Abstract
AbstractBackgroundThe amyloid deposition (A) in the 2018 ATN classification of Alzheimer disease can be assessed by CSF Aβ 1‐42 or amyloid PET. Although the agreement between them is high, it is not exact.MethodWe selected patients from the Alzheimer’s disease and other cognitive disorders Unit at Hospital Clínic of Barcelona with available amyloid PET and lumbar puncture, with a maximum difference of time of one and a half year between them. We used F18 Florbetapir (n=27), F18 Florbetaben (n=7), F18 Flutemetamol (n=16) or 11C‐PIB (n=2) as tracers for amyloid PET. CSF Aβ 1‐42, total tau (tTau) and phosphorylated tau (pTau) were measured using INNOTEST® Fujirebio until June 2019 and using LUMIPULSE® Fujirebio after June 2019. We analyzed the agreement between amyloid PET and CSF biomarkers.ResultWe included 52 patients. They had been diagnosed of Alzheimer disease (n=32), frontotemporal dementia (n=11), Lewy body disease (n=2) and psychiatric disorders (n=7) (Table 1).There was a perfect agreement between CSF biomarkers and amyloid PET when CSF biomarkers were all normal or all altered (Figure 1): All patients with CSF A+T+N+ (n=19) had a positive amyloid PET and all patients with CSF A‐T‐N‐ (n=7) had a negative amyloid PET. Agreement decreased with other CSF results. Only 11/19 patients with CSF A+T‐N‐ had a positive amyloid PET. 31/32 (97%) patients with positive amyloid PET had low Aβ 1‐42 levels (A+) but only 11/20 (55%) patients with negative amyloid PET had normal Aβ 1‐42 levels (A‐).ConclusionCSF biomarkers and amyloid PET showed a perfect agreement when CSF biomarkers were all normal or all altered. For other CSF ATN results, agreement with amyloid PET was much lower.
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