Cerebral amyloid angiopathy in Down syndrome and sporadic and autosomal‐dominant Alzheimer's disease

Carmona-Iragui, María; Balasa, Mircea; Benejam, Bessy; Alcolea, Daniel; Fernández, Susana; Videla, Laura; Sala, Isabel; Sánchez-Saudinós, María Belén; Morenas‐Rodríguez, Estrella; Ribosa-Nogué, Roser; Illán-Gala, Ignacio; González‐Ortiz, Sofía; Clarimón, Jordi; Schmitt, Frederick A.; Powell, David K.; Bosch, Beatríz; Lladó, Albert; Rafii, Michael S.; Head, Elizabeth; Molinuevo, José Luís; Blesa, Rafael; Videla, Sebastián; Lleó, Alberto; Sánchez‐Valle, Raquel; Fortea, Juan

doi:10.1016/j.jalz.2017.03.007

Cited by 60 publications

(74 citation statements)

References 40 publications

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“…A β 1‐42, A β 1‐40, tTau and pTau levels in CSF from participants of this study had been measured previously using other immunoassays (INNOTEST β ‐AMYLOID (1‐42) , INNOTEST hTAU Ag, and INNOTEST PHOSPHO‐TAU (181P) , Fujirebio Europe; and High Sensitivity Human Amyloid β 40, Merck‐Millipore), and these results were available in our database for their comparison with the LUMIPULSE analyses …”

Section: Methodsmentioning

confidence: 99%

Agreement of amyloid PET and CSF biomarkers for Alzheimer's disease on Lumipulse

Alcolea

Pegueroles

Muñoz

et al. 2019

Ann Clin Transl Neurol

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Objective To determine the cutoffs that optimized the agreement between 18F‐Florbetapir positron emission tomography (PET) and Aβ1‐42, Aβ1‐40, tTau, pTau and their ratios measured in cerebrospinal fluid (CSF) on the LUMIPULSE G600II instrument, we quantified the levels of these four biomarkers in 94 CSF samples from participants of the Sant Pau Initiative on Neurodegeneration (SPIN cohort) using the Lumipulse G System with available 18F‐Florbetapir imaging. Methods Participants had mild cognitive impairment (n = 35), AD dementia (n = 12), other dementias or neurodegenerative diseases (n = 41), or were cognitively normal controls (n = 6). Levels of Aβ1‐42 were standardized to certified reference material. Amyloid scans were assessed visually and through automated quantification. We determined the cutoffs of CSF biomarkers that optimized their agreement with 18F‐Florbetapir PET and evaluated concordance between markers of the amyloid category. Results Aβ1‐42, tTau and pTau (but not Aβ1‐40) and the ratios with Aβ1‐42 had good diagnostic agreement with 18F‐Florbetapir PET. As a marker of amyloid pathology, the Aβ1‐42/Aβ1‐40 ratio had higher agreement and better correlation with amyloid PET than Aβ1‐42 alone. Interpretation CSF biomarkers measured with the Lumipulse G System show good agreement with amyloid imaging in a clinical setting with heterogeneous presentations of neurological disorders. Combination of Aβ1‐42 with Aβ1‐40 increases the agreement between markers of amyloid pathology.

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Section: Methodsmentioning

confidence: 99%

Agreement of amyloid PET and CSF biomarkers for Alzheimer's disease on Lumipulse

Alcolea

Pegueroles

Muñoz

et al. 2019

Ann Clin Transl Neurol

Self Cite

130

137

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“…As in amyloid plaques, Aβ in CAA also contributes to amyloid PET ligand retention in vivo (Bacskai et al, 2007;Lockhart et al, 2007). Although variable, severity of CAA lesions in DS was reported to be higher than in sporadic AD Mann et al, 2018), a finding also reflected in studies of CAA-associated MRI neuroimaging features in DS (Carmona-Iragui et al, 2017). However, the time of onset of CAA lesions in DS, and its implications for amyloid PET imaging are not well-understood.…”

Section: Cerebral Amyloid Angiopathymentioning

confidence: 99%

Neuropathological correlates of amyloid PET imaging in Down syndrome

Abrahamson

Head

Lott

et al. 2019

Developmental Neurobiology

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Down syndrome (DS) results in an overproduction of amyloid‐β (Aβ) peptide associated with early onset of Alzheimer's disease (AD). DS cases have Aβ deposits detectable histologically as young as 12–30 years of age, primarily in the form of diffuse plaques, the type of early amyloid pathology also seen at pre‐clinical (i.e., pathological aging) and prodromal stages of sporadic late onset AD. In DS subjects aged >40 years, levels of cortical Aβ deposition are similar to those observed in late onset AD and in addition to diffuse plaques involve cored plaques associated with dystrophic neurites (neuritic plaques), which are of neuropathological diagnostic significance in AD. The purpose of this review is to summarize and discuss findings from amyloid PET imaging studies of DS in reference to postmortem amyloid‐based neuropathology. PET neuroimaging applied to subjects with DS has the potential to (a) track the natural progression of brain pathology, including the earliest stages of amyloid accumulation, and (b) determine whether amyloid PET biomarkers predict the onset of dementia. In addition, the question that is still incompletely understood and relevant to both applications is the ability of amyloid PET to detect Aβ deposits in their earliest form.

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“…High Sensitivity Human Amyloid β 40, Merck-Millipore), and these results were available in our database for their comparison with the LUMIPULSE analyses [23][24][25][26][27]. The personnel involved in the CSF analyses for this study were blinded to the clinical diagnosis and to previous biomarker determinations.…”

Section: Innotest Htau Ag and Innotest Phospho-tau (181p) Fujirebimentioning

confidence: 99%

Agreement between ¹⁸F-Florbetapir PET imaging and cerebrospinal fluid Aβ1-42, Aβ1-40, tTau and pTau measured on the LUMIPULSE G fully automated platform

Alcolea

Pegueroles

Muñoz

et al. 2018

Preprint

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INTRODUCTION: The development of fully automated immunoassay platforms has improved the technical reliability of cerebrospinal fluid (CSF) biomarkers for Alzheimer's disease. METHODS:We quantified Aβ1-42, Aβ1-40, tTau and pTau levels using the Lumipulse G System in 94 CSF samples from participants of the SPIN cohort with available 18 F-Florbetapir imaging. Amyloid scans were assessed visually and through automated quantification. We determined the cutoffs of CSF biomarkers that optimized their agreement with 18 F-Florbetapir PET and evaluated concordance between markers of the amyloid category.RESULTS: Aβ1-42, tTau and pTau (but not Aβ1-40) and the ratios with Aβ1-42 had good diagnostic agreement with 18 F-Florbetapir PET. As a marker of amyloid pathology, the Aβ1-42/Aβ1-40 ratio had higher agreement and better correlation with amyloid PET than Aβ1-42 alone.DISCUSSION: CSF biomarkers measured with the Lumipulse G System show good agreement with amyloid imaging. Combination of Aβ1-42 with Aβ1-40 increases the agreement between markers of amyloid pathology.

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Cerebral amyloid angiopathy in Down syndrome and sporadic and autosomal‐dominant Alzheimer's disease

Cited by 60 publications

References 40 publications

Agreement of amyloid PET and CSF biomarkers for Alzheimer's disease on Lumipulse

Agreement of amyloid PET and CSF biomarkers for Alzheimer's disease on Lumipulse

Neuropathological correlates of amyloid PET imaging in Down syndrome

Agreement between ¹⁸F-Florbetapir PET imaging and cerebrospinal fluid Aβ1-42, Aβ1-40, tTau and pTau measured on the LUMIPULSE G fully automated platform

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Cerebral amyloid angiopathy in Down syndrome and sporadic and autosomal‐dominant Alzheimer's disease

Cited by 60 publications

References 40 publications

Agreement of amyloid PET and CSF biomarkers for Alzheimer's disease on Lumipulse

Agreement of amyloid PET and CSF biomarkers for Alzheimer's disease on Lumipulse

Neuropathological correlates of amyloid PET imaging in Down syndrome

Agreement between 18F-Florbetapir PET imaging and cerebrospinal fluid Aβ1-42, Aβ1-40, tTau and pTau measured on the LUMIPULSE G fully automated platform

Contact Info

Product

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Agreement between ¹⁸F-Florbetapir PET imaging and cerebrospinal fluid Aβ1-42, Aβ1-40, tTau and pTau measured on the LUMIPULSE G fully automated platform