Please use this identifier to cite or link to this item: https://hdl.handle.net/20.500.12530/56901
Title: Microglia, neurodegeneration and loss of neuroendocrine control.
Authors: Chowen, Julie A
Garcia-Segura, Luis M
Keywords: 
Mesh: 
Issue Date: 9-Nov-2019
Citation: Prog Neurobiol.2020;(184):101720
Abstract: Microglia, the primary regulators of inflammatory responses in the brain, suffer deterioration during aging culminating in their inability to generate adequate adaptive responses to maintain physiological homeostasis in brain tissue. Microglia affect the function of other glial cells and neurons, including those involved in the hypothalamic control of body homeostasis. Microglial dysfunction with aging in cognitive areas such as the hippocampus is known to associate with cognitive decline; more recently, microglial alterations in the hypothalamus during midlife was suggested to participate in changes in the endocrine and metabolic control exerted by this brain region. Consequently, the feed-back loops between endocrine glands and the hypothalamus are altered. This generates a vicious circle in which the plasma levels of key neuroprotective hormones, such as gonadal hormones, insulin-like growth factor-1, growth hormone and leptin and their hypothalamic signaling are decreased, which further enhances microglial alterations and deterioration of hypothalamic function. Hypothalamic dysfunction is a risk factor for neurodegenerative diseases and these diseases in turn promote additional alterations in hypothalamic microglial cells, which are unable to cope with the neurodegenerative process, resulting in permanent damage of the neuronal-glial circuits controlling endocrine homeostasis, food intake and body metabolism. Thus, a "vicious cycle" may such be initiated.
PMID: 31715222
URI: https://hdl.handle.net/20.500.12530/56901
Appears in Collections:Fundaciones e Institutos de Investigación > FIB H. Infantil U. Niño Jesús > Artículos

Files in This Item:
The file with the full text of this item is not available due to copyright restrictions or because there is no digital version. Authors can contact the head of the repository of their center to incorporate the corresponding file.


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.