Relationship between white matter connectivity loss and cortical thinning in cerebral amyloid angiopathy
Patients with cerebral amyloid angiopathy (CAA) show loss of white matter connectivity and cortical thinning on MRI, primarily in posterior brain regions. Here we examined whether a potential causal relationship exists between these markers of subcortical and cortical brain injury by examining wheth...
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Published in | Human brain mapping Vol. 38; no. 7; pp. 3723 - 3731 |
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Main Authors | , , , , , , , , , , |
Format | Journal Article |
Language | English |
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United States
John Wiley and Sons Inc
01.07.2017
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Abstract | Patients with cerebral amyloid angiopathy (CAA) show loss of white matter connectivity and cortical thinning on MRI, primarily in posterior brain regions. Here we examined whether a potential causal relationship exists between these markers of subcortical and cortical brain injury by examining whether changes in cortical thickness progress in tandem with changes in their underlying connections. Thirty‐one patients with probable CAA with brain MRI at two time points were included (follow‐up time: 1.3 ± 0.4 years). Brain networks were reconstructed using diffusion MRI‐based fiber tractography. Of each network node, we calculated the change in fractional anisotropy‐weighted connectivity strength over time and the change in cortical thickness. The association between change in connectivity strength and cortical thickness was assessed with (hierarchical) linear regression models. Our results showed that decline in posterior network connectivity over time was strongly related to thinning of the occipital cortex (β = 0.65 (0.35–0.94), P < 0.001), but not to thinning of the other posterior or frontal cortices. However, at the level of individual network nodes, we found no association between connectivity strength and cortical thinning of the corresponding node (β = 0.009 ± 0.04, P = 0.80). Associations were independent of age, sex, and other brain MRI markers of CAA. To conclude, CAA patients with greater progressive loss of posterior white matter connectivity also have greater progression of occipital cortical thinning, but our results do not support a direct causal relationship between them. The association can be better explained by a shared underlying mechanism, which may form a potential target for future treatments. Hum Brain Mapp 38:3723–3731, 2017. © 2017 Wiley Periodicals, Inc. |
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AbstractList | Patients with cerebral amyloid angiopathy (CAA) show loss of white matter connectivity and cortical thinning on MRI, primarily in posterior brain regions. Here we examined whether a potential causal relationship exists between these markers of subcortical and cortical brain injury by examining whether changes in cortical thickness progress in tandem with changes in their underlying connections. Thirty‐one patients with probable CAA with brain MRI at two time points were included (follow‐up time: 1.3 ± 0.4 years). Brain networks were reconstructed using diffusion MRI‐based fiber tractography. Of each network node, we calculated the change in fractional anisotropy‐weighted connectivity strength over time and the change in cortical thickness. The association between change in connectivity strength and cortical thickness was assessed with (hierarchical) linear regression models. Our results showed that decline in posterior network connectivity over time was strongly related to thinning of the occipital cortex (
β
= 0.65 (0.35–0.94),
P
< 0.001), but not to thinning of the other posterior or frontal cortices. However, at the level of individual network nodes, we found no association between connectivity strength and cortical thinning of the corresponding node (
β
= 0.009 ± 0.04,
P
= 0.80). Associations were independent of age, sex, and other brain MRI markers of CAA. To conclude, CAA patients with greater progressive loss of posterior white matter connectivity also have greater progression of occipital cortical thinning, but our results do not support a direct causal relationship between them. The association can be better explained by a shared underlying mechanism, which may form a potential target for future treatments.
Hum Brain Mapp 38:3723–3731, 2017
. ©
2017 Wiley Periodicals, Inc. Patients with cerebral amyloid angiopathy (CAA) show loss of white matter connectivity and cortical thinning on MRI, primarily in posterior brain regions. Here we examined whether a potential causal relationship exists between these markers of subcortical and cortical brain injury by examining whether changes in cortical thickness progress in tandem with changes in their underlying connections. Thirty-one patients with probable CAA with brain MRI at two time points were included (follow-up time: 1.3 ± 0.4 years). Brain networks were reconstructed using diffusion MRI-based fiber tractography. Of each network node, we calculated the change in fractional anisotropy-weighted connectivity strength over time and the change in cortical thickness. The association between change in connectivity strength and cortical thickness was assessed with (hierarchical) linear regression models. Our results showed that decline in posterior network connectivity over time was strongly related to thinning of the occipital cortex (β = 0.65 (0.35-0.94), P < 0.001), but not to thinning of the other posterior or frontal cortices. However, at the level of individual network nodes, we found no association between connectivity strength and cortical thinning of the corresponding node (β = 0.009 ± 0.04, P = 0.80). Associations were independent of age, sex, and other brain MRI markers of CAA. To conclude, CAA patients with greater progressive loss of posterior white matter connectivity also have greater progression of occipital cortical thinning, but our results do not support a direct causal relationship between them. The association can be better explained by a shared underlying mechanism, which may form a potential target for future treatments. Hum Brain Mapp 38:3723-3731, 2017. © 2017 Wiley Periodicals, Inc. Abstract Patients with cerebral amyloid angiopathy (CAA) show loss of white matter connectivity and cortical thinning on MRI, primarily in posterior brain regions. Here we examined whether a potential causal relationship exists between these markers of subcortical and cortical brain injury by examining whether changes in cortical thickness progress in tandem with changes in their underlying connections. Thirty‐one patients with probable CAA with brain MRI at two time points were included (follow‐up time: 1.3 ± 0.4 years). Brain networks were reconstructed using diffusion MRI‐based fiber tractography. Of each network node, we calculated the change in fractional anisotropy‐weighted connectivity strength over time and the change in cortical thickness. The association between change in connectivity strength and cortical thickness was assessed with (hierarchical) linear regression models. Our results showed that decline in posterior network connectivity over time was strongly related to thinning of the occipital cortex ( β = 0.65 (0.35–0.94), P < 0.001), but not to thinning of the other posterior or frontal cortices. However, at the level of individual network nodes, we found no association between connectivity strength and cortical thinning of the corresponding node ( β = 0.009 ± 0.04, P = 0.80). Associations were independent of age, sex, and other brain MRI markers of CAA. To conclude, CAA patients with greater progressive loss of posterior white matter connectivity also have greater progression of occipital cortical thinning, but our results do not support a direct causal relationship between them. The association can be better explained by a shared underlying mechanism, which may form a potential target for future treatments. Hum Brain Mapp 38:3723–3731, 2017 . © 2017 Wiley Periodicals, Inc. |
Author | Riley, Grace A. Gurol, M. Edip Xiong, Li Fotiadis, Panagiotis van Veluw, Susanne J. Martinez‐Ramirez, Sergi Schwab, Kristin Viswanathan, Anand Greenberg, Steven M. Charidimou, Andreas Reijmer, Yael D. |
AuthorAffiliation | 1 Hemorrhagic Stroke Research Program, Department of Neurology Massachusetts General Hospital, Harvard Medical School Boston Massachusetts 2 Department of Neurology University Medical Center Utrecht, Brain Center Rudolf Magnus Utrecht The Netherlands |
AuthorAffiliation_xml | – name: 1 Hemorrhagic Stroke Research Program, Department of Neurology Massachusetts General Hospital, Harvard Medical School Boston Massachusetts – name: 2 Department of Neurology University Medical Center Utrecht, Brain Center Rudolf Magnus Utrecht The Netherlands |
Author_xml | – sequence: 1 givenname: Yael D. orcidid: 0000-0002-2566-7122 surname: Reijmer fullname: Reijmer, Yael D. email: yaelreijmer@gmail.com organization: University Medical Center Utrecht, Brain Center Rudolf Magnus – sequence: 2 givenname: Panagiotis surname: Fotiadis fullname: Fotiadis, Panagiotis organization: Massachusetts General Hospital, Harvard Medical School – sequence: 3 givenname: Andreas surname: Charidimou fullname: Charidimou, Andreas organization: Massachusetts General Hospital, Harvard Medical School – sequence: 4 givenname: Susanne J. surname: van Veluw fullname: van Veluw, Susanne J. organization: Massachusetts General Hospital, Harvard Medical School – sequence: 5 givenname: Li surname: Xiong fullname: Xiong, Li organization: Massachusetts General Hospital, Harvard Medical School – sequence: 6 givenname: Grace A. surname: Riley fullname: Riley, Grace A. organization: Massachusetts General Hospital, Harvard Medical School – sequence: 7 givenname: Sergi surname: Martinez‐Ramirez fullname: Martinez‐Ramirez, Sergi organization: Massachusetts General Hospital, Harvard Medical School – sequence: 8 givenname: Kristin surname: Schwab fullname: Schwab, Kristin organization: Massachusetts General Hospital, Harvard Medical School – sequence: 9 givenname: Anand surname: Viswanathan fullname: Viswanathan, Anand organization: Massachusetts General Hospital, Harvard Medical School – sequence: 10 givenname: M. Edip surname: Gurol fullname: Gurol, M. Edip organization: Massachusetts General Hospital, Harvard Medical School – sequence: 11 givenname: Steven M. surname: Greenberg fullname: Greenberg, Steven M. organization: Massachusetts General Hospital, Harvard Medical School |
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Snippet | Patients with cerebral amyloid angiopathy (CAA) show loss of white matter connectivity and cortical thinning on MRI, primarily in posterior brain regions. Here... Abstract Patients with cerebral amyloid angiopathy (CAA) show loss of white matter connectivity and cortical thinning on MRI, primarily in posterior brain... |
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SubjectTerms | atrophy cerebral small vessel diseases connectome diffusion tensor imaging diffusion tractography |
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Title | Relationship between white matter connectivity loss and cortical thinning in cerebral amyloid angiopathy |
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