| Autor: |
Dekens DW; Department of Neurology and Alzheimer Research Center, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.; Department of Molecular Neurobiology, University of Groningen, Groningen, The Netherlands., Naudé PJ; Department of Neurology and Alzheimer Research Center, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.; Department of Molecular Neurobiology, University of Groningen, Groningen, The Netherlands., Engelborghs S; Department of Neurology and Memory Clinic, Hospital Network Antwerp (ZNA), Antwerp, Belgium.; Laboratory of Neurochemistry and Behavior, Biobank, Institute Born-Bunge, University of Antwerp, Antwerp, Belgium., Vermeiren Y; Department of Neurology and Alzheimer Research Center, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.; Laboratory of Neurochemistry and Behavior, Biobank, Institute Born-Bunge, University of Antwerp, Antwerp, Belgium., Van Dam D; Department of Neurology and Alzheimer Research Center, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.; Laboratory of Neurochemistry and Behavior, Biobank, Institute Born-Bunge, University of Antwerp, Antwerp, Belgium., Oude Voshaar RC; University Center of Psychiatry & Interdisciplinary Center of Psychopathology of Emotion Regulation, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands., Eisel UL; Department of Molecular Neurobiology, University of Groningen, Groningen, The Netherlands.; University Center of Psychiatry & Interdisciplinary Center of Psychopathology of Emotion Regulation, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands., De Deyn PP; Department of Neurology and Alzheimer Research Center, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.; Department of Neurology and Memory Clinic, Hospital Network Antwerp (ZNA), Antwerp, Belgium.; Laboratory of Neurochemistry and Behavior, Biobank, Institute Born-Bunge, University of Antwerp, Antwerp, Belgium. |
| Abstrakt: |
Co-existing depression worsens Alzheimer's disease (AD) pathology. Neutrophil gelatinase-associated lipocalin (NGAL) is a newly identified (neuro)inflammatory mediator in the pathophysiologies of both AD and depression. This study aimed to compare NGAL levels in healthy controls, AD without depression (AD-D), and AD with co-existing depression (AD+D) patients. Protein levels of NGAL and its receptors, 24p3R and megalin, were assessed in nine brain regions from healthy controls (n = 19), AD-D (n = 19), and AD+D (n = 21) patients. NGAL levels in AD-D patients were significantly increased in brain regions commonly associated with AD. In the hippocampus, NGAL levels were even further increased in AD+D subjects. Unexpectedly, NGAL levels in the prefrontal cortex of AD+D patients were comparable to those in controls. Megalin levels were increased in BA11 and amygdala of AD+D patients, while no changes in 24p3R were detected. These findings indicate significant differences in neuroimmunological regulation between AD patients with and without co-existing depression. Considering its known effects, elevated NGAL levels might actively promote neuropathological processes in AD with and without depression. |
