DR. AMANDINE GRIMM
News
22.08.2024
Our new study on the effects of Gelsemium on mitochondrial function in neuronal cells has been published. This is the result of a fruitful collaboration with the "Laboratoire Boiron, France".
24.07.2024
Check out our latest publication on an in vitro neuronal aging model that reflects the mitochondrial aging signature. Congratulations Nimmy for this nice work !!
03.07.2024
I am delighted to share with you our latest review on TSPO and Alzheimer's disease in collaboration with Lauren Fairley and Anna Barron.
Lauren, you did a really great job! Congratulations!
05.2024
Our project about mitochondrial transplantation has been highlighted in the newletter of the Synapsis Foundation, Dementia Research Switzerland.
Many thanks for their support in funding our research.
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 !
13.11.2023
A glimpse of the Neurobiology Laboratory (Research Cluster, Molecular and Cognitive Neurosciences (MCN)) in the video presentation of the University Psychiatric Clinics (Universitäre Psychiatrische Kliniken (UPK)) in Basel.
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"