DR. AMANDINE GRIMM
News
09.12.2024
I'm very proud to announce that our new review article, "Mitochondrial Transplantation in Brain Disorders: Achievements, Methods, and Challenges,” has been published in Neuroscience & Biobehavioral Reviews.
The review highlights promising preclinical studies where mitochondrial transplantation has been shown to restore mitochondrial function, reduce inflammation, and improve cognitive and motor functions in several animal models of brain disorders.
It also addresses significant challenges that must be overcome before this therapy can be clinically applied. Current efforts to overcome these challenges, including advancements in isolation techniques, cryopreservation methods, finding an appropriate mitochondria source, and potential delivery routes, are discussed.
This is the first article of my PhD students, Aurélien Riou and Aline Broeglin. I congratulate them on their excellent work!!
26.01.2024
Check out our latest publication in the journal Biochimie !
We provide evidence that the TSPO-specific ligands Ro5-4864 and XBD173 attenuate mitophagy deficits and mitochondrial fragmentation in a cellular model of Alzheimer's disease overexpressing the human amyloid precursor protein.
Many thanks to Lauren for all her hard work!
24.01.2024
Delighted to share the latest publication in collaboration with Eline Pecho-Vrieseling's group on the propagation of mutant huntingtin across the human neuromuscular synapse. Many thanks to Eline and Marga for taking us on board in this wonderful project !
04.07.2023
It is my greatest pleasure to announce that our manuscript titled "ER‐mitochondria contacts and cholesterol metabolism are disrupted by disease‐associated tau protein" is now published in EMBO Reports.
I would like to warmly thank all the co-authors and collaborators that made this fascinating study possible.
In this study, we show that abnormal tau protein disrupts ER—mitochondria contacts, impairing cholesterol metabolism and pregnenolone synthesis within mitochondria. Our key findings are that:
- Contact points between the endoplasmic reticulum (ER) and mitochondria are decreased in the presence of P301L mutant tau protein.
- P301Ltau disturbs cholesterol metabolism and its conversion to pregnenolone within mitochondria.
- P301Ltau expression and tau knockout show opposite effects on ER-mitochondria association and cholesterol metabolism.
- The P301Ltau-induced disruption of ER-mitochondria contacts and cholesterol homeostasis is restored by GSK3β inhibition.
For more details, see:
ER-mitochondria contacts and cholesterol metabolism are disrupted by disease-associated tau protein
13.05.2023
Thrilled to share our latest publication about the impat of tau mutations on mitochondria published in Cells MDPI. In this study, we show that triple tau-mutant induced pluripotent stem cells, bearing the pathogenic N279K, P301L, and E10+16 mutations, exhibit deficits in mitochondrial bioenergetics and present altered parameters linked to the metabolic regulation of mitochondria.
For more details, see:
10.03.2023
I am happy to share our latest publication about the effects of spermidine on tau-induced mitochondrial dysfunction. In this article published in the International Journal of Molecular Science (MDPI), we showed that a treatment with spermidine improves mitochondrial bioenergetics and restores tau-induced impairments in mitophagy in a cellular model of tauopathy.
For more details, see:
"Spermidine Rescues Bioenergetic and Mitophagy Deficits Induced by Disease-Associated Tau Protein"