Mutations in transcription Factor 4 (TCF4) gene have been associated with several neuropsychiatric disorders, however, their effect on the human neuronal function is poorly understood.

Patient-derived organoids empower the patient-centric approach to research, with a precise dissection of molecular and cellular pathways that underly human-specific neuropsychiatric disorders.
Human brain organoids derived from children with Pitt-Hopkins Syndrome, carrying clinically relevant mutations in TCF4 gene, faithfully recapitulate the patients' neural phenotype (aberrant morphology, severly impaired electrical activity).

Transcriptomics and gene set enrichment analysis show that TCF4 loss-of-function leads to downregulation in the expression of Wnt signaling pathway, resulting in reduced proliferation of neural progenitor cells and increased cellular senescence.

Brain organoids represent a robust, rapid, and cost-effective tool for patient-specific drug screening.
Reduced cortical neuron content and impaired electrical activity in patient-derived organoids were rescued after correction of TCF4 expression by virus-mediated over-expression of TCF4 gene and by pharmacological modulation of Wnt signaling.

Mutations in transcription Factor 4 (TCF4) gene have been associated with several neuropsychiatric disorders, however, their effect on the human neuronal function is poorly understood.

Patient-derived organoids empower the patient-centric approach to research, with a precise dissection of molecular and cellular pathways that underly human-specific neuropsychiatric disorders.
Human brain organoids derived from children with Pitt-Hopkins Syndrome, carrying clinically relevant mutations in TCF4 gene, faithfully recapitulate the patients' neural phenotype (aberrant morphology, severly impaired electrical activity).

Transcriptomics and gene set enrichment analysis show that TCF4 loss-of-function leads to downregulation in the expression of Wnt signaling pathway, resulting in reduced proliferation of neural progenitor cells and increased cellular senescence.

Brain organoids represent a robust, rapid, and cost-effective tool for patient-specific drug screening.
Reduced cortical neuron content and impaired electrical activity in patient-derived organoids were rescued after correction of TCF4 expression by virus-mediated over-expression of TCF4 gene and by pharmacological modulation of Wnt signaling.

Mutations in transcription Factor 4 (TCF4) gene have been associated with several neuropsychiatric disorders, however, their effect on the human neuronal function is poorly understood.

Patient-derived organoids empower the patient-centric approach to research, with a precise dissection of molecular and cellular pathways that underly human-specific neuropsychiatric disorders.
Human brain organoids derived from children with Pitt-Hopkins Syndrome, carrying clinically relevant mutations in TCF4 gene, faithfully recapitulate the patients' neural phenotype (aberrant morphology, severly impaired electrical activity).

Transcriptomics and gene set enrichment analysis show that TCF4 loss-of-function leads to downregulation in the expression of Wnt signaling pathway, resulting in reduced proliferation of neural progenitor cells and increased cellular senescence.

Brain organoids represent a robust, rapid, and cost-effective tool for patient-specific drug screening.
Reduced cortical neuron content and impaired electrical activity in patient-derived organoids were rescued after correction of TCF4 expression by virus-mediated over-expression of TCF4 gene and by pharmacological modulation of Wnt signaling.

Mutations in transcription Factor 4 (TCF4) gene have been associated with several neuropsychiatric disorders, however, their effect on the human neuronal function is poorly understood.

Patient-derived organoids empower the patient-centric approach to research, with a precise dissection of molecular and cellular pathways that underly human-specific neuropsychiatric disorders.
Human brain organoids derived from children with Pitt-Hopkins Syndrome, carrying clinically relevant mutations in TCF4 gene, faithfully recapitulate the patients' neural phenotype (aberrant morphology, severly impaired electrical activity).

Transcriptomics and gene set enrichment analysis show that TCF4 loss-of-function leads to downregulation in the expression of Wnt signaling pathway, resulting in reduced proliferation of neural progenitor cells and increased cellular senescence.

Brain organoids represent a robust, rapid, and cost-effective tool for patient-specific drug screening.
Reduced cortical neuron content and impaired electrical activity in patient-derived organoids were rescued after correction of TCF4 expression by virus-mediated over-expression of TCF4 gene and by pharmacological modulation of Wnt signaling.

Mutations in transcription Factor 4 (TCF4) gene have been associated with several neuropsychiatric disorders, however, their effect on the human neuronal function is poorly understood.

Patient-derived organoids empower the patient-centric approach to research, with a precise dissection of molecular and cellular pathways that underly human-specific neuropsychiatric disorders.
Human brain organoids derived from children with Pitt-Hopkins Syndrome, carrying clinically relevant mutations in TCF4 gene, faithfully recapitulate the patients' neural phenotype (aberrant morphology, severly impaired electrical activity).

Transcriptomics and gene set enrichment analysis show that TCF4 loss-of-function leads to downregulation in the expression of Wnt signaling pathway, resulting in reduced proliferation of neural progenitor cells and increased cellular senescence.

Brain organoids represent a robust, rapid, and cost-effective tool for patient-specific drug screening.
Reduced cortical neuron content and impaired electrical activity in patient-derived organoids were rescued after correction of TCF4 expression by virus-mediated over-expression of TCF4 gene and by pharmacological modulation of Wnt signaling.

Mutations in transcription Factor 4 (TCF4) gene have been associated with several neuropsychiatric disorders, however, their effect on the human neuronal function is poorly understood.

Patient-derived organoids empower the patient-centric approach to research, with a precise dissection of molecular and cellular pathways that underly human-specific neuropsychiatric disorders.
Human brain organoids derived from children with Pitt-Hopkins Syndrome, carrying clinically relevant mutations in TCF4 gene, faithfully recapitulate the patients' neural phenotype (aberrant morphology, severly impaired electrical activity).

Transcriptomics and gene set enrichment analysis show that TCF4 loss-of-function leads to downregulation in the expression of Wnt signaling pathway, resulting in reduced proliferation of neural progenitor cells and increased cellular senescence.

Brain organoids represent a robust, rapid, and cost-effective tool for patient-specific drug screening.
Reduced cortical neuron content and impaired electrical activity in patient-derived organoids were rescued after correction of TCF4 expression by virus-mediated over-expression of TCF4 gene and by pharmacological modulation of Wnt signaling.

Mutations in transcription Factor 4 (TCF4) gene have been associated with several neuropsychiatric disorders, however, their effect on the human neuronal function is poorly understood.

Patient-derived organoids empower the patient-centric approach to research, with a precise dissection of molecular and cellular pathways that underly human-specific neuropsychiatric disorders.
Human brain organoids derived from children with Pitt-Hopkins Syndrome, carrying clinically relevant mutations in TCF4 gene, faithfully recapitulate the patients' neural phenotype (aberrant morphology, severly impaired electrical activity).

Transcriptomics and gene set enrichment analysis show that TCF4 loss-of-function leads to downregulation in the expression of Wnt signaling pathway, resulting in reduced proliferation of neural progenitor cells and increased cellular senescence.

Brain organoids represent a robust, rapid, and cost-effective tool for patient-specific drug screening.
Reduced cortical neuron content and impaired electrical activity in patient-derived organoids were rescued after correction of TCF4 expression by virus-mediated over-expression of TCF4 gene and by pharmacological modulation of Wnt signaling.

Mutations in transcription Factor 4 (TCF4) gene have been associated with several neuropsychiatric disorders, however, their effect on the human neuronal function is poorly understood.

Patient-derived organoids empower the patient-centric approach to research, with a precise dissection of molecular and cellular pathways that underly human-specific neuropsychiatric disorders.
Human brain organoids derived from children with Pitt-Hopkins Syndrome, carrying clinically relevant mutations in TCF4 gene, faithfully recapitulate the patients' neural phenotype (aberrant morphology, severly impaired electrical activity).

Transcriptomics and gene set enrichment analysis show that TCF4 loss-of-function leads to downregulation in the expression of Wnt signaling pathway, resulting in reduced proliferation of neural progenitor cells and increased cellular senescence.

Brain organoids represent a robust, rapid, and cost-effective tool for patient-specific drug screening.
Reduced cortical neuron content and impaired electrical activity in patient-derived organoids were rescued after correction of TCF4 expression by virus-mediated over-expression of TCF4 gene and by pharmacological modulation of Wnt signaling.

Mutations in transcription Factor 4 (TCF4) gene have been associated with several neuropsychiatric disorders, however, their effect on the human neuronal function is poorly understood.

Patient-derived organoids empower the patient-centric approach to research, with a precise dissection of molecular and cellular pathways that underly human-specific neuropsychiatric disorders.
Human brain organoids derived from children with Pitt-Hopkins Syndrome, carrying clinically relevant mutations in TCF4 gene, faithfully recapitulate the patients' neural phenotype (aberrant morphology, severly impaired electrical activity).

Transcriptomics and gene set enrichment analysis show that TCF4 loss-of-function leads to downregulation in the expression of Wnt signaling pathway, resulting in reduced proliferation of neural progenitor cells and increased cellular senescence.

Brain organoids represent a robust, rapid, and cost-effective tool for patient-specific drug screening.
Reduced cortical neuron content and impaired electrical activity in patient-derived organoids were rescued after correction of TCF4 expression by virus-mediated over-expression of TCF4 gene and by pharmacological modulation of Wnt signaling.

Mutations in transcription Factor 4 (TCF4) gene have been associated with several neuropsychiatric disorders, however, their effect on the human neuronal function is poorly understood.

Patient-derived organoids empower the patient-centric approach to research, with a precise dissection of molecular and cellular pathways that underly human-specific neuropsychiatric disorders.
Human brain organoids derived from children with Pitt-Hopkins Syndrome, carrying clinically relevant mutations in TCF4 gene, faithfully recapitulate the patients' neural phenotype (aberrant morphology, severly impaired electrical activity).

Transcriptomics and gene set enrichment analysis show that TCF4 loss-of-function leads to downregulation in the expression of Wnt signaling pathway, resulting in reduced proliferation of neural progenitor cells and increased cellular senescence.

Brain organoids represent a robust, rapid, and cost-effective tool for patient-specific drug screening.
Reduced cortical neuron content and impaired electrical activity in patient-derived organoids were rescued after correction of TCF4 expression by virus-mediated over-expression of TCF4 gene and by pharmacological modulation of Wnt signaling.