Baseline long‐term potentiation‐like cortical plasticity is associated with longitudinal cortical thinning in healthy adults and in adults with bipolar disorder type II

The precise neurobiological processes underlying cerebral cortical thinning in aging and psychiatric illnesses remain undetermined, yet aging‐ and synaptic dysfunction‐related loss of synapses are potentially important mechanisms. We used long‐term potentiation‐like plasticity of the visual evoked p...

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Published inThe European journal of neuroscience Vol. 58; no. 3; pp. 2824 - 2837
Main Authors Zak, Nathalia, Moberget, Torgeir, Bøen, Erlend, Boye, Birgitte, Rygvold, Trine W., Malt, Ulrik F., Andreassen, Ole A., Andersson, Stein, Westlye, Lars T., Elvsåshagen, Torbjørn
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Published France Wiley Subscription Services, Inc 01.08.2023
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Abstract The precise neurobiological processes underlying cerebral cortical thinning in aging and psychiatric illnesses remain undetermined, yet aging‐ and synaptic dysfunction‐related loss of synapses are potentially important mechanisms. We used long‐term potentiation‐like plasticity of the visual evoked potential as an index of synaptic function in the cortex and hypothesized that plasticity at baseline would be negatively associated with future cortical thinning in healthy adults and in adults with bipolar disorder type II. Thirty‐two healthy adults and 15 adults with bipolar disorder type II underwent electroencephalography‐based measurement of visual evoked potential plasticity and 3T magnetic resonance imaging of the brain at baseline and a follow‐up brain scan on average 2.3 years later. The relationships between visual evoked potential plasticity at baseline and longitudinal cortical thickness changes were examined using Freesurfer and the Permutation Analysis of Linear Models tool. The analyses showed a negative association between the plasticity of the N1 visual evoked potential amplitude at baseline and thinning rate in the medial and lateral parietal and medial occipital cortices in healthy adults and in the right medial occipital cortex in the total sample of healthy adults and adults with bipolar disorder type II, indicating greater thinning over time in subjects with less N1 plasticity (pFWER < .05). Although preliminary, the results indicate an association between visual evoked potential plasticity and the future rate of cortical thinning in healthy adults and in bipolar disorder type II, supporting the hypothesis that cortical thinning might be related to synaptic dysfunction. Long‐term potentiation‐like plasticity of the visual evoked potential (VEP), that is, an index of synaptic function in the cortex, at baseline was associated with future cortical thinning in healthy adults and in adults with bipolar disorder (BPD) type II. Lower N1 amplitude plasticity levels at baseline were associated with an increased cortical thinning rate in healthy adults and in the total sample, supporting the hypothesis that cortical thinning in aging and in psychiatric illnesses might be related to synaptic dysfunction.
AbstractList The precise neurobiological processes underlying cerebral cortical thinning in aging and psychiatric illnesses remain undetermined, yet aging‐ and synaptic dysfunction‐related loss of synapses are potentially important mechanisms. We used long‐term potentiation‐like plasticity of the visual evoked potential as an index of synaptic function in the cortex and hypothesized that plasticity at baseline would be negatively associated with future cortical thinning in healthy adults and in adults with bipolar disorder type II. Thirty‐two healthy adults and 15 adults with bipolar disorder type II underwent electroencephalography‐based measurement of visual evoked potential plasticity and 3T magnetic resonance imaging of the brain at baseline and a follow‐up brain scan on average 2.3 years later. The relationships between visual evoked potential plasticity at baseline and longitudinal cortical thickness changes were examined using Freesurfer and the Permutation Analysis of Linear Models tool. The analyses showed a negative association between the plasticity of the N1 visual evoked potential amplitude at baseline and thinning rate in the medial and lateral parietal and medial occipital cortices in healthy adults and in the right medial occipital cortex in the total sample of healthy adults and adults with bipolar disorder type II, indicating greater thinning over time in subjects with less N1 plasticity (pFWER < .05). Although preliminary, the results indicate an association between visual evoked potential plasticity and the future rate of cortical thinning in healthy adults and in bipolar disorder type II, supporting the hypothesis that cortical thinning might be related to synaptic dysfunction.
The precise neurobiological processes underlying cerebral cortical thinning in aging and psychiatric illnesses remain undetermined, yet aging‐ and synaptic dysfunction‐related loss of synapses are potentially important mechanisms. We used long‐term potentiation‐like plasticity of the visual evoked potential as an index of synaptic function in the cortex and hypothesized that plasticity at baseline would be negatively associated with future cortical thinning in healthy adults and in adults with bipolar disorder type II. Thirty‐two healthy adults and 15 adults with bipolar disorder type II underwent electroencephalography‐based measurement of visual evoked potential plasticity and 3T magnetic resonance imaging of the brain at baseline and a follow‐up brain scan on average 2.3 years later. The relationships between visual evoked potential plasticity at baseline and longitudinal cortical thickness changes were examined using Freesurfer and the Permutation Analysis of Linear Models tool. The analyses showed a negative association between the plasticity of the N1 visual evoked potential amplitude at baseline and thinning rate in the medial and lateral parietal and medial occipital cortices in healthy adults and in the right medial occipital cortex in the total sample of healthy adults and adults with bipolar disorder type II, indicating greater thinning over time in subjects with less N1 plasticity ( p FWER  < .05). Although preliminary, the results indicate an association between visual evoked potential plasticity and the future rate of cortical thinning in healthy adults and in bipolar disorder type II, supporting the hypothesis that cortical thinning might be related to synaptic dysfunction.
Abstract The precise neurobiological processes underlying cerebral cortical thinning in aging and psychiatric illnesses remain undetermined, yet aging‐ and synaptic dysfunction‐related loss of synapses are potentially important mechanisms. We used long‐term potentiation‐like plasticity of the visual evoked potential as an index of synaptic function in the cortex and hypothesized that plasticity at baseline would be negatively associated with future cortical thinning in healthy adults and in adults with bipolar disorder type II. Thirty‐two healthy adults and 15 adults with bipolar disorder type II underwent electroencephalography‐based measurement of visual evoked potential plasticity and 3T magnetic resonance imaging of the brain at baseline and a follow‐up brain scan on average 2.3 years later. The relationships between visual evoked potential plasticity at baseline and longitudinal cortical thickness changes were examined using Freesurfer and the Permutation Analysis of Linear Models tool. The analyses showed a negative association between the plasticity of the N1 visual evoked potential amplitude at baseline and thinning rate in the medial and lateral parietal and medial occipital cortices in healthy adults and in the right medial occipital cortex in the total sample of healthy adults and adults with bipolar disorder type II, indicating greater thinning over time in subjects with less N1 plasticity ( p FWER  < .05). Although preliminary, the results indicate an association between visual evoked potential plasticity and the future rate of cortical thinning in healthy adults and in bipolar disorder type II, supporting the hypothesis that cortical thinning might be related to synaptic dysfunction.
The precise neurobiological processes underlying cerebral cortical thinning in aging and psychiatric illnesses remain undetermined, yet aging- and synaptic dysfunction-related loss of synapses are potentially important mechanisms. We used long-term potentiation-like plasticity of the visual evoked potential as an index of synaptic function in the cortex and hypothesized that plasticity at baseline would be negatively associated with future cortical thinning in healthy adults and in adults with bipolar disorder type II. Thirty-two healthy adults and 15 adults with bipolar disorder type II underwent electroencephalography-based measurement of visual evoked potential plasticity and 3T magnetic resonance imaging of the brain at baseline and a follow-up brain scan on average 2.3 years later. The relationships between visual evoked potential plasticity at baseline and longitudinal cortical thickness changes were examined using Freesurfer and the Permutation Analysis of Linear Models tool. The analyses showed a negative association between the plasticity of the N1 visual evoked potential amplitude at baseline and thinning rate in the medial and lateral parietal and medial occipital cortices in healthy adults and in the right medial occipital cortex in the total sample of healthy adults and adults with bipolar disorder type II, indicating greater thinning over time in subjects with less N1 plasticity (p  < .05). Although preliminary, the results indicate an association between visual evoked potential plasticity and the future rate of cortical thinning in healthy adults and in bipolar disorder type II, supporting the hypothesis that cortical thinning might be related to synaptic dysfunction.
The precise neurobiological processes underlying cerebral cortical thinning in aging and psychiatric illnesses remain undetermined, yet aging‐ and synaptic dysfunction‐related loss of synapses are potentially important mechanisms. We used long‐term potentiation‐like plasticity of the visual evoked potential as an index of synaptic function in the cortex and hypothesized that plasticity at baseline would be negatively associated with future cortical thinning in healthy adults and in adults with bipolar disorder type II. Thirty‐two healthy adults and 15 adults with bipolar disorder type II underwent electroencephalography‐based measurement of visual evoked potential plasticity and 3T magnetic resonance imaging of the brain at baseline and a follow‐up brain scan on average 2.3 years later. The relationships between visual evoked potential plasticity at baseline and longitudinal cortical thickness changes were examined using Freesurfer and the Permutation Analysis of Linear Models tool. The analyses showed a negative association between the plasticity of the N1 visual evoked potential amplitude at baseline and thinning rate in the medial and lateral parietal and medial occipital cortices in healthy adults and in the right medial occipital cortex in the total sample of healthy adults and adults with bipolar disorder type II, indicating greater thinning over time in subjects with less N1 plasticity (pFWER < .05). Although preliminary, the results indicate an association between visual evoked potential plasticity and the future rate of cortical thinning in healthy adults and in bipolar disorder type II, supporting the hypothesis that cortical thinning might be related to synaptic dysfunction. Long‐term potentiation‐like plasticity of the visual evoked potential (VEP), that is, an index of synaptic function in the cortex, at baseline was associated with future cortical thinning in healthy adults and in adults with bipolar disorder (BPD) type II. Lower N1 amplitude plasticity levels at baseline were associated with an increased cortical thinning rate in healthy adults and in the total sample, supporting the hypothesis that cortical thinning in aging and in psychiatric illnesses might be related to synaptic dysfunction.
The precise neurobiological processes underlying cerebral cortical thinning in aging and psychiatric illnesses remain undetermined, yet aging- and synaptic dysfunction-related loss of synapses are potentially important mechanisms. We used long-term potentiation-like plasticity of the visual evoked potential as an index of synaptic function in the cortex and hypothesized that plasticity at baseline would be negatively associated with future cortical thinning in healthy adults and in adults with bipolar disorder type II. Thirty-two healthy adults and 15 adults with bipolar disorder type II underwent electroencephalography-based measurement of visual evoked potential plasticity and 3T magnetic resonance imaging of the brain at baseline and a follow-up brain scan on average 2.3 years later. The relationships between visual evoked potential plasticity at baseline and longitudinal cortical thickness changes were examined using Freesurfer and the Permutation Analysis of Linear Models tool. The analyses showed a negative association between the plasticity of the N1 visual evoked potential amplitude at baseline and thinning rate in the medial and lateral parietal and medial occipital cortices in healthy adults and in the right medial occipital cortex in the total sample of healthy adults and adults with bipolar disorder type II, indicating greater thinning over time in subjects with less N1 plasticity (pFWER  < .05). Although preliminary, the results indicate an association between visual evoked potential plasticity and the future rate of cortical thinning in healthy adults and in bipolar disorder type II, supporting the hypothesis that cortical thinning might be related to synaptic dysfunction.The precise neurobiological processes underlying cerebral cortical thinning in aging and psychiatric illnesses remain undetermined, yet aging- and synaptic dysfunction-related loss of synapses are potentially important mechanisms. We used long-term potentiation-like plasticity of the visual evoked potential as an index of synaptic function in the cortex and hypothesized that plasticity at baseline would be negatively associated with future cortical thinning in healthy adults and in adults with bipolar disorder type II. Thirty-two healthy adults and 15 adults with bipolar disorder type II underwent electroencephalography-based measurement of visual evoked potential plasticity and 3T magnetic resonance imaging of the brain at baseline and a follow-up brain scan on average 2.3 years later. The relationships between visual evoked potential plasticity at baseline and longitudinal cortical thickness changes were examined using Freesurfer and the Permutation Analysis of Linear Models tool. The analyses showed a negative association between the plasticity of the N1 visual evoked potential amplitude at baseline and thinning rate in the medial and lateral parietal and medial occipital cortices in healthy adults and in the right medial occipital cortex in the total sample of healthy adults and adults with bipolar disorder type II, indicating greater thinning over time in subjects with less N1 plasticity (pFWER  < .05). Although preliminary, the results indicate an association between visual evoked potential plasticity and the future rate of cortical thinning in healthy adults and in bipolar disorder type II, supporting the hypothesis that cortical thinning might be related to synaptic dysfunction.
Author Bøen, Erlend
Zak, Nathalia
Malt, Ulrik F.
Andreassen, Ole A.
Boye, Birgitte
Westlye, Lars T.
Moberget, Torgeir
Rygvold, Trine W.
Elvsåshagen, Torbjørn
Andersson, Stein
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Keywords cerebral cortex
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synaptic plasticity
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2005; 10
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Snippet The precise neurobiological processes underlying cerebral cortical thinning in aging and psychiatric illnesses remain undetermined, yet aging‐ and synaptic...
The precise neurobiological processes underlying cerebral cortical thinning in aging and psychiatric illnesses remain undetermined, yet aging- and synaptic...
Abstract The precise neurobiological processes underlying cerebral cortical thinning in aging and psychiatric illnesses remain undetermined, yet aging‐ and...
SourceID cristin
proquest
pubmed
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wiley
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Publisher
StartPage 2824
SubjectTerms Adult
Aging
Auditory evoked potentials
Bipolar disorder
Bipolar Disorder - diagnostic imaging
cerebral cortex
Cerebral Cortex - diagnostic imaging
Cerebral Cortical Thinning
Cortex (parietal)
EEG
Event-related potentials
Evoked Potentials, Visual
Humans
Long-Term Potentiation
Magnetic Resonance Imaging
mood disorder
Neuroimaging
Neuroplasticity
Occipital lobe
Potentiation
synaptic function
synaptic plasticity
Thinning
Visual evoked potentials
Visual plasticity
Title Baseline long‐term potentiation‐like cortical plasticity is associated with longitudinal cortical thinning in healthy adults and in adults with bipolar disorder type II
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fejn.16038
https://www.ncbi.nlm.nih.gov/pubmed/37163975
https://www.proquest.com/docview/2844936298
https://www.proquest.com/docview/2812507159
http://hdl.handle.net/10852/106975
Volume 58
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