P Shahim1, R Rejdak, P Ksiazek, K Blennow, H Zetterberg, N Mattsson, K Rejdak. 1. Clinical Neurochemistry Laboratory, Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, University of Gothenburg, Sahlgrenska University Hospital/Mölndal, Mölndal, Sweden.
Abstract
BACKGROUND AND PURPOSE: The main objectives of this study were to investigate if epileptic seizures have effects on brain metabolism of β-amyloid (Aβ), as reflected by cerebrospinal fluid (CSF) levels of different isoforms of Aβ peptides and soluble amyloid precursor protein (APP), and neuronal degeneration, as reflected by CSF biomarker signs of acute neuronal injury. METHODS: Forty-five patients were included, 21 of whom had single generalized tonic-clonic seizures sGTCS), 11 had repetitive GTCS, 7 had repetitive partial seizures (rPS), 6 had single partial seizure (sPS) and 4 fulfilled the criterion for non-convulsive status epilepticus (nSE). CSF was analyzed for Aβx-38, Aβx-40, Aβx-42, Aβ1-42, soluble APP fragments (sAPP-α/β), total-tau (T-tau) and phosphorylated tau (P-tau), as well as heart-type fatty acid binding protein (H-FABP). RESULTS: Patients with seizures had decreased levels of T-tau (P = 0.0016) and P-tau (P = 0.0028) compared with controls, but no differences in H-FABP (P = 0.67). There were no overall differences in Aβ or sAPP peptides between seizure patients and controls. In patients with rPS, the levels of Aβx-38 and Aβx-40 were elevated compared with nSE (P < 0.01), sPS (P < 0.05) and controls (P < 0.05), and Aβx-42 was elevated in rPS relative to nSE (P < 0.05). CONCLUSIONS: The findings of this study argue against acute neuronal injury following medically treated seizures but suggest that seizures may reduce CSF levels of tau. Although seizures generally did not affect CSF levels of Aβ or sAPP peptides, our findings suggest that different types of seizures may have different effects on APP metabolism.
BACKGROUND AND PURPOSE: The main objectives of this study were to investigate if epileptic seizures have effects on brain metabolism of β-amyloid (Aβ), as reflected by cerebrospinal fluid (CSF) levels of different isoforms of Aβ peptides and soluble amyloid precursor protein (APP), and neuronal degeneration, as reflected by CSF biomarker signs of acute neuronal injury. METHODS: Forty-five patients were included, 21 of whom had single generalized tonic-clonic seizures sGTCS), 11 had repetitive GTCS, 7 had repetitive partial seizures (rPS), 6 had single partial seizure (sPS) and 4 fulfilled the criterion for non-convulsive status epilepticus (nSE). CSF was analyzed for Aβx-38, Aβx-40, Aβx-42, Aβ1-42, soluble APP fragments (sAPP-α/β), total-tau (T-tau) and phosphorylated tau (P-tau), as well as heart-type fatty acid binding protein (H-FABP). RESULTS:Patients with seizures had decreased levels of T-tau (P = 0.0016) and P-tau (P = 0.0028) compared with controls, but no differences in H-FABP (P = 0.67). There were no overall differences in Aβ or sAPP peptides between seizurepatients and controls. In patients with rPS, the levels of Aβx-38 and Aβx-40 were elevated compared with nSE (P < 0.01), sPS (P < 0.05) and controls (P < 0.05), and Aβx-42 was elevated in rPS relative to nSE (P < 0.05). CONCLUSIONS: The findings of this study argue against acute neuronal injury following medically treated seizures but suggest that seizures may reduce CSF levels of tau. Although seizures generally did not affect CSF levels of Aβ or sAPP peptides, our findings suggest that different types of seizures may have different effects on APP metabolism.