Alzheimer's Disease, Sleep Disordered Breathing, and Microglia: Puzzling out a Common Link.

Sleep Disordered Breathing (SDB) and Alzheimer's Disease (AD) are strongly associated clinically, but it is unknown if they are mechanistically associated. Here, we review data covering both the cellular and molecular responses in SDB and AD with an emphasis on the overlapping neuroimmune responses in both diseases. We extensively discuss the use of animal models of both diseases and their relative utilities in modeling human disease.

Prior Hypoxia Exposure Enhances Murine Microglial Inflammatory Gene Expression Without Concomitant H3K4me3 Enrichment.

Hypoxia (Hx) is a component of multiple disorders, including stroke and sleep-disordered breathing, which often precede or are comorbid with neurodegenerative diseases. However, little is known about how hypoxia affects the ability of microglia, resident CNS macrophages, to respond to subsequent inflammatory challenges that are often present during neurodegenerative processes. We, therefore, tested the hypothesis that hypoxia would enhance or "prime" microglial pro-inflammatory gene expression in response to a later inflammatory challenge without programmatically increasing basal levels of pro-inflammatory cytokine expression.

All roads lead to inflammation: Is maternal immune activation a common culprit behind environmental factors impacting offspring neural control of breathing?

Despite numerous studies investigating how prenatal exposures impact the developing brain, there remains very little known about how these in utero exposures impact the life-sustaining function of breathing. While some exposures such as alcohol and drugs of abuse are well-known to alter respiratory function, few studies have evaluated other common maternal environmental stimuli, such as maternal infection, inhalation of diesel exhaust particles prevalent in urban areas, or obstructive sleep apnea during pregnancy, just to name a few. The goals of this review article are thus to: 1) highlight data on gestational exposures that impair respiratory function, 2) discuss what is known about the potential role of inflammation in the effects of these maternal exposures, and 3) identify less studied but potential in utero exposures that could negatively impact CNS regions important in respiratory motor control, perhaps by impacting maternal or fetal inflammation.