Einblick - Neuroscience - # Neural Development and CNTN4-APP Interaction

CNTN4 Modulates Neural Elongation Through Interaction with APP

Q: How does the interaction between CNTN4 and APP impact synaptic plasticity?

The interaction between CNTN4 and APP plays a crucial role in synaptic plasticity. CNTN4 is known to be involved in neurite outgrowth, spine formation, and synapse stability. When CNTN4 interacts with APP, it contributes to the regulation of dendritic spine density and morphology. This interaction helps in maintaining the balance of excitatory and inhibitory inputs at the synapse, which is essential for proper synaptic function. Studies have shown that loss of either CNTN4 or APP can lead to abnormalities in spine density, maturation, and neuronal connectivity. The binding between these two proteins influences the development of dendritic spines by modulating their growth patterns and shapes. Additionally, this interaction may affect neurotransmitter release and receptor localization at the synapse, further impacting synaptic transmission.

Q: What implications do these findings have for understanding neurodevelopmental disorders beyond ASD?

These findings provide valuable insights into neurodevelopmental disorders beyond Autism Spectrum Disorder (ASD). The role of CNTN4-APP interaction in regulating neuronal morphology, migration, and connectivity suggests its involvement in various neurodevelopmental processes. Abnormalities in this pathway could contribute to a range of neurological conditions characterized by altered brain structure or function. Understanding how disruptions in the CNTN4-APP pathway impact synaptic plasticity can shed light on the underlying mechanisms of other neurodevelopmental disorders such as intellectual disabilities, schizophrenia, ADHD (Attention Deficit Hyperactivity Disorder), bipolar disorder etc. Targeting this pathway could potentially offer new therapeutic strategies for treating a broader spectrum of neurological conditions associated with abnormal brain development.

Q: How might targeting the CNTN4-APP interaction offer therapeutic benefits for conditions like Alzheimer's disease?

Targeting the interaction between CNTN4 and APP holds promise for therapeutic interventions in Alzheimer's disease (AD). In AD pathology, aberrant processing of APP leads to an accumulation of amyloid-beta plaques which are toxic to neurons. By modulating or stabilizing the interactions between these proteins through pharmacological agents or gene therapies: Reduced Amyloid-Beta Production: Modulation of this interaction could potentially reduce amyloid-beta production by altering cleavage pathways leading to less plaque formation. Enhanced Synaptic Function: Stabilizing this protein-protein interaction may improve synaptic function by promoting proper neurite outgrowth and spine formation. Neuroprotection: By preserving normal neuronal morphology through targeted intervention on this pathway could protect against degeneration seen in AD. Overall, targeting the CNTN4-APP interplay offers a novel approach towards developing treatments that address not only symptom management but also potential disease-modifying effects on Alzheimer's disease progression within neural networks affected by pathological changes related to AD pathogenesis.

Kernkonzepte

CNTN4 contributes to cortical development and controls neural elongation through its interaction with APP.

Zusammenfassung

The study investigates the role of CNTN4 in the cortex, revealing reduced cortical thickness in Cntn4-/- mice. Neuronal morphology changes were observed in the motor cortex, indicating CNTN4's involvement in neuron structure. The interaction between CNTN4 and APP was identified, showing their relationship in controlling neural elongation. Knockout human cells confirmed the importance of this interaction for cell morphology and neurite outgrowth. These findings enhance our understanding of Alzheimer's disease, ASD, and neurodevelopment mechanisms.

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Statistiken

Reduced cortical thickness observed in the motor cortex of Cntn4-/- mice.
Significant morphological changes in neurons in the M1 region.
Interaction between CNTN4 and APP controls neural elongation.

Zitate

"The study demonstrates that CNTN4 contributes to cortical development."
"CNTN4 is involved in neuronal morphology and spine density."
"The interaction between CNTN4 and APP controls neural elongation."

Wichtige Erkenntnisse aus

CNTN4 modulates neural elongation through interplay with APP

by Bamford,R. A... um www.biorxiv.org 08-28-2023

https://www.biorxiv.org/content/10.1101/2023.08.25.554833v2

Tiefere Fragen

How does the interaction between CNTN4 and APP impact synaptic plasticity?

The interaction between CNTN4 and APP plays a crucial role in synaptic plasticity. CNTN4 is known to be involved in neurite outgrowth, spine formation, and synapse stability. When CNTN4 interacts with APP, it contributes to the regulation of dendritic spine density and morphology. This interaction helps in maintaining the balance of excitatory and inhibitory inputs at the synapse, which is essential for proper synaptic function.
Studies have shown that loss of either CNTN4 or APP can lead to abnormalities in spine density, maturation, and neuronal connectivity. The binding between these two proteins influences the development of dendritic spines by modulating their growth patterns and shapes. Additionally, this interaction may affect neurotransmitter release and receptor localization at the synapse, further impacting synaptic transmission.

What implications do these findings have for understanding neurodevelopmental disorders beyond ASD?

These findings provide valuable insights into neurodevelopmental disorders beyond Autism Spectrum Disorder (ASD). The role of CNTN4-APP interaction in regulating neuronal morphology, migration, and connectivity suggests its involvement in various neurodevelopmental processes. Abnormalities in this pathway could contribute to a range of neurological conditions characterized by altered brain structure or function.
Understanding how disruptions in the CNTN4-APP pathway impact synaptic plasticity can shed light on the underlying mechanisms of other neurodevelopmental disorders such as intellectual disabilities, schizophrenia, ADHD (Attention Deficit Hyperactivity Disorder), bipolar disorder etc. Targeting this pathway could potentially offer new therapeutic strategies for treating a broader spectrum of neurological conditions associated with abnormal brain development.

How might targeting the CNTN4-APP interaction offer therapeutic benefits for conditions like Alzheimer's disease?

Targeting the interaction between CNTN4 and APP holds promise for therapeutic interventions in Alzheimer's disease (AD). In AD pathology, aberrant processing of APP leads to an accumulation of amyloid-beta plaques which are toxic to neurons. By modulating or stabilizing the interactions between these proteins through pharmacological agents or gene therapies:

Reduced Amyloid-Beta Production: Modulation of this interaction could potentially reduce amyloid-beta production by altering cleavage pathways leading to less plaque formation.

Enhanced Synaptic Function: Stabilizing this protein-protein interaction may improve synaptic function by promoting proper neurite outgrowth and spine formation.

Neuroprotection: By preserving normal neuronal morphology through targeted intervention on this pathway could protect against degeneration seen in AD.

Overall, targeting the CNTN4-APP interplay offers a novel approach towards developing treatments that address not only symptom management but also potential disease-modifying effects on Alzheimer's disease progression within neural networks affected by pathological changes related to AD pathogenesis.