Skip to main content Accessibility help
×
Home

Canadian Consensus Guidelines on Use of Amyloid Imaging in Canada: Update and Future Directions from the Specialized Task Force on Amyloid imaging in Canada

  • Robert Laforce (a1) (a2), Pedro Rosa-Neto (a3) (a4), Jean-Paul Soucy (a5) (a6) (a7), Gil D. Rabinovici (a8), Bruno Dubois (a9) (a10) and S. Gauthier (a4)...

Abstract

Positron emission tomography (PET) imaging of brain amyloid beta is now clinically available in several countries including the United States and the United Kingdom, but not Canada. It has become an established technique in the field of neuroimaging of aging and dementia, with data incorporated in the new consensus guidelines for the diagnosis of Alzheimer disease and predementia Alzheimer’s disease–related conditions. At this point, there are three US Food and Drug Administration– and European Union–approved tracers. Guided by appropriate use criteria developed in 2013 by the Alzheimer’s Association and the Society of Nuclear Medicine and Molecular Imaging, the utility of amyloid imaging in medical practice is now supported by a growing body of research. In this paper, we aimed to provide an update on the 2012 Canadian consensus guidelines to dementia care practitioners on proper use of amyloid imaging. We also wished to generate momentum for the industry to submit a new drug proposal to Health Canada. A group of local, national, and international dementia experts and imaging specialists met to discuss scenarios in which amyloid PET could be used appropriately. Peer-reviewed and published literature between January 2004 and May 2015 was searched. Technical and regulatory considerations pertaining to Canada were considered. The results of a survey of current practices in Canadian dementia centers were considered. A set of specific clinical and research guidelines was agreed on that defines the types of patients and clinical circumstances in which amyloid PET could be used in Canada. Future research directions were also outlined, notably the importance of studies that would assess the pharmaco-economics of amyloid imaging.

Lignes directrices consensuelles quant à l’utilisation de l’imagerie amyloïde au Canada : mise à jour et pistes pour l’avenir proposées par le Groupe d’étude canadien sur l’imagerie amyloïde. La tomographie par émission de positons (TEP), examen d’imagerie de la protéine bêta-amyloïde du cerveau, est désormais disponible sur le plan clinique dans de nombreux pays, dont les États-Unis et le Royaume-Uni, mais pas encore au Canada. La TEP s’est imposée comme une technique reconnue dans le champ de la neuro-imagerie associé au vieillissement et aux démences. Les données ainsi recueillies ont été intégrées à de nouvelles lignes directrices consensuelles en ce qui concerne le diagnostic de la maladie d’Alzheimer et des problèmes liés à sa phase pré-démentielle. À l’heure actuelle, trois traceurs ont été approuvés par la Food and Drug Administration des États-Unis ainsi que par l’Union européenne. S’appuyant sur des critères d’utilisation appropriés (« AUC » en anglais) élaborés en 2013 par l’Alzheimer’s Association et la Society of Nuclear Medicine and Molecular Imaging, l’utilité de l’imagerie amyloïde en médecine est dorénavant étayée par un nombre grandissant de travaux de recherche. Dans cet article, nous entendons proposer une mise à jour des lignes directrices consensuelles établies au Canada en 2012 quant à une utilisation appropriée de l’imagerie amyloïde. Ces lignes directrices sont destinées aux professionnels de la santé appelés à traiter la démence. Nous souhaitons également susciter un élan dans l’industrie pharmaceutique visant à soumettre des propositions de nouveaux médicaments à Santé Canada. À cet égard, un groupe d’experts nationaux et internationaux en matière de démence, de même que des spécialistes en imagerie, se sont rencontrés afin d’examiner les situations en vertu desquelles la TEP pourrait être utilisée de manière appropriée. Pour notre part, nous avons d’abord effectué une revue de la littérature scientifique soumise à examen collégial et publiée entre janvier 2004 et mai 2015. Nous nous sommes penchés ensuite sur les considérations techniques et réglementaires propres au Canada ainsi que sur les résultats d’un sondage portant sur les pratiques en vigueur dans les centres canadiens de soins de la démence. Nous avons ainsi convenu d’un ensemble de lignes directrices spécifiques concernant le travail clinique et la recherche. Ces lignes directrices visent à définir les types de patients et les circonstances cliniques en vertu desquels la TEP pourrait être utilisée au Canada. Enfin, de futurs axes de recherche ont également été soulignés, en particulier l’importance d’études pouvant évaluer la dimension pharmaco-économique de l’imagerie amyloïde.

  • View HTML
    • Send article to Kindle

      To send this article to your Kindle, first ensure no-reply@cambridge.org is added to your Approved Personal Document E-mail List under your Personal Document Settings on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part of your Kindle email address below. Find out more about sending to your Kindle. Find out more about sending to your Kindle.

      Note you can select to send to either the @free.kindle.com or @kindle.com variations. ‘@free.kindle.com’ emails are free but can only be sent to your device when it is connected to wi-fi. ‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.

      Find out more about the Kindle Personal Document Service.

      Canadian Consensus Guidelines on Use of Amyloid Imaging in Canada: Update and Future Directions from the Specialized Task Force on Amyloid imaging in Canada
      Available formats
      ×

      Send article to Dropbox

      To send this article to your Dropbox account, please select one or more formats and confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your <service> account. Find out more about sending content to Dropbox.

      Canadian Consensus Guidelines on Use of Amyloid Imaging in Canada: Update and Future Directions from the Specialized Task Force on Amyloid imaging in Canada
      Available formats
      ×

      Send article to Google Drive

      To send this article to your Google Drive account, please select one or more formats and confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your <service> account. Find out more about sending content to Google Drive.

      Canadian Consensus Guidelines on Use of Amyloid Imaging in Canada: Update and Future Directions from the Specialized Task Force on Amyloid imaging in Canada
      Available formats
      ×

Copyright

Corresponding author

Correspondence to: Dr. Robert Laforce Jr., Neurologue et Neuropsychologue, Professeur Agrégé, Faculté de Médecine, Université Laval, Clinique Interdisciplinaire de Mémoire, Département des Sciences Neurologiques, CHU de Québec, 1401, 18ième rue, Québec, Canada, G1J 1Z4. Email: robert.laforce@fmed.ulaval.ca

References

Hide All
1. Patterson, CJ, Gauthier, S, Bergman, H, et al. The recognition, assessment and management of dementing disorders: conclusions from the Canadian Consensus Conference on Dementia. CMAJ. 1999;160:S1-15.
2. Chertkow, H. Diagnosis and treatment of dementia: introduction. Introducing a series based on the Third Canadian Consensus Conference on the Diagnosis and Treatment of Dementia. CMAJ. 2008;178:316-321.
3. Gauthier, S, Patterson, C, Chertkow, H, et al. 4th Canadian Consensus Conference on the Diagnosis and Treatment of Dementia. Can J Neurol Sci. 2012;39:S1-S8.
4. Assessing dementia: the Canadian consensus. Organizing Committee, Canadian Consensus Conference on the Assessment of Dementia. Can Med Assoc J. 1991;144:851-853.
5. Dubois, B, Feldman, H, Jacova, C, et al. Research criteria for the diagnosis of Alzheimer’s disease: revisiting the NINCDS-ADRDA criteria. Lancet Neurol. 2007;6:734-746.
6. Dubois, B, Feldman, HH, Jacova, C, et al. Revising the definition of Alzheimer’s disease: a new lexicon. Lancet Neurol. 2010;9:1118-1127.
7. McKhann, G, Knopman, D, Chertkow, H, et al. The diagnosis of dementia due to Alzheimer’s disease: recommendations from the National Institute on Aging and the Alzheimer’s Association workgroup. Alzheimers Dement. 2011;7:263-269.
8. Albert, M, DeKosky, S, Dickson, D, 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 9.
9. Sperling, RA, Aisen, PS, Beckett, LA, et al. Toward defining the preclinical stages of Alzheimer’s disease: recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease. Alzheimers Dement. 2011;7:280-292.
10. Burhan, A, Bartha, R, Bocti, C, et al. Role of emerging neuroimaging modalities in patients with cognitive impairment: a review from the Canadian Consensus Conference on the Diagnosis and Treatment of Dementia 2012. Alzheimers Res Ther. 2013;5:S4.
11. Soucy, J-P, Bartha, R, Bocti, C, et al. Clinical applications of neuroimaging in patients with Alzheimer’s disease: a review from the Fourth Canadian Consensus Conference on the Diagnosis and Treatment of Dementia 2012. Alzheimers Res Ther. 2013;5:S3.
12. Klunk, WE, Engler, H, Nordberg, A, et al. Imaging brain amyloid in Alzheimer’s disease with Pittsburgh Compound-B. Ann Neurol. 2004;55:306-319.
13. Jack, CR Jr., Wiste, HJ, Weigand, SD, et al. Amyloid-first and neurodegeneration-first profiles characterize incident amyloid PET positivity. Neurology. 2013;81:1732-1740.
14. Sperling, RA, Rentz, DM, Johnson, KA, et al. The A4 study: stopping AD before symptoms begin? Sci Transl Med. 2014;6:228fs13.
15. Farlow, M, Arnold, SE, van Dyck, CH, et al. Safety and biomarker effects of solanezumab in patients with Alzheimer’s disease. Alzheimers Dement. 2012;8:261-271.
16. Rinne, JO, Brooks, DJ, Rossor, MN, et al. 11C-PiB PET assessment of change in fibrillar amyloid-beta load in patients with Alzheimer’s disease treated with bapineuzumab: a phase 2, double-blind, placebo-controlled, ascending-dose study. Lancet Neurol. 2010;9:363-372.
17. Keller, D. Finally, a big win for a monoclonal in Alzheimer’s. AD/PD 2015: International Conference on Alzheimer’s and Parkinson’s Diseases 2015 [cited 2015, July 31]. Available from: http://www.medscape.com/viewarticle/841856.
18. Clark, C, Pontecorvo, M, Beach, T, et al. Cerebral PET with florbetapir compared with neuropathology at autopsy for detection of neuritic amyloid-beta plaques: a prospective cohort study. Lancet Neurol. 2012;11:669-678.
19. Wolk, DA, Grachev, ID, Buckley, C, et al. Association between in vivo fluorine 18-labeled flutemetamol amyloid positron emission tomography imaging and in vivo cerebral cortical histopathology. Arch Neurol. 2011;68:1398-1403.
20. Rowe, CC, Ackerman, U, Browne, W, et al. Imaging of amyloid beta in Alzheimer’s disease with 18F-BAY94-9172, a novel PET tracer: proof of mechanism. Lancet Neurol. 2008;7:129-135.
21. Ossenkoppele, R, Prins, ND, Pijnenburg, YA, et al. Impact of molecular imaging on the diagnostic process in a memory clinic. Alzheimers Dement. 2013;9:414-421.
22. Sanchez-Juan, P, Ghosh, PM, Hagen, J, et al. Practical utility of amyloid and FDG-PET in an academic dementia center. Neurology. 2014;82:230-238.
23. Rabinovici, G, Rosen, H, Alkalay, A, et al. Amyloid versus FDG PET in the differential diagnosis of AD and FTLD. Neurology. 2011;77:2034-2042.
24. Wolk, DA, Price, JC, Madeira, C, et al. Amyloid imaging in dementias with atypical presentation. Alzheimers Dement. 2012;8:389-398.
25. Bensaïdane, M, Fortin, M, Damasse, G, Chenard, M, Dionne, C. Clinical utility of amyloid imaging in a complex case of corticobasal syndrome presenting with psychiatric symptoms. J Neurol Disord. 2014;2:2.
26. Grundman, M, Pontecorvo, MJ, Salloway, SP, et al. Potential impact of amyloid imaging on diagnosis and intended management in patients with progressive cognitive decline. Alzheimers Dis Assoc Disord. 2013;27:4-15.
27. Zannas, AS, Doraiswamy, PM, Shpanskaya, KS, et al. Impact of 18F-florbetapir PET imaging of beta-amyloid neuritic plaque density on clinical decision-making. Neurocase. 2014;20:466-473.
28. Mitsis, E, Bender, H, Kostakoglu, L, et al. A consecutive case series experience with [18F] florbetapir PET imaging in an urban dementia center: impact on quality of life, decision making, and disposition. Mol Neurodegener. 2014;9:10.
29. Bensaïdane MR, Beauregard JM, Poulin S, et al. (forthcoming). Clinical utility of amyloid PET Imaging in the differential diagnosis of atypical dementias and its impact on caregivers. J Alzheimers Dis. 2016.
30. Pike, K, Savage, G, Villemagne, V, et al. Beta-amyloid imaging and memory in nondemented individuals: evidence for preclinical Alzheimer’s disease. Brain. 2007;130:2837-2844.
31. Rowe, C, Ellis, K, Rimajova, M, et al. Amyloid imaging results from the Australian Imaging, Biomarkers and Lifestyle (AIBL) study of aging. Neurobiol Aging. 2010;31:1275-1283.
32. Jack, CR Jr., Wiste, HJ, Weigand, SD, et al. Age-specific population frequencies of cerebral beta-amyloidosis and neurodegeneration among people with normal cognitive function aged 50-89 years: a cross-sectional study. Lancet Neurol. 2014;13:997-1005.
33. Petersen, RC. Mild cognitive impairment as a diagnostic entity. J Intern Med. 2004;256:183-194.
34. Petersen, RC. MIld cognitive impairment or questionable dementia? Arch Neurol. 2000;57:643-644.
35. Kantarci, K, Lowe, V, Przybelski, SA, et al. APOE modifies the association between Aβ load and cognition in cognitively normal older adults. Neurology. 2012;78:232-240.
36. Mormino, EC, Betensky, RA, Hedden, T, et al. Synergistic effect of beta-amyloid and neurodegeneration on cognitive decline in clinically normal individuals. JAMA Neurol. 2014;71:1379-1385.
37. Dickerson, BC, Bakkour, A, Salat, DH, et al. The cortical signature of Alzheimer’s disease: regionally specific cortical thinning relates to symptom severity in very mild to mild AD dementia and is detectable in asymptomatic amyloid-positive individuals. Cereb Cortex. 2009;19:497-510.
38. Roe, CM, Fagan, AM, Grant, EA, et al. Amyloid imaging and CSF biomarkers in predicting cognitive impairment up to 7.5 years later. Neurology. 2013;80:1784-1791.
39. Klunk, WE. Amyloid imaging as a biomarker for cerebral beta-amyloidosis and risk prediction for Alzheimer dementia. Neurobiol Aging. 2011;32:S20-S36.
40. Ostrowitzki, S, Deptula, D, Thurfjell, L, et al. Mechanism of amyloid removal in patients with Alzheimer disease treated with gantenerumab. Arch Neurol. 2012;69:198-207.
41. Pontecorvo, M, Mintun, M. PET amyloid imaging as a tool for early diagnosis and identifying patients at risk for progression to Alzheimer’s disease. Alzheimers Res Ther. 2011;3:11.
42. Wolk, DA, Price, JC, Saxton, JA, et al. Amyloid imaging in mild cognitive impairment subtypes. Ann Neurol. 2009;65:557-568.
43. Okello, A, Koivunen, J, Edison, P, et al. Conversion of amyloid positive and negative MCI to AD over 3 years: an 11C-PIB PET study. Neurology. 2009;73:754-760.
44. Ellis, KA, Lim, YY, Harrington, K, et al. Decline in cognitive function over 18 months in healthy older adults with high amyloid-beta. J Alzheimers Dis. 2013;34:861-871.
45. Rabinovici, GD, Jagust, WJ, Furst, AJ, et al. Abeta amyloid and glucose metabolism in three variants of primary progressive aphasia. Ann Neurol. 2008;64:388-401.
46. de Souza, LC, Corlier, F, Habert, MO, et al. Similar amyloid-beta burden in posterior cortical atrophy and Alzheimer’s disease. Brain. 2011;134:2036-2043.
47. Laforce, R, Buteau, J, Paquet, N, Verret, L, Houde, M, Bouchard, R. The value of PET in mild cognitive impairment, typical and atypical/unclear dementias: a retrospective memory clinic study. Am J Alzheimers Dis Other Dement. 2010;25:324-332.
48. Ratnavalli, E, Brayne, C, Dawson, K, Hodges, JR. The prevalence of frontotemporal dementia. Neurology. 2002;58:1615-1621.
49. Alladi, S, Xuereb, J, Bak, T, et al. Focal cortical presentations of Alzheimer’s disease. Brain. 2007;130:2636-2645.
50. Villemagne, VL, Ong, K, Mulligan, RS, et al. Amyloid imaging with (18)F-florbetaben in Alzheimer disease and other dementias. J Nucl Med. 2011;52:1210-1217.
51. Beach, TG, Monsell, SE, Phillips, LE, Kukull, W. Accuracy of the clinical diagnosis of Alzheimer disease at National Institute on Aging Alzheimer Disease Centers, 2005-2010. J Neuropathol Exp Neurol. 2012;71:266-273.
52. Ossenkoppele, R, Jansen, WJ, Rabinovici, GD, et al. Prevalence of amyloid pet positivity in dementia syndromes: a meta-analysis. JAMA. 2015;313:1939-1950.
53. Cselényi, Z, Jönhagen, ME, Forsberg, A, et al. Clinical validation of 18F-AZD4694, an amyloid-β–specific PET radioligand. J Nucl Med. 2012;53:415-424.
54. Juréus, A, Swahn, BM, Sandell, J, et al. Characterization of AZD4694, a novel fluorinated Aβ plaque neuroimaging PET radioligand. J Neurochem. 2010;114:784-794.
55. Rowe, CC, Pejoska, S, Mulligan, RS, et al. Head-to-head comparison of 11C-PiB and 18F-AZD4694 (NAV4694) for beta-amyloid imaging in aging and dementia. J Nucl Med. 2013;54:880-886.
56. Lee, JH, Kim, SH, Kim, GH, et al. Identification of pure subcortical vascular dementia using 11C-Pittsburgh compound B. Neurology. 2011;77:18-25.
57. Johnson, KA, Gregas, M, Becker, JA, et al. Imaging of amyloid burden and distribution in cerebral amyloid angiopathy. Ann Neurol. 2007;62:229-234.
58. Maetzler, W, Liepelt, I, Reimold, M, et al. Cortical PIB binding in Lewy body disease is associated with Alzheimer-like characteristics. Neurobiol Dis. 2009;34:107-112.
59. Johnson, K, Minoshima, S, Bohnen, N, et al. Appropriate use criteria for amyloid PET: a report of the Amyloid Imaging Task Force, the Society of Nuclear Medicine and Molecular Imaging, and the Alzheimer’s Association. Alzheimers Dement. 2013;9:1-15.
60. Jagust, WJ. Amyloid imaging: liberal or conservative? Let the data decide. Arch Neurol. 2011;68:1377-1378.
61. Johnson, KA, Minoshima, S, Bohnen, NI, et al. Update on appropriate use criteria for amyloid PET imaging: dementia experts, mild cognitive impairment, and education. J Nucl Med. 2013;54:1011-1013.
62. Curtis, C, Gamez, JE, Singh, U, et al. Phase 3 trial of flutemetamol labeled with radioactive fluorine 18 imaging and neuritic plaque density. JAMA Neurol. 2015;72:287-294.
63. Sabri, O, Sabbagh, MN, Seibyl, J, et al. Florbetaben PET imaging to detect amyloid beta plaques in Alzheimer’s disease: phase 3 study. Alzheimers Dement. 2015;11:964-974.
64. Guyatt, GH, Oxman, AD, Vist, GE, et al. GRADE: an emerging consensus on rating quality of evidence and strength of recommendations. BMJ. 2008;336:924-926.
65. Harkins, K, Sankar, P, Sperling, R, et al. Development of a process to disclose amyloid imaging results to cognitively normal older adult research participants. Alzheimers Res Ther. 2015;7:26.
66. Laforce, R, Rabinovici, G. Amyloid imaging in the differential diagnosis of dementia: review and potential clinical applications. Alzheimers Res Ther. 2011;3:31.
67. Ducharme, S, Guiot, M-C, Nikelski, J, Chertkow, H. Does a positive Pittsburgh Compound B scan in a patient with dementia equal Alzheimer disease? JAMA Neurol. 2013;70:912-914.
68. Bohnen, N, Djang, D, Herholz, K, Anzai, Y, Minoshima, S. Effectiveness and safety of 18F-FDG PET in the evaluation of dementia: a review of the recent literature. J Nucl Med. 2012;53:59-71.
69. Jagust, W, Reed, B, Mungas, D, Ellis, W, Decarli, C. What does fluorodeoxyglucose PET imaging add to a clinical diagnosis of dementia? Neurology. 2007;69:871-877.
70. Mosconi, L. Brain glucose metabolism in the early and specific diagnosis of Alzheimer’s disease. FDG-PET studies in MCI and AD. Eur J Nucl Med Mol Imaging. 2005;32:486-510.
71. Mosconi, L, Tsui, WH, Herholz, K, et al. Multicenter standardized 18F-FDG PET diagnosis of mild cognitive impairment, Alzheimer’s disease, and other dementias. J Nucl Med. 2008;49:390-398.
72. Silverman, D, Small, G, Chang, C, et al. Positron emission tomography in evaluation of dementia - regional brain metabolism and long-term outcome. JAMA. 2001;286:2120-2127.
73. Silverman, DH, Gambhir, SS, Huang, HW, et al. Evaluating early dementia with and without assessment of regional cerebral metabolism by PET: a comparison of predicted costs and benefits. J Nucl Med. 2002;43:253-266.
74. Jack, C, Wiste, H, Vemuri, P, et al. Brain beta-amyloid measure and magnetic resonance imaging atrophy both predict time-to-progression from mild cognitive impairment to Alzheimer’s disease. Brain. 2010;133:3336-3348.
75. Bateman, RJ, Xiong, C, Benzinger, TL, et al. Clinical and biomarker changes in dominantly inherited Alzheimer’s disease. N Engl J Med. 2012;367:795-804.
76. Fagan, AM, Head, D, Shah, AR, et al. Decreased CSF Aβ42 correlates with brain atrophy in cognitively normal elderly. Ann Neurol. 2009;65:176-183.
77. Palmqvist, S, Zetterberg, H, Blennow, K, et al. Accuracy of brain amyloid detection in clinical practice using cerebrospinal fluid beta-amyloid 42: a cross-validation study against amyloid positron emission tomography. JAMA Neurol. 2014;71:1282-1289.
78. Landau, SM, Lu, M, Joshi, AD, et al. Comparing positron emission tomography imaging and cerebrospinal fluid measurements of beta-amyloid. Ann Neurol. 2013;74:826-836.
79. Hampel, H, Bürger, K, Teipel, SJ, Bokde, AL, Zetterberg, H, Blennow, K. Core candidate neurochemical and imaging biomarkers of Alzheimer’s disease. Alzheimers Dement. 2008;4:38-48.
80. Mulder, C, Verwey, NA, van der Flier, WM, et al. Amyloid-beta(1-42), total tau, and phosphorylated tau as cerebrospinal fluid biomarkers for the diagnosis of Alzheimer disease. Clin Chem. 2010;56:248-253.
81. Rosa-Neto, P, Hsiung, G-Y, Masellis, M, on behalf of the CCDTD4 participants. Fluid biomarkers for diagnosing dementia: rationale and the Canadian Consensus on Diagnosis and Treatment of Dementia recommendations for Canadian physicians. Alzheimers Res Ther. 2013;5:S8.
82. Hampel, H, Teipel, SJ. Total and phosphorylated tau proteins: evaluation as core biomarker candidates in frontotemporal dementia. Dement Geriatr Cogn Disord. 2004;17:350-354.
83. Bian, H, Van Swieten, JC, Leight, S, et al. CSF biomarkers in frontotemporal lobar degeneration with known pathology. Neurology. 2008;70:1827-1835.
84. Borroni, B, Malinverno, M, Gardoni, F, et al. Tau forms in CSF as a reliable biomarker for progressive supranuclear palsy. Neurology. 2008;71:1796-1803.
85. Kapaki, E, Paraskevas, GP, Papageorgiou, SG, et al. Diagnostic value of CSF biomarker profile in frontotemporal lobar degeneration. Alzheimer Dis Assoc Disord. 2008;22:47-53.
86. Hu, WT, Watts, K, Grossman, M, et al. Reduced CSF p-tau181 to tau ratio is a biomarker for FTLD-TDP. Neurology. 2013;81:1945-1952.
87. Bibl, M, Mollenhauer, B, Lewczuk, P, et al. Cerebrospinal fluid tau, p-tau 181 and amyloid-beta38/40/42 in frontotemporal dementias and primary progressive aphasias. Dement Geriatr Cogn Disord. 2011;31:37-44.
88. Global Biomarker Standardization Consortium. Biomarker Standardization Projects. 2015 [cited 2015, Aug 29]; Available from: http://www.alz.org/research/funding/global_biomarker_projects.asp.
89. Landau, SM, Mintun, MA, Joshi, AD, et al. Amyloid deposition, hypometabolism, and longitudinal cognitive decline. Ann Neurol. 2012;72:578-586.

Keywords

Canadian Consensus Guidelines on Use of Amyloid Imaging in Canada: Update and Future Directions from the Specialized Task Force on Amyloid imaging in Canada

  • Robert Laforce (a1) (a2), Pedro Rosa-Neto (a3) (a4), Jean-Paul Soucy (a5) (a6) (a7), Gil D. Rabinovici (a8), Bruno Dubois (a9) (a10) and S. Gauthier (a4)...

Metrics

Altmetric attention score

Full text views

Total number of HTML views: 0
Total number of PDF views: 0 *
Loading metrics...

Abstract views

Total abstract views: 0 *
Loading metrics...

* Views captured on Cambridge Core between <date>. This data will be updated every 24 hours.

Usage data cannot currently be displayed