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Life Sciences › Neuroscience › Developmental Neuroscience
Dysregulation of BDNF/TrkB signaling mediated by NMDAR/Ca²+/calpain might contribute to postoperative cognitive dysfunction in aging mice
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Conflicts of Interest
Identified Weaknesses
Rating Explanation
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Paper Summary
Paperzilla title
Zapping Brain Spark: How Anesthesia Messes with Memory (and a Potential Fix!)
Anesthesia and surgery can trigger neuroinflammation, leading to overactivation of NMDARs and calpain, which in turn messes with BDNF/TrkB signaling, causing memory problems in older mice. Luckily, blocking NMDARs or calpain seemed to protect the mice's brains and memories!
Possible Conflicts of Interest
None identified
Identified Weaknesses
Limited long-term cognitive assessment
The study primarily focuses on short-term cognitive outcomes, which limits the generalizability of the findings to longer-term POCD effects. More comprehensive assessment of cognitive function over a longer period is needed.
Lack of selective NMDAR subunit investigation
While memantine's mechanism is explored, the study doesn't investigate the specific roles of GluN2A and GluN2B subunits using selective antagonists. This would provide a more detailed understanding of NMDAR involvement.
Incomplete analysis of TrkB receptor isoforms
The study identifies a 32-kDa TrkB fragment (TrkB-ICD) but doesn't investigate other truncated TrkB receptor isoforms. A more comprehensive analysis of TrkB receptor alterations is needed.
Rating Explanation
This study presents strong evidence for the role of neuroinflammation, NMDARs, and calpain in POCD, offering a potential therapeutic target. The methodology is generally sound, but the short-term focus and limited investigation of specific NMDAR subunits and TrkB isoforms prevent a perfect score.
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File Information
Original Title:
Dysregulation of BDNF/TrkB signaling mediated by NMDAR/Ca²+/calpain might contribute to postoperative cognitive dysfunction in aging mice
File Name:
s12974-019-1695-x.pdf
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File Size:
3.04 MB
Uploaded:
July 14, 2025 at 11:18 AM
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