Abstract
Obstructive sleep apnea (OSA) is well known for its metabolic as well as neurobehavioral consequences. Chronic intermittent hypoxia (IH) is a major component of OSA. In recent years, substantial advances have been made in elucidating the cellular and molecular mechanisms underlying the effect of chronic IH on neurocognitive functions, many of which are based on studies in animal models. A number of hypotheses have been put forward to explain chronic IH-induced neurological dysfunctions. Among these, the roles of oxidative stress and apoptosis-related neural injury are widely accepted. Here, focusing on results derived from animal studies, we highlight a possible role of reduced expression of brain-derived neurotrophic factor (BDNF) in causing impairment in long-term synaptic plasticity and neurocognitive functions during chronic IH. The possible relationship between BDNF and previous findings on this subject will be elucidated. © 2012 CPS and SIMM. All rights reserved.
| Original language | English |
|---|---|
| Pages (from-to) | 5-10 |
| Journal | Acta Pharmacologica Sinica |
| Volume | 33 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - Jan 2012 |
| Externally published | Yes |
Bibliographical note
Publication details (e.g. title, author(s), publication statuses and dates) are captured on an “AS IS” and “AS AVAILABLE” basis at the time of record harvesting from the data source. Suggestions for further amendments or supplementary information can be sent to [email protected].Funding
The authors' work described in this article was supported by the Research Grants Council of Hong Kong, China (Project No 478308).
Research Keywords
- brain-derived neurotrophic factor
- intermittent hypoxia
- long-term potentiation
- obstructive sleep apnea
- synaptic plasticity