Please use this identifier to cite or link to this item:
|Potential role of aminoprocalcitonin in the pathogenesis of alzheimer disease
López González, Irene
Ferrer, Isidro (Ferrer Abizanda)
Miñano, Francisco J.
|Increasing evidence suggests that inflammatory responses cause brain atrophy and play a prominent and early role in the progression of Alzheimer disease. Recent findings show that the neuroendocrine peptide aminoprocalcitonin (NPCT) plays a critical role in the development of systemic inflammatory response; however, the presence, possible function, regulation, and mechanisms by which NPCT may be involved in Alzheimer disease neuropathology remain unknown. We explored the expression of NPCT and its interaction with amyloid-b (Ab), and proinflammatory and neurogenic effects. By using brain samples of Alzheimer disease patients and APP/PS1 transgenic mice, we evaluated the potential role of NPCT on Ab-related pathology. We found that NPCT is expressed in hippocampal and cortical neurons and Ab-induced up-regulation of NPCT expression. Peripherally administered antibodies against NPCT decreased microglial activation, decreased circulating levels of proinflammatory cytokines, and prevented Ab-induced neurotoxicity in experimental models of Alzheimer disease. Remarkably, anti-NPTC therapy resulted in a significant improvement in the behavioral status of APP/PS1 mice. Our results indicate a central role of NPCT in Alzheimer disease pathogenesis and suggest NPCT as a potential biomarker and therapeutic target.
|Versió postprint del document publicat a: https://doi.org/10.1016/j.ajpath.2016.06.006
|It is part of:
|American Journal of Pathology, 2016, vol. 186, num. 10, p. 2723-2735
|Appears in Collections:
|Articles publicats en revistes (Institut d'lnvestigació Biomèdica de Bellvitge (IDIBELL))
Articles publicats en revistes (Patologia i Terapèutica Experimental)
This item is licensed under a Creative Commons License