Vagus nerve stimulation as a potential therapy in early Alzheimer’s disease: a review
Vagus nerve stimulation as a potential therapy in early Alzheimer’s disease: a review
Cognitive dysfunction in Alzheimer’s disease (AD) is caused by disturbances in neuronal circuits of the brain underpinned by synapse loss, neuronal dysfunction and neuronal death. Amyloid beta and tau protein cause these pathological changes and enhance neuroinflammation, which in turn modifies disease progression and severity. Vagal nerve stimulation (VNS), via activation of the locus coeruleus (LC), results in the release of catecholamines in the hippocampus and neocortex, which can enhance synaptic plasticity and reduce inflammatory signalling. Vagal nerve stimulation has shown promise to enhance cognitive ability in animal models. Research in rodents has shown that VNS can have positive effects on basal synaptic function and synaptic plasticity, tune inflammatory signalling, and limit the accumulation of amyloid plaques. Research in humans with invasive and non-invasive VNS devices has shown promise for the modulation of cognition. However, the direct stimulation of the vagus nerve afforded with the invasive procedure carries surgical risks. In contrast, non-invasive VNS has the potential to be a broadly available therapy to manage cognitive symptoms in early AD, however, the magnitude and specificity of its effects remains to be elucidated, and the non-inferiority of the effects of non-invasive VNS as compared with invasive VNS still needs to be established. Ongoing clinical trials with healthy individuals and patients with early AD will provide valuable information to clarify the potential benefits of non-invasive VNS in cognition and AD. Whether invasive or non-invasive VNS can produce a significant improvement on memory function and whether its effects can modify the progression of AD will require further investigation.
Alzheimer, MCI, memory, noradrenaline, norepinepherine, plasticity, vagal, vagus
Vargas-Caballero, Mariana
de2178ac-77fd-4748-9fe5-109ab8ad93e1
Warming, Hannah
52e41d3f-0cf4-440f-b0c9-cec47ed3b23a
Walker, Robert
9368ac2d-f1e9-4bd9-a4b4-4a161c4aa140
Holmes, Clive
ada5abf3-8459-4cf7-be40-3f4e9391cc96
Cruickshank, Garth
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Patel, Bipin
a1ba298c-2f06-4b54-86ee-a7ec5f130708
29 April 2022
Vargas-Caballero, Mariana
de2178ac-77fd-4748-9fe5-109ab8ad93e1
Warming, Hannah
52e41d3f-0cf4-440f-b0c9-cec47ed3b23a
Walker, Robert
9368ac2d-f1e9-4bd9-a4b4-4a161c4aa140
Holmes, Clive
ada5abf3-8459-4cf7-be40-3f4e9391cc96
Cruickshank, Garth
f7656619-ab1d-4cea-be4e-f6bc097736d2
Patel, Bipin
a1ba298c-2f06-4b54-86ee-a7ec5f130708
Vargas-Caballero, Mariana, Warming, Hannah, Walker, Robert, Holmes, Clive, Cruickshank, Garth and Patel, Bipin
(2022)
Vagus nerve stimulation as a potential therapy in early Alzheimer’s disease: a review.
Frontiers in Human Neuroscience, 16, [866434].
(doi:10.3389/fnhum.2022.866434).
Abstract
Cognitive dysfunction in Alzheimer’s disease (AD) is caused by disturbances in neuronal circuits of the brain underpinned by synapse loss, neuronal dysfunction and neuronal death. Amyloid beta and tau protein cause these pathological changes and enhance neuroinflammation, which in turn modifies disease progression and severity. Vagal nerve stimulation (VNS), via activation of the locus coeruleus (LC), results in the release of catecholamines in the hippocampus and neocortex, which can enhance synaptic plasticity and reduce inflammatory signalling. Vagal nerve stimulation has shown promise to enhance cognitive ability in animal models. Research in rodents has shown that VNS can have positive effects on basal synaptic function and synaptic plasticity, tune inflammatory signalling, and limit the accumulation of amyloid plaques. Research in humans with invasive and non-invasive VNS devices has shown promise for the modulation of cognition. However, the direct stimulation of the vagus nerve afforded with the invasive procedure carries surgical risks. In contrast, non-invasive VNS has the potential to be a broadly available therapy to manage cognitive symptoms in early AD, however, the magnitude and specificity of its effects remains to be elucidated, and the non-inferiority of the effects of non-invasive VNS as compared with invasive VNS still needs to be established. Ongoing clinical trials with healthy individuals and patients with early AD will provide valuable information to clarify the potential benefits of non-invasive VNS in cognition and AD. Whether invasive or non-invasive VNS can produce a significant improvement on memory function and whether its effects can modify the progression of AD will require further investigation.
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fnhum-16-866434
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More information
Accepted/In Press date: 6 April 2022
e-pub ahead of print date: 29 April 2022
Published date: 29 April 2022
Additional Information:
Funding Information:
HW is funded by the Gerald Kerkut Trust and the Institute for Life Sciences, University of Southampton.
Publisher Copyright:
Copyright © 2022 Vargas-Caballero, Warming, Walker, Holmes, Cruickshank and Patel.
Keywords:
Alzheimer, MCI, memory, noradrenaline, norepinepherine, plasticity, vagal, vagus
Identifiers
Local EPrints ID: 471403
URI: http://eprints.soton.ac.uk/id/eprint/471403
ISSN: 1662-5161
PURE UUID: 332b4303-12aa-4979-83da-58807b7af18d
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Date deposited: 07 Nov 2022 17:32
Last modified: 17 Mar 2024 03:53
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Author:
Garth Cruickshank
Author:
Bipin Patel
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