summary: New research reveals a critical role for the protein contactin 4 (CNTN4) in neuronal development, with implications for both neurodevelopmental disorders and Alzheimer’s disease. Researchers found that CNTN4, which is associated with autism, interacts with the Alzheimer’s-related protein APP and affects the growth of neurons in the brain cortex.
This finding highlights the codependent relationships that are essential for healthy brain development. This finding provides new insights into the overlap between developmental and neurodegenerative diseases.
Important facts:
- major protein: CNTN4 is essential for neuron development and is associated with autism and Alzheimer’s disease.
- protein interactions:The interaction of CNTN4 and APP is essential for healthy brain function.
- neuron impact: Knocking out CNTN4 alters the growth of neurons in the brain cortex.
sauce: University of Exeter
New research reveals complex interactions between cellular proteins and how they affect neurons in neurodevelopmental disorders and Alzheimer’s disease.
New research led by the University of Exeter Royal Society Open Biology found that the protein contactin 4 (encoded by the gene CNTN4) plays an important role in neuron formation.
Researchers began studying CNTN4 because it was known to be involved in autism, but its functional role was not fully understood. The research team investigated how CNTN4 functions in the brain, particularly its interactions with proteins involved in neurodegenerative diseases such as Alzheimer’s disease.
For the first time, researchers studied mice in which the CNTN4 gene was knocked out in the cortex, a region of the brain responsible for important functions such as memory, thinking, and reasoning. They found that neurons develop differently in cortical areas.
Researchers have demonstrated for the first time in human cells an interaction between the gene CNTN4 and the gene APP, which is strongly associated with Alzheimer’s disease, revealing a codependent relationship essential for healthy brain development, particularly the growth of neurons.
They found that CNTN4 not only contributes to neural outgrowth in frontal cortical regions of the brain, but also that CNTN4 expression is regulated through its relationship with APP.
Using studies in genetically engineered human cells, the research team also discovered that a complex interaction exists between CNTN4 and APP. When CNTN4 is knocked out, APP levels decrease but do not go to zero. Scientists believe that APP may compensate for the loss of her CNTN4 and vice versa.
Lead author of the study, Dr Rosemary Bamford from the University of Exeter’s School of Medicine, said: “The discovery that CNTN4, a gene associated with developmental processes, also plays a role in regulating factors involved in Alzheimer’s disease is a huge breakthrough. “It was noteworthy.”
“This intersection of developmental and neurodegenerative pathways provides exciting new insights into the broader implications of these proteins.”
Lead author Dr. Asami Oguro Ando, from the University of Exeter’s School of Medicine, said: “Looking to the future, my group is keen to further dissect the molecular mechanisms underlying the interaction between CNTN4 and APP and investigate their broader impact on diseases such as Alzheimer’s and autism. is a spectrum disorder.
“Our next steps include determining how the CNTN4-APP interaction affects neural activity. Understanding this interaction will help improve neurodevelopmental disorders and This is extremely important as it is a fundamental step towards a comprehensive understanding of degenerative disorders.”
About this autism and Alzheimer’s disease research news
author: Louise Vennels
sauce: University of Exeter
contact: Louise Vennels – University of Exeter
image: Image credited to Neuroscience News
Original research: Open access.
“CNTN4 regulates nerve outgrowth through interaction with APPWritten by Rosemary Bamford et al. Royal Society Open Biology
abstract
CNTN4 regulates nerve outgrowth through interaction with APP
Neural cell adhesion molecule contactin-4 (CNTN4) are genetically linked to autism spectrum disorder (ASD) and other psychiatric disorders.
Cntn4A CNTN4-deficient mouse model previously showed that CNTN4 plays an important role in hippocampal axon guidance and synaptic plasticity.
However, the pathogenesis and functional role of CNTN4 in the cortex remains to be investigated.
In our study, we found that the cortical thickness of the motor cortex was reduced. Cntn4 −/− However, cortical cell migration and differentiation were not affected. Significant morphological changes were observed in neurons in the her M1 area of the motor cortex, indicating that CNTN4 is also involved in the morphology and spine density of neurons in the motor cortex.
Additionally, mass spectrometry analysis identified interaction partners of CNTN4 and confirmed the interaction of CNTN4 with amyloid precursor protein (APP). Human cells with CNTN4 and/or APP knocked out revealed a relationship between CNTN4 and APP.
This study demonstrates that CNTN4 contributes to cortical development and its binding and interaction with APP controls neuronal outgrowth. This is an important discovery in understanding the physiological function of APP, a key protein in Alzheimer’s disease.
The bond between CNTN4 and APP, which is involved in neurodevelopment, is essential for healthy neuronal outgrowth.
