Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Obstructive sleep apnea (OSA) may be associated with myriad clinical consequences such as increased risk of systemic hypertension, coronary vascular disease, congestive heart failure, cerebrovascular disease, glucose intolerance, impotence, obesity, pulmonary hypertension, gastroesophageal reflux, and impaired concentration. Nonetheless, OSA remains undiagnosed in 82% of men and 93% of women with the condition. Early identification and treatment of OSA provides significant relief for individuals, prevents complications of OSA, and reduces overall health care costs. Better understanding of the pathogenesis, risk factors, diagnosis, and treatment of OSA has the potential to improve early recognition of OSA and prevention of adverse effects on the individual and society.
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PMID:Snoring and obstructive sleep apnea. 2073 12

A wide range of clinical consequences may be associated with obstructive sleep apnea (OSA) including systemic hypertension, cardiovascular disease, pulmonary hypertension, congestive heart failure, cerebrovascular disease, glucose intolerance, impotence, gastroesophageal reflux, and obesity, to name a few. Despite this, 82 % of men and 93 % of women with OSA remain undiagnosed. OSA affects many body systems, and induces major alterations in metabolic, autonomic, and cerebral functions. Typically, OSA is characterized by recurrent chronic intermittent hypoxia (CIH), hypercapnia, hypoventilation, sleep fragmentation, peripheral and central inflammation, cerebral hypoperfusion, and cerebral glucose hypometabolism. Upregulation of oxidative stress in OSA plays an important pathogenic role in the milieu of hypoxia-induced cerebral and cardiovascular dysfunctions. Strong evidence underscores that cerebral amyloidogenesis and tau phosphorylation--two cardinal features of Alzheimer's disease (AD), are triggered by hypoxia. Mice subjected to hypoxic conditions unambiguously demonstrated upregulation in cerebral amyloid plaque formation and tau phosphorylation, as well as memory deficit. Hypoxia triggers neuronal degeneration and axonal dysfunction in both cortex and brainstem. Consequently, neurocognitive impairment in apneic/hypoxic patients is attributable to a complex interplay between CIH and stimulation of several pathological trajectories. The framework presented here helps delineate the emergence and progression of cognitive decline, and may yield insight into AD neuropathogenesis. The global impact of CIH should provide a strong rationale for treating OSA and snoring clinically, in order to ameliorate neurocognitive impairment in aged/AD patients.
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PMID:Death by a thousand cuts in Alzheimer's disease: hypoxia--the prodrome. 2340 Jun 34