See the published version of this preprint at Molecular Autism.
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Autism Spectrum Disorder (ASD) is a neurodevelopmental disorder with main core symptoms including deficits in social-communication abilities and repetitive behaviors/restricted interests. ASD affects 1 of 88 children worldwide and currently there is no sufficiently effective treatment that alleviates its core deficits. In our previous studies, we have shown that both MSC and MSC-exo can ameliorate core ASD-like symptoms of the BTBR multifactorial mouse model of autism. Furthermore, we have demonstrated that the MSC-exo migrate to distinct neuropathological areas in several mouse models, including the frontal cortex and cerebellum in BTBR mice. In contrast to BTBR mice, which is a multifactorial model of autism, the Shank3B KO mouse is used to study ASD which develops due to a specific genetic mutation. Here we demonstrate that intranasal treatment with MSC-exo improves the social behavior deficit in multiple paradigms, increases vocalization and reduces repetitive behaviors. We also observed an increase of GABRB1 in the prefrontal cortex. Taken together, our data indicate that intranasal treatment with MSC-exo improves the core ASD-like deficits of in this mouse model autism and therefore has the potential to treat ASD patients carrying the Shank3 mutation.
Keywords
Autism Spectrum Disorder (ASD),Mesenchymal Stem Cells (MSC)
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CURRENT STATUS: Published
View the published article at Molecular Autism.
No community comments so far
Editorial decision: Accept
On 20 Jul, 2020
Editor assigned
On 17 Jul, 2020
Submission checks complete
On 16 Jul, 2020
Editor invited
On 16 Jul, 2020
No comments provided
Editorial decision: Minor revision
On 07 Jul, 2020
Review #1 received
Received 05 Jul, 2020
Review #2 received
Received 04 Jul, 2020
Reviewer #2 agreed
On 22 Jun, 2020
Editor assigned
On 21 Jun, 2020
Reviewers invited
Invitations sent on 21 Jun, 2020
Reviewer #1 agreed
On 21 Jun, 2020
Submission checks complete
On 20 Jun, 2020
Editor invited
On 20 Jun, 2020
Version 1
Posted 13 Mar, 2020
No comments provided
Editorial decision: Major revision
On 10 Apr, 2020
Review #2 received
Received 09 Apr, 2020
Review #1 received
Received 09 Apr, 2020
Reviewer #1 agreed
On 20 Mar, 2020
Reviewer #2 agreed
On 20 Mar, 2020
Reviewers invited
Invitations sent on 19 Mar, 2020
Editor invited
On 18 Mar, 2020
Editor assigned
On 18 Mar, 2020
Submission checks complete
On 11 Mar, 2020
First submitted
On 08 Mar, 2020
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Subject Areas
Cellular & Molecular Neuroscience
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A new preprint design is coming!
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See the published version of this preprint at Molecular Autism.
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
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 Molecular Autism.
No community comments so far
Editorial decision: Accept
On 20 Jul, 2020
Editor assigned
On 17 Jul, 2020
Submission checks complete
On 16 Jul, 2020
Editor invited
On 16 Jul, 2020
No comments provided
Editorial decision: Minor revision
On 07 Jul, 2020
Review #1 received
Received 05 Jul, 2020
Review #2 received
Received 04 Jul, 2020
Reviewer #2 agreed
On 22 Jun, 2020
Editor assigned
On 21 Jun, 2020
Reviewers invited
Invitations sent on 21 Jun, 2020
Reviewer #1 agreed
On 21 Jun, 2020
Submission checks complete
On 20 Jun, 2020
Editor invited
On 20 Jun, 2020
Version 1
Posted 13 Mar, 2020
No comments provided
Editorial decision: Major revision
On 10 Apr, 2020
Review #2 received
Received 09 Apr, 2020
Review #1 received
Received 09 Apr, 2020
Reviewer #1 agreed
On 20 Mar, 2020
Reviewer #2 agreed
On 20 Mar, 2020
Reviewers invited
Invitations sent on 19 Mar, 2020
Editor invited
On 18 Mar, 2020
Editor assigned
On 18 Mar, 2020
Submission checks complete
On 11 Mar, 2020
First submitted
On 08 Mar, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Cellular & Molecular Neuroscience
License:
This work is licensed under a CC BY 4.0 License. Read Full License
View the published article at Molecular Autism.
Autism Spectrum Disorder (ASD) is a neurodevelopmental disorder with main core symptoms including deficits in social-communication abilities and repetitive behaviors/restricted interests. ASD affects 1 of 88 children worldwide and currently there is no sufficiently effective treatment that alleviates its core deficits. In our previous studies, we have shown that both MSC and MSC-exo can ameliorate core ASD-like symptoms of the BTBR multifactorial mouse model of autism. Furthermore, we have demonstrated that the MSC-exo migrate to distinct neuropathological areas in several mouse models, including the frontal cortex and cerebellum in BTBR mice. In contrast to BTBR mice, which is a multifactorial model of autism, the Shank3B KO mouse is used to study ASD which develops due to a specific genetic mutation. Here we demonstrate that intranasal treatment with MSC-exo improves the social behavior deficit in multiple paradigms, increases vocalization and reduces repetitive behaviors. We also observed an increase of GABRB1 in the prefrontal cortex. Taken together, our data indicate that intranasal treatment with MSC-exo improves the core ASD-like deficits of in this mouse model autism and therefore has the potential to treat ASD patients carrying the Shank3 mutation.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
This is a list of supplementary files associated with this preprint. Click to download.
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