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Current Neurology and Neuroscience Reports

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01.10.2017 | Neuroimaging (N Pavese, Section Editor)

Molecular Imaging and Updated Diagnostic Criteria in Lewy Body Dementias

verfasst von: Nicolaas I. Bohnen, Martijn L. T. M. Müller, Kirk A. Frey

Erschienen in: Current Neurology and Neuroscience Reports | Ausgabe 10/2017

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Abstract

Purpose of Review

The aims of the study were to review recent advances in molecular imaging in the Lewy body dementias (LBD) and determine if these may support the clinical but contested temporal profile distinction between Parkinson disease (PD) with dementia (PDD) versus dementia with Lewy bodies (DLB).

Recent Findings

There do not appear to be major regional cerebral metabolic or neurotransmitter distinctions between PDD and DLB. However, recent studies highlight the relative discriminating roles of Alzheimer proteinopathies. PDD patients have lower cortical β-amyloid deposition than DLB. Preliminary tau PET studies suggest a gradient of increasing tau binding from cognitively normal PD (absent to lowest) to cognitively impaired PD (low) to DLB (intermediate) to Alzheimer disease (AD; highest). However, tau binding in DLB, including the medial temporal lobe, is substantially lower than in AD.

Summary

Alzheimer-type proteinopathies appear to be more common in DLB compared to PDD with relative but no absolute differences. Given the spectrum of overlapping pathologies, future α-synuclein ligands are expected to have the best potential to distinguish the LBD from pure AD.

Harding AJ, Halliday GM. Cortical Lewy body pathology in the diagnosis of dementia. Acta Neuropathol. 2001;102:355–63.PubMed

Jellinger KA, Attems J. Prevalence and impact of vascular and Alzheimer pathologies in Lewy body disease. Acta Neuropathol. 2008;115:427–36.CrossRefPubMed

Howlett DR, Whitfield D, Johnson M, Attems J, O'Brien JT, Aarsland D, et al. Regional multiple pathology scores are associated with cognitive decline in Lewy body dementias. Brain Pathol. 2015;25:401–8.

Compta Y, Parkkinen L, Kempster P, Selikhova M, Lashley T, Holton JL, et al. The significance of alpha-synuclein, amyloid-beta and tau pathologies in Parkinson’s disease progression and related dementia. Neurodegener Dis. 2014;13:154–6.

Kotzbauer PT, Cairns NJ, Campbell MC, Willis AW, Racette BA, Tabbal SD, et al. Pathologic accumulation of alpha-synuclein and Abeta in Parkinson disease patients with dementia. Arch Neurol. 2012;69:1–6.

Irwin DJ, White MT, Toledo JB, Xie SX, Robinson JL, Van Deerlin V, et al. Neuropathologic substrates of Parkinson disease dementia. Ann Neurol. 2012;72:587–98.

Toledo JB, Gopal P, Raible K, Irwin DJ, Brettschneider J, Sedor S, et al. Pathological alpha-synuclein distribution in subjects with coincident Alzheimer’s and Lewy body pathology. Acta Neuropathol. 2016;131:393–409.

Gaspar P, Gray F. Dementia in idiopathic Parkinson’s disease. A neuropathological study of 32 cases. Acta Neuropathol (Berl). 1984;64:43–52.CrossRef

Hirsch EC, Graybiel AM, Duyckaerts C, Javoy-Agid F. Neuronal loss in the pedunculopontine tegmental nucleus in Parkinson disease and in progressive supranuclear palsy. Proc Natl Acad Sci U S A. 1987;84:5976–80.CrossRefPubMedPubMedCentral

10.

Jellinger KA. Post mortem studies in Parkinson’s disease—is it possible to detect brain areas for specific symptoms? J Neural Transm Suppl. 1999;56:1–29.CrossRefPubMed

11.

Kalaitzakis ME, Pearce RK. The morbid anatomy of dementia in Parkinson’s disease. Acta Neuropathol. 2009;118:587–98.CrossRefPubMed

12.

McKeith IG, Galasko D, Kosaka K, Perry EK, Dickson DW, Hansen LA, et al. Consensus guideline for the clinical and pathological diagnosis of dementia with Lewy bodies (LBD): report of the Consortium on DLB International Workshop. Neurology. 1996;47:1113–24.

13.

Postuma RB, Berg D, Stern M, Poewe W, Olanow CW, Oertel W, et al. MDS clinical diagnostic criteria for Parkinson’s disease. Mov Disord. 2015;30:1591–601.

14.

McKeith IG, Boeve BF, Dickson DW, Halliday G, Taylor JP, Weintraub D, et al. Diagnosis and management of dementia with Lewy bodies: fourth consensus report of the DLB Consortium. Neurology. 2017;89:88–100.

15.

Frey KA, Petrou M. Imaging amyloidopathy in Parkinson disease and parkinsonian dementia syndromes. Clin Transl Imaging. 2015;3:57–64.CrossRefPubMedPubMedCentral

16.

Bohnen NI, Koeppe RA, Minoshima S, Giordani B, Albin RL, Frey KA, et al. Cerebral glucose metabolic features of Parkinson disease and incident dementia: longitudinal study. J Nucl Med. 2011;52:848–55.

17.

Minoshima S, Foster NL, Sima AA, Frey KA, Albin RL, Kuhl DE. Alzheimer’s disease versus dementia with Lewy bodies: cerebral metabolic distinction with autopsy confirmation. Ann Neurol. 2001;50:358–65.CrossRefPubMed

18.

Granert O, Drzezga AE, Boecker H, Perneczky R, Kurz A, Gotz J, et al. Metabolic topology of neurodegenerative disorders: influence of cognitive and motor deficits. J Nucl Med. 2015;56:1916–21.

19.

Firbank MJ, Lloyd J, O'Brien JT. The relationship between hallucinations and FDG-PET in dementia with Lewy bodies. Brain Imaging Behav. 2016;10:636–9.CrossRefPubMed

20.

Lim SM, Katsifis A, Villemagne VL, Best R, Jones G, Saling M, et al. The 18F-FDG PET cingulate island sign and comparison to 123I-beta-CIT SPECT for diagnosis of dementia with Lewy bodies. J Nucl Med. 2009;50:1638–45.

21.

Imabayashi E, Yokoyama K, Tsukamoto T, Sone D, Sumida K, Kimura Y, et al. The cingulate island sign within early Alzheimer’s disease-specific hypoperfusion volumes of interest is useful for differentiating Alzheimer’s disease from dementia with Lewy bodies. EJNMMI Res. 2016;6:67.

22.

• Graff-Radford J, Murray ME, Lowe VJ, Boeve BF, Ferman TJ, Przybelski SA, et al. Dementia with Lewy bodies: basis of cingulate island sign. Neurology. 2014;83:801–9. Study showing evidence of neuropathological correlate of the cingulate island sign in DLB.

23.

Iizuka T, Kameyama M. Cingulate island sign on FDG-PET is associated with medial temporal lobe atrophy in dementia with Lewy bodies. Ann Nucl Med. 2016;30:421–9.CrossRefPubMed

24.

• Whitwell JL, Graff-Radford J, Singh TD, Drubach DA, Senjem ML, Spychalla AJ, et al. ¹⁸F-FDG PET in posterior cortical atrophy and dementia with lewy bodies. J Nucl Med. 2017;58:632–8. Comprehensive study comparing FDG metabolic difference and overlap between PCA and DLB.

25.

Crutch SJ, Schott JM, Rabinovici GD, Murray M, Snowden JS, van der Flier WM, Dickerson BC, Vandenberghe R, Ahmed S, Bak TH, Boeve BF, Butler C, Cappa SF, Ceccaldi M, de Souza LC, Dubois B, Felician O, Galasko D, Graff-Radford J, Graff-Radford NR, Hof PR, Krolak-Salmon P, Lehmann M, Magnin E, Mendez MF, Nestor PJ, Onyike CU, Pelak VS, Pijnenburg Y, Primativo S, Rossor MN, Ryan NS, Scheltens P, Shakespeare TJ, Suarez Gonzalez A, Tang-Wai DF, Yong KX, Carrillo M, Fox NC. Alzheimer’s Association, IAAsD, Associated Syndromes Professional Interest, A. Consensus classification of posterior cortical atrophy. Alzheimers Dement. 2017;13:870–84.

26.

Spehl TS, Hellwig S, Amtage F, Weiller C, Bormann T, Weber WA, et al. Syndrome-specific patterns of regional cerebral glucose metabolism in posterior cortical atrophy in comparison to dementia with Lewy bodies and Alzheimer’s disease—a [F-18]-FDG pet study. J Neuroimaging. 2015;25:281–8.

27.

Walker Z, Jaros E, Walker RW, Lee L, Costa DC, Livingston G, et al. Dementia with Lewy bodies: a comparison of clinical diagnosis, FP-CIT single photon emission computed tomography imaging and autopsy. J Neurol Neurosurg Psychiatry. 2007;78:1176–81.

28.

McKeith I, O’Brien J, Walker Z, Tatsch K, Booij J, Darcourt J, et al. Sensitivity and specificity of dopamine transporter imaging with 123I-FP-CIT SPECT in dementia with Lewy bodies: a phase III, multicentre study. Lancet Neurol. 2007;6:305–13.CrossRefPubMed

29.

Koeppe RA, Gilman S, Junck L, Wernette K, Frey KA. Differentiating Alzheimer’s disease from dementia with Lewy bodies and Parkinson’s disease with (+)-[11C]dihydrotetrabenazine positron emission tomography. Alzheimers Dement. 2008;4:S67–76.CrossRefPubMed

30.

Albin RL, Fisher-Hubbard A, Shanmugasundaram K, Koeppe RA, Burke JF, Camelo-Piragua S, et al. Post-mortem evaluation of amyloid-dopamine terminal positron emission tomography dementia classifications. Ann Neurol. 2015;78:824–30.

31.

Colloby SJ, McParland S, O'Brien JT, Attems J. Neuropathological correlates of dopaminergic imaging in Alzheimer’s disease and Lewy body dementias. Brain. 2012;135:2798–808.CrossRefPubMed

32.

Christopher L, Marras C, Duff-Canning S, Koshimori Y, Chen R, Boileau I, et al. Combined insular and striatal dopamine dysfunction are associated with executive deficits in Parkinson’s disease with mild cognitive impairment. Brain. 2014;137:565–75.

33.

Klein JC, Eggers C, Kalbe E, Weisenbach S, Hohmann C, Vollmar S, et al. Neurotransmitter changes in dementia with Lewy bodies and Parkinson disease dementia in vivo. Neurology. 2010;74:885–92.

34.

Bohnen NI, Kaufer DI, Ivanco LS, Lopresti B, Koeppe RA, Davis JG, et al. Cortical cholinergic function is more severely affected in parkinsonian dementia than in Alzheimer disease: an in vivo positron emission tomographic study. Arch Neurol. 2003;60:1745–8.

35.

Williams-Gray CH, Foltynie T, Brayne CE, Robbins TW, Barker RA. Evolution of cognitive dysfunction in an incident Parkinson’s disease cohort. Brain. 2007;130:1787–98.CrossRefPubMed

36.

Kehagia AA, Barker RA, Robbins TW. Cognitive impairment in Parkinson’s disease: the dual syndrome hypothesis. Neurodegener Dis. 2013;11:79–92.CrossRefPubMed

37.

Bohnen NI, Albin RL, Muller ML, Petrou M, Kotagal V, Koeppe RA, et al. Frequency of cholinergic and caudate nucleus dopaminergic deficits across the predemented cognitive spectrum of Parkinson disease and evidence of interaction effects. JAMA Neurol. 2015;72:194–200.

38.

Calabresi P, Picconi B, Parnetti L, Di Filippo M. A convergent model for cognitive dysfunctions in Parkinson’s disease: the critical dopamine-acetylcholine synaptic balance. Lancet Neurol. 2006;5:974–83.CrossRefPubMed

39.

Sarter M, Albin RL, Kucinski A, Lustig C. Where attention falls: increased risk of falls from the converging impact of cortical cholinergic and midbrain dopamine loss on striatal function. Exp Neurol. 2014;257C:120–9.CrossRef

40.

Orimo S, Uchihara T, Nakamura A, Mori F, Kakita A, Wakabayashi K, et al. Axonal alpha-synuclein aggregates herald centripetal degeneration of cardiac sympathetic nerve in Parkinson’s disease. Brain. 2008;131:642–50.

41.

Yoshita M, Arai H, Arai H, Arai T, Asada T, Fujishiro H, et al. Diagnostic accuracy of ¹²³I-meta-iodobenzylguanidine myocardial scintigraphy in dementia with Lewy bodies: a multicenter study. PLoS One. 2015;10:e0120540.

42.

Shimizu S, Hirao K, Kanetaka H, Namioka N, Hatanaka H, Hirose D, et al. Utility of the combination of DAT SPECT and MIBG myocardial scintigraphy in differentiating dementia with Lewy bodies from Alzheimer’s disease. Eur J Nucl Med Mol Imaging. 2016;43:184–92.

43.

Mashima K, Ito D, Kameyama M, Osada T, Tabuchi H, Nihei Y, et al. Extremely low prevalence of amyloid positron emission tomography positivity in Parkinson’s disease without dementia. Eur Neurol. 2017;77:231–7.

44.

Donaghy P, Thomas AJ, O'Brien JT. Amyloid PET imaging in Lewy body disorders. Am J Geriatr Psychiatry. 2015;23:23–37.CrossRefPubMed

45.

Gomperts SN, Locascio JJ, Rentz D, Santarlasci A, Marquie M, Johnson KA, et al. Amyloid is linked to cognitive decline in patients with Parkinson disease without dementia. Neurology. 2013;80:85–91.

46.

Gomperts SN, Marquie M, Locascio JJ, Bayer S, Johnson KA, Growdon JH. PET radioligands reveal the basis of dementia in Parkinson’s disease and dementia with Lewy bodies. Neurodegener Dis. 2016;16:118–24.CrossRefPubMed

47.

Kalaitzakis ME, Graeber MB, Gentleman SM, Pearce RK. Striatal beta-amyloid deposition in Parkinson disease with dementia. J Neuropathol Exp Neurol. 2008;67:155–61.CrossRefPubMed

48.

Halliday GM, Song YJ, Harding AJ. Striatal beta-amyloid in dementia with Lewy bodies but not Parkinson’s disease. J Neural Transm. 2011;118:713–9.CrossRefPubMed

49.

Dugger BN, Serrano GE, Sue LI, Walker DG, Adler CH, Shill HA, et al. Presence of striatal amyloid plaques in Parkinson’s disease dementia predicts concomitant Alzheimer’s disease: usefulness for amyloid imaging. J Parkinson’s Dis. 2012;2:57–65.

50.

Kalaitzakis ME, Walls AJ, Pearce RK, Gentleman SM. Striatal Abeta peptide deposition mirrors dementia and differentiates DLB and PDD from other Parkinsonian syndromes. Neurobiol Dis. 2011;41:377–84.CrossRefPubMed

51.

Shah N, Frey KA, Müller MLTM, Petrou M, Kotagal V, Koeppe RA, et al. Striatal and cortical beta-amyloidopathy and cognition in Parkinson’s disease. Mov Disord. 2016;31:111–7.

52.

• Gomperts SN, Locascio JJ, Makaretz SJ, Schultz A, Caso C, Vasdev N, et al. Tau positron emission tomographic imaging in the Lewy body diseases. JAMA Neurol. 2016;73:1334–41. Study showing evidence of cognitive correlates of in vivo tau imaging in Lewy body patients.

53.

•• Kantarci K, Lowe VJ, Boeve BF, Senjem ML, Tosakulwong N, Lesnick TG, et al. AV-1451 tau and beta-amyloid positron emission tomography imaging in dementia with Lewy bodies. Ann Neurol. 2017;81:58–67. This multi-modal imaging study is the largest study to date showing the spectrum of tau pathology between AD, DLB, and control subjects.

54.

Hansen AK, Damholdt MF, Fedorova TD, Knudsen K, Parbo P, Ismail R, et al. In vivo cortical tau in Parkinson’s disease using 18F-AV-1451 positron emission tomography. Mov Disord. 2017;32:922–7.

55.

Mrak RE, Griffin WS. Common inflammatory mechanisms in Lewy body disease and Alzheimer disease. J Neuropathol Exp Neurol. 2007;66:683–6.CrossRefPubMed

56.

Iannaccone S, Cerami C, Alessio M, Garibotto V, Panzacchi A, Olivieri S, et al. In vivo microglia activation in very early dementia with Lewy bodies, comparison with Parkinson’s disease. Parkinsonism Relat Disord. 2013;19:47–52.

57.

Edison P, Ahmed I, Fan Z, Hinz R, Gelosa G, Ray Chaudhuri K, et al. Microglia, amyloid, and glucose metabolism in Parkinson’s disease with and without dementia. Neuropsychopharmacology. 2013;38:938–49.

58.

Fan Z, Aman Y, Ahmed I, Chetelat G, Landeau B, Ray Chaudhuri K, et al. Influence of microglial activation on neuronal function in Alzheimer’s and Parkinson’s disease dementia. Alzheimers Dement. 2015;11:608–21. e7.

59.

Femminella GD, Ninan S, Atkinson R, Fan Z, Brooks DJ, Edison P. Does microglial activation influence hippocampal volume and neuronal function in Alzheimer’s disease and Parkinson’s disease dementia? J Alzheimers Dis. 2016;51:1275–89.CrossRefPubMed

60.

Stefaniak J, O'Brien J. Imaging of neuroinflammation in dementia: a review. J Neurol Neurosurg Psychiatry. 2016;87:21–8.CrossRefPubMed

61.

Varley J, Brooks DJ, Edison P. Imaging neuroinflammation in Alzheimer’s disease and other dementias: recent advances and future directions. Alzheimers Dement. 2015;11:1110–20.CrossRefPubMed

62.

Modreanu R, Cerquera SC, Marti MJ, Rios J, Sanchez-Gomez A, Camara A, et al. Cross-sectional and longitudinal associations of motor fluctuations and non-motor predominance with cerebrospinal tau and Abeta as well as dementia-risk in Parkinson’s disease. J Neurol Sci. 2017;373:223–9.

63.

Petrou M, Bohnen NI, Muller ML, Koeppe RA, Albin RL, Frey KA. Abeta-amyloid deposition in patients with Parkinson disease at risk for development of dementia. Neurology. 2012;79:1161–7.CrossRefPubMedPubMedCentral

64.

Tsigelny IF, Crews L, Desplats P, Shaked GM, Sharikov Y, Mizuno H, et al. Mechanisms of hybrid oligomer formation in the pathogenesis of combined Alzheimer’s and Parkinson’s diseases. PLoS One. 2008;3:e3135.

65.

Compta Y, Parkkinen L, O'Sullivan SS, Vandrovcova J, Holton JL, Collins C, et al. Lewy- and Alzheimer-type pathologies in Parkinson’s disease dementia: which is more important? Brain. 2011;134:1493–505.

66.

Lebedev AV, Westman E, Simmons A, Lebedeva A, Siepel FJ, Pereira JB, et al. Large-scale resting state network correlates of cognitive impairment in Parkinson’s disease and related dopaminergic deficits. Front Syst Neurosci. 2014;8:45.

67.

Gratwicke J, Jahanshahi M, Foltynie T. Parkinson’s disease dementia: a neural networks perspective. Brain. 2015;138:1454–76.CrossRefPubMedPubMedCentral

68.

Caminiti SP, Tettamanti M, Sala A, Presotto L, Iannaccone S, Cappa SF, et al. Metabolic connectomics targeting brain pathology in dementia with Lewy bodies. J Cereb Blood Flow Metab. 2017;37:1311–25.CrossRefPubMed

69.

Niethammer M, Eidelberg D. Metabolic brain networks in translational neurology: concepts and applications. Ann Neurol. 2012;72:635–47.CrossRefPubMedPubMedCentral

70.

Niethammer M, Tang CC, Ma Y, Mattis PJ, Ko JH, Dhawan V, et al. Parkinson’s disease cognitive network correlates with caudate dopamine. NeuroImage. 2013;78:204–9.

71.

Mattis PJ, Niethammer M, Sako W, Tang CC, Nazem A, Gordon ML, et al. Distinct brain networks underlie cognitive dysfunction in Parkinson and Alzheimer diseases. Neurology. 2016;87:1925–33.

72.

Taylor JP, Colloby SJ, McKeith IG, O'Brien JT. Covariant perfusion patterns provide clues to the origin of cognitive fluctuations and attentional dysfunction in dementia with Lewy bodies. Int Psychogeriatr. 2013;25:1917–28.CrossRefPubMedPubMedCentral

73.

Colloby SJ, McKeith IG, Burn DJ, Wyper DJ, O'Brien JT, Taylor JP. Cholinergic and perfusion brain networks in Parkinson disease dementia. Neurology. 2016;87:178–85.CrossRefPubMedPubMedCentral

74.

Burke JF, Albin RL, Koeppe RA, Giordani B, Kilbourn MR, Gilman S, et al. Assessment of mild dementia with amyloid and dopamine terminal positron emission tomography. Brain. 2011;134:1647–57.

Titel: Molecular Imaging and Updated Diagnostic Criteria in Lewy Body Dementias
verfasst von: Nicolaas I. Bohnen
Martijn L. T. M. Müller
Kirk A. Frey
Publikationsdatum: 01.10.2017
Verlag: Springer US
Erschienen in: Current Neurology and Neuroscience Reports / Ausgabe 10/2017
Print ISSN: 1528-4042
Elektronische ISSN: 1534-6293
DOI: https://doi.org/10.1007/s11910-017-0789-z

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