Protein interacting with C-kinase 1 (PICK1) regulates synaptic function and reversal learning in a mouse model for schizophrenia

Neuropsychopharmacology, Год журнала: 2025, Номер unknown

Опубликована: Фев. 22, 2025

Язык: Английский

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The “don’t eat me” signal CD47 is associated with microglial phagocytosis defects and autism-like behaviors in 16p11.2 deletion mice

Proceedings of the National Academy of Sciences, Год журнала: 2025, Номер 122(16)

Опубликована: Апрель 16, 2025

Various pathological characteristics of autism spectrum disorder (ASD) stem from abnormalities in brain resident immune cells, specifically microglia, to prune unnecessary synapses or neural connections during early development. Animal models ASD exhibit an abundance different regions, which is strongly linked the appearance behaviors. Overexpression CD47 on neurons acts as a “don’t eat me” signal, safeguarding inappropriate pruning by microglia. Indeed, overexpression occurs 16p11.2 deletion carriers, causing decreased synaptic phagocytosis and manifestation characteristics. However, role impairment leading phenotypes mouse model unclear. Moreover, whether blocking can alleviate mice’s behavioral deficits remains unknown. Here, we demonstrate strong link between increased expression, microglia capacity, social novelty preference mice. The reduction caused rise excitatory transmission prefrontal cortex Importantly, using specific antibody reducing expression short hairpin RNA (shRNA) enhanced reduced transmission. Reduction improved These findings that associated with mice could be promising target for development treatment ASD.

Язык: Английский

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The “don’t eat me” signal CD47 contributes to microglial phagocytosis defects and autism-like behaviors in 16p11.2 deletion mice

bioRxiv (Cold Spring Harbor Laboratory), Год журнала: 2024, Номер unknown

Опубликована: Июнь 8, 2024

Abstract Various pathological characteristics of autism spectrum disorder (ASD) stem from abnormalities in brain resident immune cells, specifically microglia, to prune unnecessary synapses or neural connections during early development. Animal models ASD exhibit an abundance different regions, which is strongly linked the appearance behaviors. Overexpression CD47 on neurons acts as a “don’t eat me” signal, safeguarding inappropriate pruning by microglia. Indeed, overexpression occurs 16p11.2 deletion carriers, causing decreased synaptic phagocytosis and manifestation characteristics. However, role impairment leading phenotypes mouse model unclear. Moreover, whether blocking can alleviate mice’s behavioral deficits remains unknown. Here, we demonstrate strong link between increased expression, microglia capacity, social novelty preference mice. The reduction caused rise excitatory transmission prefrontal cortex Importantly, using specific antibody reducing expression shRNA enhanced reduced transmission. Reduction improved These findings that contributes mice could be promising target for development treatment ASD. Significance Statement Autism neurological developmental condition characterized stereotyped behaviors cognitive deficits. therapeutic options remain limited. Activation classical complement system, innate signaling pathway component, supports microglia-mediated disease. In particular, CD47, protects clearance. investigated microglial model, demonstrating enhances phagocytose cortex. This enhancement leads function provide mechanistic insights into laying groundwork developing more effective treatments

Язык: Английский

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Resveratrol prevents offspring's behavioral impairment associated with immunogenic stress during pregnancy

Progress in Neuro-Psychopharmacology and Biological Psychiatry, Год журнала: 2024, Номер 136, С. 111188 - 111188

Опубликована: Ноя. 8, 2024

Язык: Английский

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