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• W2980329192 abstract "Frontotemporal dementia (FTD) is a neuropathologically heterogeneous disorder with different genetic and cellular mechanism. Some evidence is present for changes in the amyloid pathway due to the underlying FTD neuropathological process. Here, CSF amyloid beta (Aβ) 38, 40 and 42 were investigated in FTD patients with known underlying pathology. Additionally, a possible correlation between CSF amyloid levels and brain tissue amyloid load was studied. Levels of Aβ38, Aβ40, and Aβ42 were measured in ante-mortem obtained lumbar CSF of FTD (n=26), AD (n=25) and patients with subjective memory complaints (SMC; n=24). FTD patients with post-mortem confirmed TAR DNA binding protein 43 pathology (FTLD-TDP, n=10), FTD genetically confirmed patients (C9orf72 hexanucleotide repeat expansion (n=3), tau-gene mutation (n=3) and progranuline (n=2) mutation), as well as patients with clinical FTD with EMG confirmed motor neuron disease (association with MND-confirmed, n=8) were included. AD cases were either positive for PIB-PET during live (N=14) or positive for amyloid beta post-mortem after neuropathological assessment (n=11). The ABC score model of NIAA was applied to determine amyloid load in FTLD-TDP (n=10). Group differences for all three biomarkers were significant (Aβ38 p=0.05, Aβ40 p<0.05, Aβ42 p<0.01). Post-hoc analysis revealed lower (p<0.01) Aβ38 and Aβ40 levels for FTD compared with SMC. Aβ38 and Aβ40 in AD did not differ compared with FTD and SMC. Significant intermediate Aβ42 levels were found in FTD patients compared with SMC (p<0.05) and AD (p<0.01). As expected, in AD lower Aβ42 was found when compared with SMC (p<0.01). No correlation was found between brain amyloid load and CSF Aβ subtype concentrations in FTLD-TDP. This study shows reduced Aβ38, Aβ40 and Aβ42 levels in CSF of definite FTD patients compared to controls. Surprisingly, no relation was found between CSF Aβ subtypes and amyloid load in brain tissue, although numbers were relatively small. This is an intriguing finding, suggesting a possible interaction between TDP-43 and soluble amyloid. Further research is needed to elucidate the role of Aβ subtypes in the pathogenesis of FTD." @default.
• W2980329192 created "2019-10-25" @default.
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• W2980329192 date "2019-07-01" @default.
• W2980329192 modified "2023-09-27" @default.
• W2980329192 title "P1-433: DECREASED CSF AMYLOID BETA 38, 40 AND 42 IN GENETICALLY AND PATHOLOGICALLY CONFIRMED FTD" @default.
• W2980329192 doi "https://doi.org/10.1016/j.jalz.2019.06.1038" @default.
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