BACKGROUND/ OBJECTIVE: PrP (c) has been suggested to play a role in AD pathophysiology. CSF concentrations of PrP (c) have been shown to be reduced in AD compared with healthy controls. Furthermore, serum levels of PrP (c) have recently been reported to be associated with the cognitive status of healthy elderly subjects. Therefore, we hypothesized that CSF levels of PrP (c) could be associated with cognitive function of AD patients at the time of diagnosis. METHODS: AD patients (n = 114) included into an observational study underwent CERAD testing and lumbar puncture at time of diagnosis / study inclusion. CSF PrP (c) was determined. Generalized linear models were fitted to assess the associations of PrP (c) plus a variety of possible confounding factors and CERAD subscale measures. RESULTS: No association of CSF PrP (c) and cognitive status could be established, while other factors (i.e., use of antipsychotic drugs, use of anti-dementia drugs, female sex, pre-progression time) were related to worse cognitive function in some domains. CONCLUSION: CSF PrP (c) appears not to be a useful biochemical surrogate of cognitive status in AD at the time of diagnosis. Follow-up analyses will examine possible associations with the speed of cognitive decline.
BACKGROUND/ OBJECTIVE:PrP (c) has been suggested to play a role in AD pathophysiology. CSF concentrations of PrP (c) have been shown to be reduced in AD compared with healthy controls. Furthermore, serum levels of PrP (c) have recently been reported to be associated with the cognitive status of healthy elderly subjects. Therefore, we hypothesized that CSF levels of PrP (c) could be associated with cognitive function of ADpatients at the time of diagnosis. METHODS:ADpatients (n = 114) included into an observational study underwent CERAD testing and lumbar puncture at time of diagnosis / study inclusion. CSFPrP (c) was determined. Generalized linear models were fitted to assess the associations of PrP (c) plus a variety of possible confounding factors and CERAD subscale measures. RESULTS: No association of CSFPrP (c) and cognitive status could be established, while other factors (i.e., use of antipsychotic drugs, use of anti-dementia drugs, female sex, pre-progression time) were related to worse cognitive function in some domains. CONCLUSION:CSFPrP (c) appears not to be a useful biochemical surrogate of cognitive status in AD at the time of diagnosis. Follow-up analyses will examine possible associations with the speed of cognitive decline.
Entities:
Keywords:
Alzheimer; CSF; biomarker; cognition; prion protein
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