Laboratory of Molecular Psychiatry

Laboratory of, United States

Laboratory of Molecular Psychiatry

Laboratory of, United States
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Engel O.,Charité - Medical University of Berlin | Akyuz L.,Institute for Medical Immunology | Akyuz L.,Berlin Brandenburg Center for Regenerative Medicine | Da Costa Goncalves A.C.,Max Delbrück Center for Molecular Medicine | And 15 more authors.
Stroke | Year: 2015

Background and Purpose-Temporary immunosuppression has been identified as a major risk factor for the development of pneumonia after acute central nervous system injury. Although overactivation of the sympathetic nervous system was previously shown to mediate suppression of systemic cellular immune responses after stroke, the role of the parasympathetic cholinergic anti-inflammatory pathway in the antibacterial defense in lung remains largely elusive. Methods-The middle cerebral artery occlusion model in mice was used to examine the influence of the parasympathetic nervous system on poststroke immunosuppression. We used heart rate variability measurement by telemetry, vagotomy, α7 nicotinic acetylcholine receptor-deficient mice, and parasympathomimetics (nicotine, PNU282987) to measure and modulate parasympathetic activity. Results-Here, we demonstrate a rapidly increased parasympathetic activity in mice after experimental stroke. Inhibition of cholinergic signaling by either vagotomy or by using α7 nicotinic acetylcholine receptor-deficient mice reversed pulmonary immune hyporesponsiveness and prevented pneumonia after stroke. In vivo and ex vivo studies on the role of α7 nicotinic acetylcholine receptor on different lung cells using bone marrow chimeric mice and isolated primary cells indicated that not only macrophages but also alveolar epithelial cells are a major cellular target of cholinergic anti-inflammatory signaling in the lung. Conclusions-Thus, cholinergic pathways play a pivotal role in the development of pulmonary infections after acute central nervous system injury. © 2015 American Heart Association, Inc.


PubMed | Laboratory of Molecular Psychiatry, Hospital Of Clinicas Of Porto Alegre Hcpa, Dementia Clinic and Federal University of Rio Grande do Sul
Type: Journal Article | Journal: Dementia and geriatric cognitive disorders extra | Year: 2017

Hippocampal atrophy is a recognized biomarker of Alzheimer disease (AD) pathology. Serum brain-derived neurotrophic factor (BDNF) reduction has been associated with neurodegeneration. We aimed to evaluate BDNF serum levels and hippocampal volume in clinical AD (dementia and mild cognitive impairment [MCI]).Participants were 10 patients with MCI and 13 with dementia due to AD as well as 10 healthy controls. BDNF serum levels were determined by ELISA and volumetric measures with NeuroQuant.MCI and dementia patients presented lower BDNF serum levels than healthy participants; dementia patients presented a smaller hippocampal volume than MCI patients and healthy participants.The findings support that the decrease in BDNF might start before the establishment of neuronal injury expressed by the hippocampal reduction.

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