Q Wang

University of California, San Diego

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Marie‐Christine Birling

Université de Strasbourg

Helin Atas-Özcan

Institut de génétique et de biologie moléculaire et cellulaire

Yann Hérault

Institut de génétique et de biologie moléculaire et cellulaire

Michel Simonneau

Inserm

Valérie Hindie

Hybrigenics (France)

Bernard Malissen

Aix-Marseille Université

Ida Chiara Guerrera

Inserm

Luisa Ciobanu

Université Paris-Saclay

B Zhang

Icahn School of Medicine at Mount Sinai

Yoshifumi Abe

Keio University

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Inserm

Centre National de la Recherche Scientifique

Université Paris-Saclay

Institut de Psychiatrie et Neurosciences de Paris

Université Paris Cité

University of California, San Diego

Université de Strasbourg

Institut de génétique et de biologie moléculaire et cellulaire

Icahn School of Medicine at Mount Sinai

Commissariat à l'Énergie Atomique et aux Énergies Alternatives

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BIN1 Genetic Risk Factor for Alzheimer is Sufficient to Induce Early Structural Tract Alterations in Entorhinal-Hippocampal Area and Memory-Related Hippocampal Multi-Scale Impairments

SSRN Electronic Journal (2021)

Rachel Daudin Damien Maréchal Roxane Golgolab Q Wang Yoshifumi Abe

Genetic factors are known to contribute to Late Onset Alzheimer’s disease (LOAD) but their contribution to pathophysiology, specially to prodomic phases accessible to therapeutic approaches are far to be understood. To translate genetic risk of Alzheimer's disease (AD) into mechanistic insight, we generated transgenic mouse lines that express a ~195 kbp human BAC that includes only BIN1, a gene associated to LOAD. This model gives a modest BIN1 overexpression, dependent of the number of BAC copies. At 6 months of age, we detected impaired entorhinal cortex (EC)-hippocampal pathways with specific impairments in EC-dentate gyrus synaptic long-term potentiation, dendritic spines of granular cells and recognition episodic memory. Structural changes were quantified using MRI. Their whole-brain functional impact were analyzed using resting state fMRI with a hypoconnectivity centered on entorhinal cortex. These early phenotype defects independent of any changes in A-beta can be instrumental in the search for new AD drug targets.

Entorhinal cortex

Memory Impairment

10.2139/ssrn.3816953

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Citations (1)

Impact of liver fibrosis on prognosis following liver resection for hepatitis B-associated hepatocellular carcinoma

British Journal of Cancer (2013)

Q Wang M. Isabel Fiel Sima Blank Wei Luan Hena Kadri

This study aims to evaluate the impact of liver fibrosis severity on prognosis following liver resection among HBV–HCC patients. Data were extracted from a prospective database of 189 HBV–HCC patients treated at Mount Sinai between 1995 and 2008. Fibrosis staging of each surgical resection specimen using the modified Ishak method was performed by a single liver pathologist. A wide range of Ishak fibrosis stage was observed among this patient population, with 29% having established cirrhosis (Ishak stage 6). Ishak stage 6 was independently associated with poor overall and recurrence-free survival. In patients with Ishak stage 1–5, Ishak stage did not affect survival; rather, tumour size was associated with poor overall survival, and tumour size, histologic activity index and serum AFP>20 ng ml−1 were associated with poor recurrence-free survival. In patients with Ishak stage 6, poorly differentiated histology and tumour size were associated with poor overall survival, and tumour size was associated with poor recurrence-free survival. HBV–HCC develops with varying degrees of underlying liver fibrosis; however, progressive liver fibrosis does not affect the outcomes following resection until cirrhosis is reached. Established cirrhosis, as defined histologically by Ishak stage 6, is an independent predictor of poor overall and recurrence-free survival among these patients.

Hepatitis B

Hepatitis C

10.1038/bjc.2013.352

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Citations (70)

Viral vector-mediated transgene delivery with novel recombinase systems for targeting neuronal populations defined by multiple features

Neuron (2023)

Minju Jeong Jun‐Hyeok Choi Hyeonseok Jang Dong Hyun Sohn Q Wang

A comprehensive understanding of neuronal diversity and connectivity is essential for understanding the anatomical and cellular mechanisms that underlie functional contributions. With the advent of single-cell analysis, growing information regarding molecular profiles leads to the identification of more heterogeneous cell types. Therefore, the need for additional orthogonal recombinase systems is increasingly apparent, as heterogeneous tissues can be further partitioned into increasing numbers of specific cell types defined by multiple features. Critically, new recombinase systems should work together with pre-existing systems without cross-reactivity in vivo. Here, we introduce novel site-specific recombinase systems based on ΦC31 bacteriophage recombinase for labeling multiple cell types simultaneously and a novel viral strategy for versatile and robust intersectional expression of any transgene. Together, our system will help researchers specifically target different cell types with multiple features in the same animal.

Cre recombinase

Cre-Lox recombination

Identification

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10.1016/j.neuron.2023.09.038

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BIN1 genetic risk factor for Alzheimer is sufficient to induce early structural tract alterations in entorhinal-hippocampal area and memory-related hippocampal multi-scale impairments

bioRxiv (Cold Spring Harbor Laboratory) (2018)

Rachel Daudin Damien Maréchal Roxane Golgolab Q Wang Yoshifumi Abe

Abstract Genetic factors are known to contribute to Late Onset Alzheimer’s disease (LOAD) but their contribution to pathophysiology, specially to prodomic phases accessible to therapeutic approaches are far to be understood. To translate genetic risk of Alzheimer’s disease (AD) into mechanistic insight, we generated transgenic mouse lines that express a ∼195 kbp human BAC that includes only BIN1 , a gene associated to LOAD. This model gives a modest BIN1 overexpression, dependent of the number of BAC copies. At 6 months of age, we detected impaired entorhinal cortex (EC)-hippocampal pathways with specific impairments in EC-dentate gyrus synaptic long-term potentiation, dendritic spines of granular cells and recognition episodic memory. Structural changes were quantified using MRI. Their whole-brain functional impact were analyzed using resting state fMRI with a hypoconnectivity centered on entorhinal cortex. These early phenotype defects independent of any changes in A-beta can be instrumental in the search for new AD drug targets.

Entorhinal cortex

10.1101/437228

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Citations (9)