Neutrophil Gelatinase-Associated Lipocalin and its Receptors in Alzheimer's Disease (AD) Brain Regions: Differential Findings in AD with and without DepressionDekens, D. W., Naude, P. J. W., Engelborghs, S., Vermeiren, Y., Van Dam, D., Oude Voshaar, R., Eisel, U. L. M. & De Deyn, P. P., 2017, In : Journal of alzheimers disease. 55, 2, p. 763-776 14 p.
Research output: Contribution to journal › Article › Academic › peer-review
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.
|Number of pages||14|
|Journal||Journal of alzheimers disease|
|Publication status||Published - 2017|
- 24p3R, Alzheimer's disease, depression, hippocampus, inflammation, lipocalin 2, megalin, NGAL, LATE-LIFE DEPRESSION, MILD COGNITIVE IMPAIRMENT, CENTRAL-NERVOUS-SYSTEM, AMYLOID BETA-PEPTIDE, CEREBROSPINAL-FLUID, INFLAMMATORY MARKERS, PREFRONTAL CORTEX, VASCULAR-DEMENTIA, MAJOR DEPRESSION, APOLIPOPROTEIN J