated with cerebral amyloid angiopathy but is independent of plaques and neurofibrillary tangles. Ann Neurol. 2001;50:765–72.

    Article  PubMed  Google Scholar 

  69. Gorelick PB, Scuteri A, Black SE, American Heart Association Stroke Council, Council on Epidemiology and Prevention, Council on Cardiovascular Nursing, et al. Vascular contributions to cognitive impairment and dementia: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2011;42:2672–713.

    Article  PubMed  Google Scholar 

  70. Werring DJ, Gregoire SM, Cipolotti L. Cerebral microbleeds and vascular cognitive impairment. J Neurol Sci. 2010;299:131–5.

    Article  PubMed  Google Scholar 

  71. Holland CM, Smith EE, Csapo I, et al. Spatial distribution of white-matter hyperintensities in Alzheimer disease, cerebral amyloid angiopathy, and healthy aging. Stroke. 2008;39:1127–33.

    Article  PubMed  Google Scholar 

  72. Soontornniyomkij V, Lynch MD, Mermash S, et al. Cerebral microinfarcts associated with severe cerebral beta-amyloid angiopathy. Brain Pathol. 2010;20:459–67.

    Article  PubMed  Google Scholar 

  73. Viswanathan A, Patel P, Rahman R, et al. Tissue microstructural changes are independently associated with cognitive impairment in cerebral amyloid angiopathy. Stroke. 2008;39:1988–92.

    Article  PubMed  Google Scholar 

  74. • Arvanitakis Z, Leurgans SE, Wang Z, et al. Cerebral amyloid angiopathy pathology and cognitive domains in older persons. Ann Neurol. 2011;69:320–7. This is an up to date clinical-pathologic study of more than 400 older persons showing that CAA is very common in the demented and the non-demented population and is associated with AD, and after controlling for AD, with decline in specific cognitive performances.

    Article  PubMed  Google Scholar 

  75. Palsdottir A, Snorradottir AO, Thorsteinsson L. Hereditary cystatin C amyloid angiopathy: genetic, clinical, and pathological aspects. Brain Pathol. 2006;16:55–9.

    Article  PubMed  CAS  Google Scholar 

  76. Roks G, Van Harskamp F, De Koning I, et al. Presentation of amyloidosis in carriers of the codon 692 mutation in the amyloid precursor protein gene (APP692). Brain. 2000;123:2130–40.

    Article  PubMed  Google Scholar 

  77. Vidal R, Frangione B, Rostagno A, et al. A stop-codon mutation in the BRI gene associated with familial British dementia. Nature. 1999;399:776–81.

    Article  PubMed  CAS  Google Scholar 

  78. Vidal R, Garzuly F, Budka H, et al. Meningocerebrovascular amyloidosis associated with a novel transthyretin mis-sense mutation at codon 18 (TTRD 18G). Am J Pathol. 1996;148:361–6.

    PubMed  CAS  Google Scholar 

  79. Zhang-Nunes SX, Maat-Schieman ML, van Duinen SG, et al. The cerebral beta-amyloid angiopathies: hereditary and sporadic. Brain Pathol. 2006;16:30–9.

    Article  PubMed  CAS  Google Scholar 

  80. Greenberg SM, Shin Y, Grabowski TJ, et al. Hemorrhagic stroke associated with the Iowa amyloid precursor protein mutation. Neurology. 2003;60:1020–2.

    Article  PubMed  CAS  Google Scholar 

  81. Fountain NB, Eberhard DA. Primary angiitis of the central nervous system associated with cerebral amyloid angiopathy: report of two cases and review of the literature. Neurology. 1996;46:190–7.

    Article  PubMed  CAS  Google Scholar 

  82. Eng JA, Frosch MP, Choi K, et al. Clinical manifestations of cerebral amyloid angiopathy-related inflammation. Ann Neurol. 2004;55:250–6.

    Article  PubMed  Google Scholar 

  83. Kinnecom C, Lev MH, Wendell L, et al. Course of cerebral amyloid angiopathy-related inflammation. Neurology. 2007;68:1411–6.

    Article  PubMed  CAS  Google Scholar 

  84. Kloppenborg RP, Richard E, Sprengers ME, et al. Steroid responsive encephalopathy in cerebral amyloid angiopathy: a case report and review of evidence for immunosuppressive treatment. J Neuroinflammation. 2010;7:18.

    Article  PubMed  Google Scholar 

  85. • DiFrancesco JC, Brioschi M, Brighina L, et al. Anti-Aβ autoantibodies in the CSF of a patient with CAA-related inflammation: a case report. Neurology. 2011;76:842–4. This case report demonstrated for the first time that CSF anti-Aβ antibodies might serve as a biological marker for the diagnosis, monitoring and evaluation of treatment in CAA-related inflammation.

    Article  PubMed  CAS  Google Scholar 

  86. Greenberg SM, Frosch MP. Life imitates art: anti-amyloid antibodies and inflammatory cerebral amyloid angiopathy. Neurology. 2011;76:772–3.

    Article  PubMed  Google Scholar 

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Correspondence to Steven Mark Greenberg.

Appendix

Appendix

Boston Criteria for Diagnosis of CAA-Related Hemorrhage [52]

  1. 1.

    Definite CAA

    Full postmortem examination demonstrating:

    Lobar, cortical, or corticosubcortical hemorrhage

    Severe CAA with vasculopathy

    Absence of other diagnostic lesion

  2. 2.

    Probable CAA with supporting pathology

    Clinical data and pathologic tissue (evacuated hematoma or cortical biopsy) demonstrating:

    Lobar, cortical, or corticosubcortical hemorrhage

    Some degree of CAA in specimen

    Absence of other diagnostic lesion

  3. 3.

    Probable CAA

    Clinical data and MRI or CT demonstrating:

    Multiple hemorrhages restricted to lobar, cortical, or corticosubcortical regions (cerebellar hemorrhage allowed)

    Age ≥55 years

    Absence of other cause of hemorrhage

  4. 4.

    Possible CAA

    Clinical data and MRI or CT demonstrating:

    Single lobar, cortical, or corticosubcortical hemorrhage

    Age ≥55 years

    Absence of other cause of hemorrhage

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Auriel, E., Greenberg, S.M. The Pathophysiology and Clinical Presentation of Cerebral Amyloid Angiopathy. Curr Atheroscler Rep 14, 343–350 (2012). https://doi.org/10.1007/s11883-012-0254-z

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