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Grenoble Institut des Neurosciences Grenoble Institut des Neurosciences

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Impact of Amyloid beta oligomers (Abetao) on the cellular basis of learning and memory in an Amyloid Precursor Protein (APP) Knock-out mouse


We will determine whether synaptic alterations associated with Alzheimer disease are transferred to neighboring neurons and required the expression of neuronal APP. We will also check wether the amyloïdogenic processing of APP in neighboring neurons and a subsequent production of Abetao is necessary for the spreading of the synaptopathy that characterized AD.


We will perform in vivo viral infection with a lentivirus that express mutated APP(APPswe) tagged with the Green Fluorescent Protein in wild type and APP KO cortical neurons. Since the viral infection does not target all the neurons, our objective will be to find 2 neighboring neurons: one infected next to a non-infected neuron. We will study AMPA and NMDA synaptic transmission in non-infected neurons in order to identify modifications induced by the release of Abetao by the infected neurons. This approach will also allow us to evaluate the impact of an overproduction of Abetao in the dendritic spine density of surrounding neurons. In a next step, we will evaluate that the alteration of neurotransmission by secreted Abetao occurs through a processing of APP via the amyloïdogenic pathway. APPswe-GFP will be transfected in conjunction with either APP wild type-mCherry (APPwt) or APPmv-mCherry (APPmv) in APP KO cortical neurons. APPmv is mutated in the beta-secretase cleavage site leading to a decrease of amyloïdogenic processing of APP. We will study NMDA and AMPA synaptic transmission and dendritic spine density in APPwt and APPmv neurons.


We will perform in vivo viral infection in the somatosensory cortex of wild type and APP KO neurons. We will then prepare somatosensory cortex slices and patch-clamp experiments will allow us to record AMPA and NMDA dependent synaptic transmission. Dendritic spines density will be evaluated by confocal microscopy.


  • ML.Frandemiche, S.De Seranno, T.Rush, E.Borel, A.Elie, I.Arnal, F.Lanté, A.Buisson. 2014. Activity-dependent tau protein translocation to excitatory synapse is disrupted by exposure to amyloid-beta oligomers. Journal of Neuroscience 34:6084-97
  • Bosson A, Paumier A, Boisseau S, Jacquier-Sarlin M, Buisson A, Albrieux M. 2017. TRPA1 channels promote astrocytic Ca2+ hyperactivity and synaptic dysfunction mediated by oligomeric forms of amyloid-beta peptide. Mol Neurodegener.12:53

Domaines d'expertise requis

Alzheimer disease, electrophysiology, APP KO mice, glutamatergic synaptic transmission, somatosensory cortex


Fabien Lanté, Maître de Conférences UGA
Email :

Mise à jour le 31 mai 2018


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