The amyloid precursor protein and its derived fragments concomitantly contribute to the alterations of mitochondrial transport machinery in Alzheimer’s disease Article Swipe
Loan Vaillant-Beuchot
,
Fanny Eysert
,
Blandine Duval
,
Paula Fernanda Kinoshita
,
Raphaëlle Pardossi‐Piquard
,
Charlotte Bauer
,
Sabiha Eddarkaoui
,
Luc Buée
,
Frédéric Checler
,
Mounia Chami
·
YOU?
·
· 2023
· Open Access
·
· DOI: https://doi.org/10.21203/rs.3.rs-3235215/v1
YOU?
·
· 2023
· Open Access
·
· DOI: https://doi.org/10.21203/rs.3.rs-3235215/v1
Mitochondria dysfunctions and mitophagy failure have been associated with several Alzheimer’s disease (AD) related molecular actors including amyloid beta (Aβ) and recently the amyloid precursor protein-C terminal fragments (APP-CTFs). The efficacy of the mitophagy process in neurons relies on regulated mitochondrial transport along axons involving a complex molecular machinery. The contribution of the amyloid precursor protein (APP) and its derived fragments to the mitochondrial transport machinery alterations in AD have not been investigated before. We report herein a change of the expression of mitochondrial transport proteins (SNPH and Miro1), motor adaptors (TRANK1 and TRAK2) and components of the dynein and kinesin motors (i.e. IC1,2 and Kif5 (A, B, C) isoforms) by endogenous APP and by overexpression of APP carrying the familial Swedish mutation (APPswe). We show that APP-CTFs and Aβ concomitantly regulate the expression of a set of transport proteins in APPswe cells treated with β- and γ-secretase inhibitors and by using cells Knock-down for presenilin 1 and 2. We further reported the impact of APP-CTFs on the expression of transport proteins in AAV-injected C99 mice brains. Our data also indicate that both APP-CTFs and Aβ oligomers (Aβo) impair the localization of transport proteins in mitochondria as demonstrated in differentiated SH-SY5Y-APPswe cells treated with β- and γ-secretase inhibitors and in Aβo-treated differentiated SH-SY5Y naive cells. Importantly, we uncover that the expression of a set of transport proteins is modulated in a disease-dependent manner in 3xTgAD mice and in human sporadic AD brains. This study highlights molecular mechanisms underlying mitochondrial transport defect in AD that likely contribute to mitophagy failure and disease progression.
Related Topics
Concepts
Parkin
Mitophagy
Amyloid precursor protein
Presenilin
Cell biology
Axoplasmic transport
Mitochondrion
Amyloid precursor protein secretase
Amyloid beta
Biology
Transport protein
Chemistry
Alzheimer's disease
Biochemistry
Autophagy
Parkinson's disease
Disease
Medicine
Internal medicine
Peptide
Apoptosis
Metadata
- Type
- preprint
- Language
- en
- Landing Page
- https://doi.org/10.21203/rs.3.rs-3235215/v1
- https://www.researchsquare.com/article/rs-3235215/latest.pdf
- OA Status
- gold
- Cited By
- 2
- References
- 37
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4386923728
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W4386923728Canonical identifier for this work in OpenAlex
- DOI
-
https://doi.org/10.21203/rs.3.rs-3235215/v1Digital Object Identifier
- Title
-
The amyloid precursor protein and its derived fragments concomitantly contribute to the alterations of mitochondrial transport machinery in Alzheimer’s diseaseWork title
- Type
-
preprintOpenAlex work type
- Language
-
enPrimary language
- Publication year
-
2023Year of publication
- Publication date
-
2023-09-21Full publication date if available
- Authors
-
Loan Vaillant-Beuchot, Fanny Eysert, Blandine Duval, Paula Fernanda Kinoshita, Raphaëlle Pardossi‐Piquard, Charlotte Bauer, Sabiha Eddarkaoui, Luc Buée, Frédéric Checler, Mounia ChamiList of authors in order
- Landing page
-
https://doi.org/10.21203/rs.3.rs-3235215/v1Publisher landing page
- PDF URL
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https://www.researchsquare.com/article/rs-3235215/latest.pdfDirect link to full text PDF
- Open access
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YesWhether a free full text is available
- OA status
-
goldOpen access status per OpenAlex
- OA URL
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https://www.researchsquare.com/article/rs-3235215/latest.pdfDirect OA link when available
- Concepts
-
Parkin, Mitophagy, Amyloid precursor protein, Presenilin, Cell biology, Axoplasmic transport, Mitochondrion, Amyloid precursor protein secretase, Amyloid beta, Biology, Transport protein, Chemistry, Alzheimer's disease, Biochemistry, Autophagy, Parkinson's disease, Disease, Medicine, Internal medicine, Peptide, ApoptosisTop concepts (fields/topics) attached by OpenAlex
- Cited by
-
2Total citation count in OpenAlex
- Citations by year (recent)
-
2025: 1, 2023: 1Per-year citation counts (last 5 years)
- References (count)
-
37Number of works referenced by this work
- Related works (count)
-
10Other works algorithmically related by OpenAlex
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