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Angewandte Nuklearmedizin 2022; 45(04): 256-265
DOI: 10.1055/a-1712-6110
DOI: 10.1055/a-1712-6110
Nuklearmedizinische Hirnbildgebung
Übersicht
Update Amyloid-Bildgebung in der Diagnostik der Neurodegeneration
Update on amyloid-imaging in diagnosis of neurodegeneration
Zusammenfassung
Die Amyloid-PET Bildgebung stellt ein modernes, zugelassenes Verfahren der molekularen Bildgebung dar, welches den Nachweis der für die Alzheimer-Erkrankung (AE) typischen Amyloid-Plaque-Ablagerungen im Gehirn in vivo ermöglicht. Diese Methode hat erstmals die Möglichkeit eröffnet, neurodegenerative Erkrankungen durch den direkten nicht invasiven Nachweis oder Ausschluss einer spezifischen Neuropathologie ätiologisch diagnostisch näher einzuordnen. Ein positiver Amyloid-Scan kann auf das Vorliegen einer für die AE typischen Pathologie hinweisen, ist aber nicht gleichbedeutend mit der Diagnose einer Demenz. Ein negativer Amyloid-Scan macht das Vorliegen einer ablaufenden AE dagegen sehr unwahrscheinlich. Das bildgebende Verfahren ist dabei alleine nicht ausreichend für eine Diagnosestellung, sondern muss im Kontext mit der klinisch/neuropsychologischen Information interpretiert werden. Die Amyloid-Bildgebung kann das Vorliegen von Amyloid-Ablagerungen schon in frühen Erkrankungsstadien, wie bei der leichten kognitiven Störung, visualisieren und damit auch von prognostischem Nutzen sein. Differenzialdiagnostisch kann die Amyloid-Bildgebung einerseits symptomatisch atypische Erscheinungsformen der AE identifizieren und andererseits auch klinisch fälschlich als Alzheimer-Demenz imponierende Erkrankungen anderer Ursache ausschließen. Einen klaren Stellenwert hat die Amyloid-Bildgebung darüber hinaus als Einschlusskriterium für neue Therapieverfahren, die sich gegen die Amyloid-Ablagerungen richten.
Abstract
Amyloid PET imaging represents an approved molecular imaging technique allowing the detection of amyloid plaque deposits in the brain in vivo, which are representing a hallmark of Alzheimer's disease. This method has for the first time opened up the possibility to approach neurodegenerative diseases by direct non-invasive detection or exclusion of specific neuropathology. A positive amyloid scan may indicate the presence of pathology typical of Alzheimer's disease, but is not synonymous with a diagnosis of dementia. A negative amyloid scan, on the other hand, makes the presence of ongoing Alzheimer's disease very unlikely. In this regard, imaging alone is not sufficient to make a diagnosis, but must be interpreted in the context of clinical/neuropsychological information. Amyloid imaging may detect amyloid deposits in early stages of disease, such as in mild cognitive impairment, and thus also can be of prognostic value. With respect to differential diagnosis, amyloid imaging can identify atypical manifestations of Alzheimer’s disease on the one hand, and on the other hand, exclude diseases of other causes that clinically falsely appear as Alzheimer’s dementia. Furthermore, amyloid imaging has a clear value as an inclusion criterion for new therapeutic procedures directed against amyloid deposits.
Schlüsselwörter
Alzheimer Demenz - ß-Amyloid - Plaques - Amyloid-Bildgebung - Tangles - Tau-Bildgebung - PETPublication History
Article published online:
02 December 2022
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Literatur
- 1 Bonner MF, Ash S, Grossman M. The new classification of primary progressive aphasia into semantic, logopenic, or nonfluent/agrammatic variants. Curr Neurol Neurosci Rep 2010; 10: 484-490 DOI: 10.1007/s11910-010-0140-4. (PMID: 20809401)
- 2 Davies RR, Hodges JR, Kril JJ. et al. The pathological basis of semantic dementia. Brain 2005; 128: 1984-1995 DOI: 10.1093/brain/awh582. (PMID: 16000337)
- 3 W DGM. S3-Leitlinie Demenzen. Leitlinien für Diagnostik und Therapie in der Neurologie. 2016
- 4 Johnson JK, Diehl J, Mendez MF. et al. Frontotemporal lobar degeneration: demographic characteristics of 353 patients. Arch Neurol 2005; 62: 925-930 DOI: 10.1001/archneur.62.6.925. (PMID: 15956163)
- 5 Salloway S, Sperling R, Fox NC. et al. Two phase 3 trials of bapineuzumab in mild-to-moderate Alzheimer's disease. N Engl J Med 2014; 370: 322-333 DOI: 10.1056/NEJMoa1304839. (PMID: 24450891)
- 6 Braak E, Griffing K, Arai K. et al. Neuropathology of Alzheimer’s disease: what is new since A. Alzheimer?. Eur Arch Psychiatry Clin Neurosci 1999; 249: S14-S22 DOI: 10.1007/pl00014168. (PMID: 10654095)
- 7 Davies L, Wolska B, Hilbich C. et al. A4 amyloid protein deposition and the diagnosis of Alzheimer's disease: prevalence in aged brains determined by immunocytochemistry compared with conventional neuropathologic techniques. Neurology 1988; 38: 1688-1688
- 8 Albert MS, DeKosky ST, 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. Alzheimer's & dementia 2011; 7: 270-279
- 9 McKhann GM, Knopman DS, Chertkow H. et al. The diagnosis of dementia due to Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. Alzheimer's & dementia 2011; 7: 263-269
- 10 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. Alzheimer's & dementia 2011; 7: 280-292 DOI: 10.1016/j.jalz.2011.03.003. (PMID: 21514248)
- 11 Selkoe DJ. Folding proteins in fatal ways. Nature 2003; 426: 900-904 DOI: 10.1038/nature02264. (PMID: 14685251)
- 12 Drzezga A. Amyloid-plaque imaging in early and differential diagnosis of dementia. Ann Nucl Med 2010; 24: 55-66 DOI: 10.1007/s12149-009-0330-9. (PMID: 20082230)
- 13 Villemagne VL, Klunk WE, Mathis CA. et al. Aβ Imaging: feasible, pertinent, and vital to progress in Alzheimer’s disease. Eur J Nucl Med Mol Imaging 2012; 39: 209-219
- 14 Frisoni GB, Barkhof F, Altomare D. et al. AMYPAD diagnostic and patient management study: rationale and design. Alzheimer's & Dementia 2019; 15: 388-399 DOI: 10.1016/j.jalz.2018.09.003. (PMID: 30339801)
- 15 Rabinovici GD, Gatsonis C, Apgar C. et al. Association of amyloid positron emission tomography with subsequent change in clinical management among Medicare beneficiaries with mild cognitive impairment or dementia. JAMA 2019; 321: 1286-1294 DOI: 10.1001/jama.2019.2000. (PMID: 30938796)
- 16 Herrmann N, Chau SA, Kircanski I. et al. Current and emerging drug treatment options for Alzheimer’s disease. Drugs 2011; 71: 2031-2065 DOI: 10.2165/11595870-000000000-00000. (PMID: 21985169)
- 17 Decourt B, Boumelhem F, Pope ED. et al. Critical appraisal of amyloid lowering agents in AD. Curr Neurol Neurosci Rep 2021; 21: 1-10 DOI: 10.1007/s11910-021-01125-y. (PMID: 34110536)
- 18 Klunk WE, Engler H, Nordberg A. et al. Imaging brain amyloid in Alzheimer's disease with Pittsburgh Compound-B. Annals of Neurology: Official Journal of the American Neurological Association and the Child Neurology Society 2004; 55: 306-319
- 19 Barthel H, Gertz H-J, Dresel S. et al. Cerebral amyloid-β PET with florbetaben (18F) in patients with Alzheimer's disease and healthy controls: a multicentre phase 2 diagnostic study. Lancet Neurol 2011; 10: 424-435 DOI: 10.1016/S1474-4422(11)70077-1. (PMID: 21481640)
- 20 Fleisher AS, Chen K, Liu X. et al. Using positron emission tomography and florbetapir F 18 to image cortical amyloid in patients with mild cognitive impairment or dementia due to Alzheimer disease. Arch Neurol 2011; 68: 1404-1411 DOI: 10.1001/archneurol.2011.150. (PMID: 21747008)
- 21 Vandenberghe R, Van Laere K, Ivanoiu A. et al. 18F-flutemetamol amyloid imaging in Alzheimer disease and mild cognitive impairment: a phase 2 trial. Ann Neurol 2010; 68: 319-329 DOI: 10.1002/ana.22068. (PMID: 20687209)
- 22 Bacskai BJ, Frosch MP, Freeman SH. et al. Molecular imaging with Pittsburgh Compound B confirmed at autopsy: a case report. Arch Neurol 2007; 64: 431-434 DOI: 10.1001/archneur.64.3.431. (PMID: 17353389)
- 23 Clark CM, Schneider JA, Bedell BJ. et al. Use of florbetapir-PET for imaging β-amyloid pathology. JAMA 2011; 305: 275-283 DOI: 10.1001/jama.2010.2008. (PMID: 21245183)
- 24 Ikonomovic MD, Klunk WE, Abrahamson EE. et al. Post-mortem correlates of in vivo PiB-PET amyloid imaging in a typical case of Alzheimer's disease. Brain 2008; 131: 1630-1645 DOI: 10.1093/brain/awn016. (PMID: 18339640)
- 25 Kadir A, Marutle A, Gonzalez D. et al. Positron emission tomography imaging and clinical progression in relation to molecular pathology in the first Pittsburgh Compound B positron emission tomography patient with Alzheimer’s disease. Brain 2011; 134: 301-317 DOI: 10.1093/brain/awq349. (PMID: 21149866)
- 26 Leinonen V, Alafuzoff I, Aalto S. et al. Assessment of β-amyloid in a frontal cortical brain biopsy specimen and by positron emission tomography with carbon 11–labeled Pittsburgh Compound B. Arch Neurol 2008; 65: 1304-1309
- 27 Sojkova J, Driscoll I, Iacono D. et al. In vivo fibrillar β-amyloid detected using [11C] PiB positron emission tomography and neuropathologic assessment in older adults. Arch Neurol 2011; 68: 232-240 DOI: 10.1001/archneurol.2010.357. (PMID: 21320990)
- 28 Villemagne VL, McLean CA, Reardon K. et al. 11C-PiB PET studies in typical sporadic Creutzfeldt–Jakob disease. J Neurol Neurosurg Psychiatry 2009; 80: 998-1001 DOI: 10.1136/jnnp.2008.171496. (PMID: 19332421)
- 29 Wolk DA. Amyloid imaging in atypical presentations of Alzheimer’s disease. Curr Neurol Neurosci Rep 2013; 13: 412 DOI: 10.1007/s11910-013-0412-x. (PMID: 24136459)
- 30 Klunk WE, Koeppe RA, Price JC. et al. The Centiloid Project: standardizing quantitative amyloid plaque estimation by PET. Alzheimer's & dementia 2015; 11: 1-15.e14. DOI: 10.1016/j.jalz.2014.07.003. (PMID: 25443857)
- 31 Bischof GN, Bartenstein P, Barthel H. et al. Toward a Universal Readout for 18F-Labeled Amyloid Tracers: The CAPTAINs Study. J Nucl Med 2021; 62: 999-1005 DOI: 10.2967/jnumed.120.250290. (PMID: 33712532)
- 32 Barthel H, Meyer PT, Drzezga A. et al. German Society of Nuclear Medicine procedure guideline on beta-amyloid brain PET imaging. Nuklearmedizin Nuclear Medicine 2016; 55: 129-137 DOI: 10.3413/Nukmed-0816-16-04. (PMID: 27080914)
- 33 Johnson KA, Minoshima S, Bohnen NI. 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. J Nucl Med 2013; 54: 476-490 DOI: 10.2967/jnumed.113.120618. (PMID: 23359661)
- 34 Minoshima S, Drzezga AE, Barthel H. et al. SNMMI procedure standard/EANM practice. J Nucl Med 2016; 57: 1316-22 DOI: 10.2967/jnumed.116.174615.
- 35 Pike KE, Savage G, Villemagne VL. et al. β-amyloid imaging and memory in non-demented individuals: evidence for preclinical Alzheimer's disease. Brain 2007; 130: 2837-2844 DOI: 10.1093/brain/awm238. (PMID: 17928318)
- 36 Rowe CC, Ellis KA, Rimajova M. et al. Amyloid imaging results from the Australian Imaging, Biomarkers and Lifestyle (AIBL) study of aging. Neurobiol Aging 2010; 31: 1275-1283 DOI: 10.1016/j.neurobiolaging.2010.04.007. (PMID: 20472326)
- 37 Rorden C, Brett M. Stereotaxic display of brain lesions. Behav Neurol 2000; 12: 191-200 DOI: 10.1155/2000/421719. (PMID: 11568431)
- 38 van Berckel BN, Ossenkoppele R, Tolboom N. et al. Longitudinal amyloid imaging using 11C-PiB: methodologic considerations. J Nucl Med 2013; 54: 1570-1576 DOI: 10.2967/jnumed.112.113654. (PMID: 23940304)
- 39 Tiepolt S, Hesse S, Patt M. et al. Early [18F] florbetaben and [11C] PiB PET images are a surrogate biomarker of neuronal injury in Alzheimer’s disease. Eur J Nucl Med Mol Imaging 2016; 43: 1700-1709 DOI: 10.1007/s00259-016-3353-1. (PMID: 27026271)
- 40 Forsberg A, Engler H, Almkvist O. et al. PET imaging of amyloid deposition in patients with mild cognitive impairment. Neurobiol Aging 2008; 29: 1456-1465 DOI: 10.1016/j.neurobiolaging.2007.03.029. (PMID: 17499392)
- 41 Koivunen J, Scheinin N, Virta J. et al. Amyloid PET imaging in patients with mild cognitive impairment: a 2-year follow-up study. Neurology 2011; 76: 1085-1090 DOI: 10.1212/WNL.0b013e318212015e. (PMID: 21325653)
- 42 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 DOI: 10.1212/WNL.0b013e3181b23564. (PMID: 19587325)
- 43 Villemagne VL, Pike KE, Chételat G. et al. Longitudinal assessment of Aβ and cognition in aging and Alzheimer disease. Ann Neurol 2011; 69: 181-192 DOI: 10.1002/ana.22248. (PMID: 21280088)
- 44 Zhang D, Shen D. Initiative AsDN. Predicting future clinical changes of MCI patients using longitudinal and multimodal biomarkers. PLoS One 2012; 7: e33182 DOI: 10.1371/journal.pone.0033182.
- 45 Nordberg A, Carter SF, Rinne J. et al. A European multicentre PET study of fibrillar amyloid in Alzheimer’s disease. Eur J Nucl Med Mol Imaging 2013; 40: 104-114 DOI: 10.1007/s00259-012-2237-2. (PMID: 22961445)
- 46 Mormino E, Kluth J, Madison C. et al. Episodic memory loss is related to hippocampal-mediated β-amyloid deposition in elderly subjects. Brain 2009; 132: 1310-1323 DOI: 10.1093/brain/awn320. (PMID: 19042931)
- 47 Price JC, Klunk WE, Lopresti BJ. et al. Kinetic modeling of amyloid binding in humans using PET imaging and Pittsburgh Compound-B. J Cereb Blood Flow Metab 2005; 25: 1528-1547 DOI: 10.1038/sj.jcbfm.9600146. (PMID: 15944649)
- 48 Zhang S, Han D, Tan X. et al. Diagnostic accuracy of 18F-FDG and 11C-PIB-PET for prediction of short-term conversion to Alzheimer’s disease in subjects with mild cognitive impairment. Int J Clin Pract 2012; 66: 185-198
- 49 de Wilde A, Ossenkoppele R, Pelkmans W. et al. Assessment of the appropriate use criteria for amyloid PET in an unselected memory clinic cohort: The ABIDE project. Alzheimer's & Dementia 2019; 15: 1458-1467 DOI: 10.1016/j.jalz.2019.07.003. (PMID: 31594684)
- 50 Slot RE, Sikkes SA, Berkhof J. et al. Subjective cognitive decline and rates of incident Alzheimer's disease and non–Alzheimer's disease dementia. Alzheimer's & Dementia 2019; 15: 465-476 DOI: 10.1016/j.jalz.2018.10.003. (PMID: 30555032)
- 51 Mintun M, Larossa G, Sheline Y. et al. [11C] PIB in a nondemented population: potential antecedent marker of Alzheimer disease. Neurology 2006; 67: 446-452 DOI: 10.1212/01.wnl.0000228230.26044.a4. (PMID: 16894106)
- 52 Villemagne VL, Pike KE, Darby D. et al. Aβ deposits in older non-demented individuals with cognitive decline are indicative of preclinical Alzheimer's disease. Neuropsychologia 2008; 46: 1688-1697 DOI: 10.1016/j.neuropsychologia.2008.02.008. (PMID: 18343463)
- 53 Jansen WJ, Ossenkoppele R, Knol DL. et al. Prevalence of cerebral amyloid pathology in persons without dementia: a meta-analysis. JAMA 2015; 313: 1924-1938 DOI: 10.1001/jama.2015.4668. (PMID: 25988462)
- 54 Drzezga A, Becker JA, Van Dijk KR. et al. Neuronal dysfunction and disconnection of cortical hubs in non-demented subjects with elevated amyloid burden. Brain 2011; 134: 1635-1646 DOI: 10.1093/brain/awr066. (PMID: 21490054)
- 55 Hedden T, Van Dijk KR, Becker JA. et al. Disruption of functional connectivity in clinically normal older adults harboring amyloid burden. J Neurosci 2009; 29: 12686-12694 DOI: 10.1523/JNEUROSCI.3189-09.2009. (PMID: 19812343)
- 56 Sperling RA, LaViolette PS, O'Keefe K. et al. Amyloid deposition is associated with impaired default network function in older persons without dementia. Neuron 2009; 63: 178-188 DOI: 10.1016/j.neuron.2009.07.003. (PMID: 19640477)
- 57 Grossman M. Primary progressive aphasia: clinicopathological correlations. Nature Reviews Neurology 2010; 6: 88-97 DOI: 10.1038/nrneurol.2009.216. (PMID: 20139998)
- 58 Mesulam M, Wieneke C, Rogalski E. et al. Quantitative template for subtyping primary progressive aphasia. Arch Neurol 2009; 66: 1545-1551 DOI: 10.1001/archneurol.2009.288. (PMID: 20008661)
- 59 Mesulam M-M, Weintraub S, Rogalski EJ. et al. Asymmetry and heterogeneity of Alzheimer’s and frontotemporal pathology in primary progressive aphasia. Brain 2014; 137: 1176-1192 DOI: 10.1093/brain/awu024. (PMID: 24574501)
- 60 Rabinovici GD, Jagust WJ, Furst AJ. et al. Aβ amyloid and glucose metabolism in three variants of primary progressive aphasia. Ann Neurol 2008; 64: 388-401 DOI: 10.1002/ana.21451. (PMID: 18991338)
- 61 Gorno-Tempini ML, Hillis AE, Weintraub S. et al. Classification of primary progressive aphasia and its variants. Neurology 2011; 76: 1006-1014 DOI: 10.1212/WNL.0b013e31821103e6. (PMID: 21325651)
- 62 Josephs KA, Duffy JR, Strand EA. et al. Progranulin-associated PiB-negative logopenic primary progressive aphasia. J Neurol 2014; 261: 604-614 DOI: 10.1007/s00415-014-7243-9. (PMID: 24449064)
- 63 Johnson JK, Head E, Kim R. et al. Clinical and pathological evidence for a frontal variant of Alzheimer disease. Arch Neurol 1999; 56: 1233-1239 DOI: 10.1001/archneur.56.10.1233. (PMID: 10520939)
- 64 Ossenkoppele R, Pijnenburg YA, Perry DC. et al. The behavioural/dysexecutive variant of Alzheimer’s disease: clinical, neuroimaging and pathological features. Brain 2015; 138: 2732-2749 DOI: 10.1093/brain/awv191. (PMID: 26141491)
- 65 Rabinovici G, Furst A, O'neil J. et al. 11C-PIB PET imaging in Alzheimer disease and frontotemporal lobar degeneration. Neurology 2007; 68: 1205-1212 DOI: 10.1212/01.wnl.0000259035.98480.ed. (PMID: 17420404)
- 66 Crutch SJ, Lehmann M, Schott JM. et al. Posterior cortical atrophy. Lancet Neurol 2012; 11: 170-178 DOI: 10.1093/brain/awz136. (PMID: 31219516)
- 67 Nestor P, Caine D, Fryer T. et al. The topography of metabolic deficits in posterior cortical atrophy (the visual variant of Alzheimer’s disease) with FDG-PET. J Neurol Neurosurg Psychiatry 2003; 74: 1521-1529 DOI: 10.1136/jnnp.74.11.1521. (PMID: 14617709)
- 68 De Souza LC, Corlier F, Habert M-O. et al. Similar amyloid-β burden in posterior cortical atrophy and Alzheimer's disease. Brain 2011; 134: 2036-2043 DOI: 10.1093/brain/awr130. (PMID: 21705422)
- 69 Formaglio M, Costes N, Seguin J. et al. In vivo demonstration of amyloid burden in posterior cortical atrophy: a case series with PET and CSF findings. J Neurol 2011; 258: 1841-1851 DOI: 10.1007/s00415-011-6030-0. (PMID: 21479849)
- 70 Crutch SJ, Schott JM, Rabinovici GD. et al. Consensus classification of posterior cortical atrophy. Alzheimer's & Dementia 2017; 13: 870-884 DOI: 10.1016/j.jalz.2017.01.014. (PMID: 28259709)
- 71 Ossenkoppele R, Jansen WJ, Rabinovici GD. et al. Prevalence of amyloid PET positivity in dementia syndromes: a meta-analysis. JAMA 2015; 313: 1939-1950 DOI: 10.1001/jama.2015.4669. (PMID: 25988463)
- 72 Day GS, Lim TS, Hassenstab J. et al. Differentiating cognitive impairment due to corticobasal degeneration and Alzheimer disease. Neurology 2017; 88: 1273-1281 DOI: 10.1212/WNL.0000000000003770. (PMID: 28235814)
- 73 Drzezga A, Grimmer T, Henriksen G. et al. Imaging of amyloid plaques and cerebral glucose metabolism in semantic dementia and Alzheimer’s disease. NeuroImage 2008; 39: 619-633 DOI: 10.1016/j.neuroimage.2007.09.020. (PMID: 17962045)
- 74 Zaccai J, McCracken C, Brayne C. A systematic review of prevalence and incidence studies of dementia with Lewy bodies. Age Ageing 2005; 34: 561-566 DOI: 10.1093/ageing/afi190. (PMID: 16267179)
- 75 McKeith I, Dickson DW, Lowe J. et al. Diagnosis and management of dementia with Lewy bodies: third report of the DLB Consortium. Neurology 2005; 65: 1863-1872 DOI: 10.1212/01.wnl.0000187889.17253.b1. (PMID: 16237129)
- 76 Ishii K. Clinical application of positron emission tomography for diagnosis of dementia. Ann Nucl Med 2002; 16: 515-525 DOI: 10.11477/mf.1436203655. (PMID: 29262393)
- 77 Weisman D, Cho M, Taylor C. et al. In dementia with Lewy bodies, Braak stage determines phenotype, not Lewy body distribution. Neurology 2007; 69: 356-359
- 78 Rowe CC, Ng S, Ackermann U. et al. Imaging β-amyloid burden in aging and dementia. Neurology 2007; 68: 1718-1725 DOI: 10.1212/01.wnl.0000261919.22630.ea. (PMID: 17502554)
- 79 Edison P, Rowe CC, Rinne JO. et al. Amyloid load in Parkinson’s disease dementia and Lewy body dementia measured with [11C] PIB positron emission tomography. J Neurol Neurosurg Psychiatry 2008; 79: 1331-1338 DOI: 10.1136/jnnp.2007.127878. (PMID: 18653550)
- 80 Morris GP, Clark IA, Vissel B. Inconsistencies and controversies surrounding the amyloid hypothesis of Alzheimer's disease. Acta neuropathologica communications 2014; 2: 135 DOI: 10.1186/s40478-014-0135-5. (PMID: 25231068)
- 81 Engler H, Forsberg A, Almkvist O. et al. Two-year follow-up of amyloid deposition in patients with Alzheimer's disease. Brain 2006; 129: 2856-2866 DOI: 10.1093/brain/awl178. (PMID: 16854944)
- 82 Grimmer T, Tholen S, Yousefi BH. et al. Progression of cerebral amyloid load is associated with the apolipoprotein E ε4 genotype in Alzheimer's disease. Biol Psychiatry 2010; 68: 879-884 DOI: 10.1016/j.biopsych.2010.05.013. (PMID: 20598287)
- 83 Rinne JO, Brooks DJ, Rossor MN. et al. 11C-PiB PET assessment of change in fibrillar amyloid-β 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 DOI: 10.1016/S1474-4422(10)70043-0. (PMID: 20189881)
- 84 Ratner M. Biogen's early Alzheimer's data raise hopes, some eyebrows. Nat Biotechnol 2015; 33: 438-439 DOI: 10.1038/nbt0515-438. (PMID: 25965736)
- 85 O'Gorman J, Chiao P, Bussière T. et al. Clinical Development of Aducanumab, an Anti-Aβ Human Monoclonal Antibody Being Investigated for the Treatment of Early Alzheimer's Disease. The journal of prevention of Alzheimer's disease 2017; 4: 255-263 DOI: 10.14283/jpad.2017.39. (PMID: 29181491)
- 86 Chételat G, Arbizu J, Barthel H. et al. Amyloid-PET and 18F-FDG-PET in the diagnostic investigation of Alzheimer's disease and other dementias. Lancet Neurol 2020; 19: 951-962 DOI: 10.1016/S1474-4422(20)30314-8. (PMID: 33098804)