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Biology subjects

Quesnel, K. M.

Publications and source records attributed to Quesnel, K. M..

2 recordsLinked to original sources

Assigning Targetable Molecular Pathways to Transdiagnostic Subgroups Across Autism and Related Neurodevelopmental Disorders

The heterogeneity of autism and related neurodevelopmental conditions has impeded accurate prognoses and treatment discovery. Using translational neuroimaging across 135 mouse models (3,515 mice) and two human MRI datasets (n = 1,234 and n = 1,015), we derived participant subgroups from shared neuroanatomical features. These subgroups did not distinguish autism, ADHD, or OCD diagnoses and only modestly differentiated cognitive and behavioural phenotypes. Instead, they mapped onto four molecular pathways: (1) synaptic function; (2) MAPK and Wnt signalling; (3) chromatin modification and cellular stress responses; and (4) broader chromatin, immune, and second-messenger signalling pathways. This framework bridges preclinical models and idiopathic human neurodevelopmental conditions, linking patients to biologically relevant molecular mechanisms.

neuroscience↗

A mouse model of ATRX deficiency with cognitive deficits and autistic traits

ATRX is an ATP-dependent chromatin remodeling protein with essential roles in safeguarding genome integrity and modulating gene expression. Deficiencies in this protein cause ATR-X syndrome, a condition characterized by intellectual disability and an array of developmental abnormalities, including features of autism. Previous studies demonstrated that deleting ATRX in mouse forebrain excitatory neurons postnatally resulted in male-specific memory deficits. Here, we introduce a new model where ATRX is deleted at earlier embryonic stages, resulting in a broader spectrum of impairments, including contextual fear memory deficits, decreased anxiety, hyperactivity, as well as self-injurious and stereotyped behaviours. Sex-specific alterations were also observed, with males displaying heightened aggression and impaired sensory gating, while females exhibit social avoidance. Collectively, the findings indicate that early developmental abnormalities arising from ATRX deficiency in neurons contribute to of the presentation of autistic-like behaviours. Summary StatementMice with embryonic loss of ATRX in excitatory neurons represent a clinically relevant model to study sexually dimorphic alterations in cognitive and autistic traits.

animal behavior and cognition↗