Anouar Khayachi

The paper investigates how LRRK2 activity affects dopamine release in mice, showing age- and sex-dependent changes and rapid reversal with inhibition in certain groups.

This study identifies biomarkers in the neuronal secretome of bipolar disorder patients that correlate with disease state and lithium response, revealing their impact on neuronal network function.

This study uses a computational model of the dentate gyrus to show that lithium therapy improves pattern separation in bipolar disorder patients only by normalizing spontaneous activity, not by reducing cell excitability.

This study shows that VPS35(D620N) mutation leads to increased glutamate and dopamine transmission in mice, which can be reversed by LRRK2 inhibition.

This study shows lithium partially rescues transcriptomic and epigenomic changes in AKAP11 heterozygous knockout neurons, suggesting potential therapeutic relevance for bipolar disorder and schizophrenia.

This paper uses a computational model of the hippocampal CA3 to show that excitability variance in pyramidal cells impairs pattern completion in lithium nonresponsive bipolar disorder patients.

The paper constructs a single-cell eQTL atlas of the human cerebellum and identifies ET-associated variants linked to BACE2 downregulation in oligodendrocytes, suggesting demyelination and dysfunctional interactions.

The paper identifies molecular signatures of neuronal hyperexcitability and lithium responsiveness in bipolar disorder neurons, suggesting new therapeutic strategies targeting Akt and AMPK pathways.

This study investigates transcriptomic and epigenomic changes in human neurons with heterozygous AKAP11 loss-of-function mutations, revealing dysregulation of enhancers and gene networks linked to bipolar disorder and schizophrenia.

This study shows that genetic inactivation of USP19 reduces a-synuclein ubiquitination and Lewy body-like aggregate accumulation in a mouse model of Parkinson's disease.

This study identifies convergent transcriptomic targets of propranolol and primidone in essential tremor, highlighting potential biomarkers and molecular mechanisms for drug response.

This study shows chronic lithium treatment reduces neuronal excitability and shifts the excitatory/inhibitory balance toward inhibition in mouse cortical neurons.

This study investigates a missense Fmr1 mutation in mice, showing increased spine density, synaptic defects, and cognitive deficits linked to Fragile X syndrome.

This study identifies SUSD4 as a regulator of GLUA2 degradation and synaptic plasticity, showing its role in motor learning and implications for neurodevelopmental diseases.