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Cyclophilin D deficiency attenuates mitochondrial and neuronal perturbation and ameliorates learning and memory in Alzheimer's disease

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Du, Heng, Guo, Lan, Fang, Fang, Chen, Doris, A Sosunov, Alexander, M McKhann, Guy, Yan, Yilin, Wang, Chunyu, Zhang, Hong, Molkentin, Jeffery D, Gunn-Moore, Frank J, Vonsattel, Jean Paul, Arancio, Ottavio, Chen, John Xi, Yan, Shi Du·2008·Nature Medicine

DOI 10.1038/nm.1868

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Abstract

Cyclophilin D (CypD, encoded by Ppif) is an integral part of the mitochondrial permeability transition pore, whose opening leads to cell death. Here we show that interaction of CypD with mitochondrial amyloid-β protein (Aβ) potentiates mitochondrial, neuronal and synaptic stress. The CypD-deficient cortical mitochondria are resistant to Aβ- and Ca2+-induced mitochondrial swelling and permeability transition. Additionally, they have an increased calcium buffering capacity and generate fewer mitochondrial reactive oxygen species. Furthermore, the absence of CypD protects neurons from Aβ- and oxidative stress–induced cell death. Notably, CypD deficiency substantially improves learning and memory and synaptic function in an Alzheimer's disease mouse model and alleviates Aβ-mediated reduction of long-term potentiation. Thus, the CypD-mediated mitochondrial permeability transition pore is directly linked to the cellular and synaptic perturbations observed in the pathogenesis of Alzheimer's disease. Blockade of CypD may be a therapeutic strategy in Alzheimer's disease.

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PINK1 Activation Attenuates Impaired Neuronal-Like Differentiation and Synaptogenesis and Mitochondrial Dysfunction in Alzheimer’s Disease Trans-Mitochondrial Cybrid Cells
Du, F., Yu, Q., & Yan, S. S. (2021) · Journal of Alzheimer's Disease · doi:10.3233/jad-210095 · Cited by 22
Self-citation
Identification and Characterization of Amyloid-β Accumulation in Synaptic Mitochondria
Yan, S. F., Akhter, F., Sosunov, A. A., & Yan, S. S. (2018) · Methods in Molecular Biology · doi:10.1007/978-1-4939-7816-8_25 · Cited by 15
Self-citation
The Role of Caspases in Alzheimer’s Disease: Pathophysiology Implications and Pharmacologic Modulation
Khezri, M. R., & Ghasemnejad-Berenji, M. (2023) · Journal of Alzheimer s Disease · doi:10.3233/jad-220873 · Cited by 12
Beta-amyloid oligomers: recent developments
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Authors: Du, H., Guo, L., Fang, F., Chen, D., A Sosunov, A., M McKhann, G., Yan, Y., Wang, C., Zhang, H., Molkentin, J. D., Gunn-Moore, F. J., Vonsattel, J. P., Arancio, O., Chen, J. X., & Yan, S. D.
Venue: Nature Medicine
Publisher: Springer Science and Business Media LLC
Published: 2008-09-21
Volume: 14
Issue: 10
Pages: 1097-1105
ISSN: 1078-8956 (ISSN-L)
1546-170X
DOI: 10.1038/nm.1868
OpenAlex: W1968257316
Cited by: 932
References: 15
FWCI: 36.59
Type: journal article
Language: en
Open access: green

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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.

Cyclophilin D deficiency attenuates mitochondrial and neuronal perturbation and ameliorates learning and memory in Alzheimer's disease

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