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Research article
Sekh Thanprasertsuk
Chulalongkorn University Faculty of Medicine
Corresponding Author
ORCiD: https://orcid.org/0000-0002-0267-1372
License:
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Background: Logopenic progressive aphasia (LPA) is an uncommon neurodegenerative disorder primarily characterized by word-finding difficulties and sentence repetition impairment. Prominent cortical atrophy around left temporo-parietal junction (TPJ) is a classical imaging feature of LPA. This study investigated cortical thinning pattern in clinically diagnosed LPA patients using non-demented subjects as a control group. We also aimed to explore whether there was prominent thinning of other cortical area additional to the well-recognized left TPJ.
Methods: Thicknesses of all cortical regions were measured from brain magnetic resonance images using an automated command on Freesurfer software. Cortical thickness of the LPA and control groups were compared by two methods: 1) using a general linear model (GLM) in SPSS software; and 2) using a vertex-by-vertex GLM, performed with Freesurfer’s QDEC interface.
Results: Besides the well-recognized left TPJ, cortical regions that were significantly thinner in the LPA group by both comparison methods included left caudal middle frontal gyrus (CMFG) (p=0.006 by SPSS, p=0.0003 by QDEC), left rostral middle frontal gyrus (p=0.001 by SPSS, p=0.0001 by QDEC), left parahippocampal gyrus (p=0.008 by SPSS, p=0.005 by QDEC) and right CMFG (p=0.005 by SPSS, p=0.0001 by QDEC).
Conclusions: Our results demonstrated that thinning of middle frontal gyri may be an additional feature in clinically diagnosed LPA patients. Involvement of left parahippocampal gyrus may reflect the underlying neuropathology of Alzheimer’s disease in majority of the LPA patients.
Keywords
Aphasia, primary progressive, Logopenic progressive aphasia, Magnetic resonance imaging, Alzheimer’s disease, Freesurfer, Cortical thickness
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CURRENT STATUS: Published
View the published article at BMC Neurology.
Version 3
Posted 12 Jan, 2021
No community comments so far
Editorial decision: Accept
On 27 Dec, 2020
Editor assigned
On 16 Dec, 2020
Submission checks complete
On 16 Dec, 2020
Editor invited
On 16 Dec, 2020
No comments provided
Editorial decision: Major revision
On 07 Dec, 2020
Reviewer #1 agreed
On 05 Dec, 2020
Review #1 received
Received 05 Dec, 2020
Reviewers invited
Invitations sent on 23 Nov, 2020
Editor assigned
On 13 Oct, 2020
Submission checks complete
On 12 Oct, 2020
Editor invited
On 12 Oct, 2020
No comments provided
Editorial decision: Major revision
On 01 Oct, 2020
Review #1 received
Received 08 Sep, 2020
Reviewer #1 agreed
On 30 Aug, 2020
Reviewers invited
Invitations sent on 29 Aug, 2020
Editor assigned
On 26 Aug, 2020
Submission checks complete
On 25 Aug, 2020
Editor invited
On 25 Aug, 2020
First submitted
On 18 Aug, 2020
Metrics
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PDF Downloads: ...
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See the published version of this preprint at BMC Neurology.
This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Research article
Sekh Thanprasertsuk
Chulalongkorn University Faculty of Medicine
Corresponding Author
ORCiD: https://orcid.org/0000-0002-0267-1372
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Published
View the published article at BMC Neurology.
Version 3
Posted 12 Jan, 2021
No community comments so far
Editorial decision: Accept
On 27 Dec, 2020
Editor assigned
On 16 Dec, 2020
Submission checks complete
On 16 Dec, 2020
Editor invited
On 16 Dec, 2020
No comments provided
Editorial decision: Major revision
On 07 Dec, 2020
Reviewer #1 agreed
On 05 Dec, 2020
Review #1 received
Received 05 Dec, 2020
Reviewers invited
Invitations sent on 23 Nov, 2020
Editor assigned
On 13 Oct, 2020
Submission checks complete
On 12 Oct, 2020
Editor invited
On 12 Oct, 2020
No comments provided
Editorial decision: Major revision
On 01 Oct, 2020
Review #1 received
Received 08 Sep, 2020
Reviewer #1 agreed
On 30 Aug, 2020
Reviewers invited
Invitations sent on 29 Aug, 2020
Editor assigned
On 26 Aug, 2020
Submission checks complete
On 25 Aug, 2020
Editor invited
On 25 Aug, 2020
First submitted
On 18 Aug, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
License:
This work is licensed under a CC BY 4.0 License. Read Full License
View the published article at BMC Neurology.
Background: Logopenic progressive aphasia (LPA) is an uncommon neurodegenerative disorder primarily characterized by word-finding difficulties and sentence repetition impairment. Prominent cortical atrophy around left temporo-parietal junction (TPJ) is a classical imaging feature of LPA. This study investigated cortical thinning pattern in clinically diagnosed LPA patients using non-demented subjects as a control group. We also aimed to explore whether there was prominent thinning of other cortical area additional to the well-recognized left TPJ.
Methods: Thicknesses of all cortical regions were measured from brain magnetic resonance images using an automated command on Freesurfer software. Cortical thickness of the LPA and control groups were compared by two methods: 1) using a general linear model (GLM) in SPSS software; and 2) using a vertex-by-vertex GLM, performed with Freesurfer’s QDEC interface.
Results: Besides the well-recognized left TPJ, cortical regions that were significantly thinner in the LPA group by both comparison methods included left caudal middle frontal gyrus (CMFG) (p=0.006 by SPSS, p=0.0003 by QDEC), left rostral middle frontal gyrus (p=0.001 by SPSS, p=0.0001 by QDEC), left parahippocampal gyrus (p=0.008 by SPSS, p=0.005 by QDEC) and right CMFG (p=0.005 by SPSS, p=0.0001 by QDEC).
Conclusions: Our results demonstrated that thinning of middle frontal gyri may be an additional feature in clinically diagnosed LPA patients. Involvement of left parahippocampal gyrus may reflect the underlying neuropathology of Alzheimer’s disease in majority of the LPA patients.
Figure 1
Figure 2
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