Raphaelle Piquard-Pardossi

Valbonne, 06560, France

Last Updated: 09/26/2026

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Found 18 publications

Suppression of MT5-MMP Reveals Early Modulation of Alzheimer's Pathogenic Events in Primary Neuronal Cultures of 5xFAD Mice.

Suppression of MT5-MMP Reveals Early Modulation of Alzheimer's Pathogenic Events in Primary Neuronal Cultures of 5xFAD Mice.

Journal: Biomolecules

Published: October 30, 2024

Ectodomain shedding of PLA2R1 is mediated by the metalloproteases ADAM10 and ADAM17.

Ectodomain shedding of PLA2R1 is mediated by the metalloproteases ADAM10 and ADAM17.

Journal: The Journal of biological chemistry

Published: December 03, 2023

The amyloid precursor protein and its derived fragments concomitantly contribute to the alterations of mitochondrial transport machinery in Alzheimer's disease.

The amyloid precursor protein and its derived fragments concomitantly contribute to the alterations of mitochondrial transport machinery in Alzheimer's disease.

Journal: Cell death & disease

Published: August 04, 2023

Correction to: Intraneuronal aggregation of the β‑CTF fragment of APP (C99) induces Aβ‑independent lysosomal-autophagic pathology.

Correction to: Intraneuronal aggregation of the β‑CTF fragment of APP (C99) induces Aβ‑independent lysosomal-autophagic pathology.

Journal: Acta neuropathologica

Published: August 04, 2023

The η-secretase-derived APP fragment ηCTF is localized in Golgi, endosomes and extracellular vesicles and contributes to Aβ production.

The η-secretase-derived APP fragment ηCTF is localized in Golgi, endosomes and extracellular vesicles and contributes to Aβ production.

Journal: Cellular and molecular life sciences : CMLS

Published: November 18, 2022

Is γ-secretase a beneficial inactivating enzyme of the toxic APP C-terminal fragment C99?

Is γ-secretase a beneficial inactivating enzyme of the toxic APP C-terminal fragment C99?

Journal: The Journal of biological chemistry

Published: October 09, 2020

Accumulation of amyloid precursor protein C-terminal fragments triggers mitochondrial structure, function, and mitophagy defects in Alzheimer's disease models and human brains.

Accumulation of amyloid precursor protein C-terminal fragments triggers mitochondrial structure, function, and mitophagy defects in Alzheimer's disease models and human brains.

Journal: Acta neuropathologica

Published: June 09, 2020

The Transcription Factor EB Reduces the Intraneuronal Accumulation of the Beta-Secretase-Derived APP Fragment C99 in Cellular and Mouse Alzheimer’s Disease Models.

The Transcription Factor EB Reduces the Intraneuronal Accumulation of the Beta-Secretase-Derived APP Fragment C99 in Cellular and Mouse Alzheimer’s Disease Models.

Journal: Cells

Published: April 14, 2020

Targeting γ-secretase triggers the selective enrichment of oligomeric APP-CTFs in brain extracellular vesicles from Alzheimer cell and mouse models.

Targeting γ-secretase triggers the selective enrichment of oligomeric APP-CTFs in brain extracellular vesicles from Alzheimer cell and mouse models.

Journal: Translational neurodegeneration

Published: August 10, 2019

Palmitate Is Increased in the Cerebrospinal Fluid of Humans with Obesity and Induces Memory Impairment in Mice via Pro-inflammatory TNF-α.

Palmitate Is Increased in the Cerebrospinal Fluid of Humans with Obesity and Induces Memory Impairment in Mice via Pro-inflammatory TNF-α.

Journal: Cell reports

Published: November 04, 2018

Does Intraneuronal Accumulation of Carboxyl-terminal Fragments of the Amyloid Precursor Protein Trigger Early Neurotoxicity in Alzheimer's Disease?

Does Intraneuronal Accumulation of Carboxyl-terminal Fragments of the Amyloid Precursor Protein Trigger Early Neurotoxicity in Alzheimer's Disease?

Journal: Current Alzheimer research

Published: October 26, 2018

Intraneuronal accumulation of C99 contributes to synaptic alterations, apathy-like behavior, and spatial learning deficits in 3×TgAD and 2×TgAD mice.

Intraneuronal accumulation of C99 contributes to synaptic alterations, apathy-like behavior, and spatial learning deficits in 3×TgAD and 2×TgAD mice.

Journal: Neurobiology of aging

Published: February 02, 2018

Showing 1-12 of 18

Last Updated: 09/26/2026