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181 results on '"Gillardon F"'

7. Supplementary Material for: Cerebrospinal Fluid Progranulin, but Not Serum Progranulin, Is Reduced in GRN-Negative Frontotemporal Dementia

Author

Wilke, C., Gillardon, F., Deuschle, C., Hobert, M.A., Jansen, I.E., Metzger, F.G., Heutink, P., Gasser, T., Maetzler, W., Blauwendraat, C., and Synofzik, M.

Subjects
mental disorders
Abstract

Background and Objective: Reduced progranulin levels are a hallmark of frontotemporal dementia (FTD) caused by loss-of-function (LoF) mutations in the progranulin gene (GRN). However, alterations of central nervous progranulin expression also occur in neurodegenerative disorders unrelated to GRN mutations, such as Alzheimer's disease. We hypothesised that central nervous progranulin levels are also reduced in GRN-negative FTD. Methods: Progranulin levels were determined in both cerebrospinal fluid (CSF) and serum in 75 subjects (37 FTD patients and 38 controls). All FTD patients were assessed by whole-exome sequencing for GRN mutations, yielding a target cohort of 34 patients without pathogenic mutations in GRN (GRN-negative cohort) and 3 GRN mutation carriers (2 LoF variants and 1 novel missense variant). Results: Not only the GRN mutation carriers but also the GRN-negative patients showed decreased CSF levels of progranulin (serum levels in GRN-negative patients were normal). The decreased CSF progranulin levels were unrelated to patients' increased CSF levels of total tau, possibly indicating different destructive neuronal processes within FTD neurodegeneration. The patient with the novel GRN missense variant (c.1117C>T, p.P373S) showed substantially decreased CSF levels of progranulin, comparable to the 2 patients with GRN LoF mutations, suggesting a pathogenic effect of this missense variant. Conclusions: Our results indicate that central nervous progranulin reduction is not restricted to the relatively rare cases of FTD caused by GRN LoF mutations, but also contributes to the more common GRN-negative forms of FTD. Central nervous progranulin reduction might reflect a partially distinct pathogenic mechanism underlying FTD neurodegeneration and is not directly linked to tau alterations.

Published
2016
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9. Targeted disruption of the bcl-2 gene in mice exacerbates focal ischemic brain injury

Author

Hata, R., Gillardon, F., Michaelidis, T. M., and Hossmann, K. A.

Subjects
bcl-2, apoptosis, endoplasmic-reticulum, neurons, mutant mice, transgenic mice, cerebral ischemia, cell-death, cerebral-artery occlusion, cytochrome-c, bax, focal ischemia, global-ischemia, expression
Abstract

Neuronal death after brain ischemia is mainly due to necrosis but there is also evidence for involvement of apoptosis. To test the importance of apoptosis, we investigated the effect of targeted disruption of the apoptosis-suppressive gene bcl-2 on the severity of ischemic brain injury. Transient focal ischemia for 1 hour was induced by occlusion of the middle cerebral artery in homozygous (n = 7) and heterozygous (n = 6) bcl-2 knockout mice as well as in their wildtype littermates (n = 5). Bcl-2 ablation did not influence cerebral blood flow but it significantly increased infarct size and neurological deficit score at 1 day after reperfusion in a gene-dose dependent manner. The exacerbation of tissue damage in the absence of Bcl-2 underscores the importance of apoptotic pathways for the manifestation of ischemic injury after transient vascular occlusion. Metabolic Brain Disease

Published
1999

16. Targeted Antioxidative and Neuroprotective Properties of the Dopamine Agonist Pramipexole and Its Nondopaminergic Enantiomer SND919CL2x [(+)2-Amino-4,5,6,7-tetrahydro-6-lpropylamino-benzathiazole Dihydrochloride]

Author

Danzeisen, R., primary, Schwalenstoecker, B., additional, Gillardon, F., additional, Buerger, E., additional, Krzykalla, V., additional, Klinder, K., additional, Schild, L., additional, Hengerer, B., additional, Ludolph, A. C., additional, Dorner-Ciossek, C., additional, and Kussmaul, L., additional

Published
2005
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