This study finds:
a neuroprotective effect from a non-invasive auricular (ear) Vagus Nerve Stimulation (VNS) to reduce Post-Operative Cognitive Dysfunction (POCD) symptoms.
~*~
"tickle my ear" if I ever need surgery !?!?!?
Curious... and cool...
(non-invasive!!!)(smiles)
~*~
Neuroscience Letters
Auricular {ear} vagus nerve stimulation (VNS) protects against Post-Operative Cognitive Dysfunction (POCD) by attenuating neuroinflammation and neurodegeneration in aged ratsAuthor links open overlay panel
Highlights
Abstract
Volume 703, 11 June 2019, Pages 104-110
Surgery-induced cognitive impairment in aged rats is relieved noninvasively by a vagus nerve stimulation (VNS).
- Treatment with a VNS attenuates surgery-related neuroinflammation (in aged rats).
- Treatment with a VNS reduces the apoptosis induced by surgery (in aged rats).
- aVNS also diminishes the surgery-induced Aβ production and tau phosphorylation.
Postoperative cognitive dysfunction (POCD) has been increasingly recognized as a significant complication after surgery, especially in senior patients. Vagus nerve stimulation (VNS) reportedly provides beneficial effects against various brain disorders, supporting a hypothesis of its protective role in POCD. However, direct stimulation of the vagus nerve is invasive, as it requires a surgical incision in the neck. Thus, we employed a
non-invasive VNS method by
stimulating the dermatome in the external ear, which is innervated by the vagus nerve (auricular vagus nerve stimulation; aVNS)
and sought to investigate the efficacy of this method in treating surgery-induced cognitive dysfunction in an aged rat model of POCD. We observed that the treatment of aVNS alleviated postoperative memory impairment after exploratory laparotomy surgery, as demonstrated by the shorter swimming latency and distance in Morris water maze tests.
Moreover, aVNS also reduced postoperative apoptosis in the hippocampus of the aged rats.
Concomitant with these beneficial effects, we found that treatment with aVNS attenuated postoperative neuroinflammation (i.e., the protein level of interleukin-1β and tumor necrosis factor-α, along with the nuclear protein expression of NF-κB) and Alzheimer’s-related pathology (tau phosphorylation at AT-8 and Ser396, as well as the levels of Aβ40 and Aβ42) in the hippocampus of the aged rats.
In conclusion, our study is the first to reveal the neuroprotective effect of aVNS against POCD. This effect might be attributed to the inhibition of neuroinflammation and Alzheimer’s-related pathology.
This study suggests non-invasive aVNS may serve as a promising method for clinical treatment of POCD.
Comments
Post a Comment