M. Albert Basson

This study shows that inhibiting LSD1, a histone demethylase, restores learning and memory in aged mice by reversing age-related defects in H3K4me3 dynamics and synaptic plasticity.

This paper uses mass spectrometry to identify age- and activity-dependent changes in histone post-translational modifications in mouse hippocampi, proposing a framework for integrating these findings into ageing research.

The paper identifies hypo- and hyperconnectivity subtypes in autism using cross-species fMRI, linking them to distinct biological mechanisms in mice and humans.

The paper identifies molecular pathways associated with neurodevelopmental disorder subgroups using neuroimaging data from mice and humans.

The paper identifies long-range gene regulatory interactions in cerebellar granule neuron progenitors using pcHi-C, ATAC-seq, and ChIP-seq, revealing co-regulation by Atoh1 and CHD7.

This study shows that KDM5B deficiency in mice leads to autism-like behaviors and increased brain size, which can be mitigated by NMDAR antagonists.

This study shows that CHD8 suppression reduces H3K36me3 levels and alters alternative splicing of ~2000 genes, linking CHD8 to RNA processing and ASD.

This study identifies a recessive PRDM13 mutation causing congenital hypogonadotropic hypogonadism and cerebellar hypoplasia through mouse models and human expression analysis.

This study shows that CHD7 protects auditory neurons and hair cells from stress-induced degeneration, with implications for CHARGE syndrome.

This study examines synaptic imbalances and homeostatic plasticity disruption in ASD-associated Chd8 haploinsufficient mice, revealing altered excitatory and inhibitory transmission in cortical circuits.

The paper maps spatiotemporal dynamics of resting-state fMRI activity in mice, revealing recurring brain states with oscillatory dynamics and altered states in autism-associated genetic alterations.

This study investigates the effects of CHD8 mutations on brain development in mice, finding non-linear gene expression and growth changes depending on mutation severity.

This study examines Chd8 haploinsufficient mice, finding brain overgrowth, altered gene expression, and functional connectivity changes linked to autism-like features.