In today’s western societies, a major socioeconomic concern is the increase in life expectancy and consequent dramatic rise in age related disorders, such as neurodegenerative and metabolic diseases. Although the pathogenesis of both diseases has been extensively studied, the available treatment options are still scarce, implying that additional mechanisms remain to be unraveled. Accumulating evidence suggests a strong correlation between metabolic dysfunction and neurodegeneration. Indeed, proper metabolic supply is essential to maintain a healthy brain function.
In this context, the current Research Topic aims at presenting novel evidence, supporting the link between metabolism and neurodegeneration. Ultimately it will focus on how metabolic manipulations could be used as a therapeutic tool for neurodegenerative diseases. Metabolic homeostasis requires the coordinated communication and interaction between organs, in response to metabolic cues. Interestingly, the enteric nervous system, which regulates the gastrointestinal tract independent of the central nervous system, is often called the body’s “second brain.”
Traditionally we learned that the bidirectional communication between the gastrointestinal tract and the central nervous system occurs through spinal afferents and the vagus nerve, with the contribution of several neuropeptides and hormones; new studies shed light into the emerging role of gut microbiota on neurological diseases, often associated with gut dysbiosis. In recent years, another means of wireless systemic communication captured our attention - extracellular vesicles (EVs), which are double phospholipid bilayer membrane vesicles released nearly by every cell in the body and transport specific cargo (proteins, DNA, microRNAs and lipids) along the blood circulation and trigger functional alteration in distant recipient cells. These vesicles became widely recognized as essential vehicles for communication, both in physiology and pathophysiology. Curiously, misfolded forms of proteins associated with Alzheimer's, Parkinson's, and prion diseases were found in EVs, suggesting an association with these diseases. Whether EVs are working as a spreading agent and/or a cleaning mechanism is still not clear.
The aim of this Research Topic is provide an overview of the gut-brain axis by addressing how brain and gut communicate, and its implications in health and disease, with a special focus on the role of extracellular vesicles in neurodegenerative diseases, within the scope of metabolic dysfunction. We welcome reviews addressing the following subjects:
• Evidences linking metabolism and neurodegeneration.
• Impact of aging on metabolism and neurodegeneration.
• Signaling pathways that regulate metabolisms and are shared with neurodegeneration.
• Metabolic manipulations as therapeutic approaches for neurodegenerative diseases.
• Gut brain communication: how does it work.
• Interaction between gut dysbiosis and neurodegenerative diseases.
• Exosomes in aging and neurodegeneration as vehicles of communication.
In today’s western societies, a major socioeconomic concern is the increase in life expectancy and consequent dramatic rise in age related disorders, such as neurodegenerative and metabolic diseases. Although the pathogenesis of both diseases has been extensively studied, the available treatment options are still scarce, implying that additional mechanisms remain to be unraveled. Accumulating evidence suggests a strong correlation between metabolic dysfunction and neurodegeneration. Indeed, proper metabolic supply is essential to maintain a healthy brain function.
In this context, the current Research Topic aims at presenting novel evidence, supporting the link between metabolism and neurodegeneration. Ultimately it will focus on how metabolic manipulations could be used as a therapeutic tool for neurodegenerative diseases. Metabolic homeostasis requires the coordinated communication and interaction between organs, in response to metabolic cues. Interestingly, the enteric nervous system, which regulates the gastrointestinal tract independent of the central nervous system, is often called the body’s “second brain.”
Traditionally we learned that the bidirectional communication between the gastrointestinal tract and the central nervous system occurs through spinal afferents and the vagus nerve, with the contribution of several neuropeptides and hormones; new studies shed light into the emerging role of gut microbiota on neurological diseases, often associated with gut dysbiosis. In recent years, another means of wireless systemic communication captured our attention - extracellular vesicles (EVs), which are double phospholipid bilayer membrane vesicles released nearly by every cell in the body and transport specific cargo (proteins, DNA, microRNAs and lipids) along the blood circulation and trigger functional alteration in distant recipient cells. These vesicles became widely recognized as essential vehicles for communication, both in physiology and pathophysiology. Curiously, misfolded forms of proteins associated with Alzheimer's, Parkinson's, and prion diseases were found in EVs, suggesting an association with these diseases. Whether EVs are working as a spreading agent and/or a cleaning mechanism is still not clear.
The aim of this Research Topic is provide an overview of the gut-brain axis by addressing how brain and gut communicate, and its implications in health and disease, with a special focus on the role of extracellular vesicles in neurodegenerative diseases, within the scope of metabolic dysfunction. We welcome reviews addressing the following subjects:
• Evidences linking metabolism and neurodegeneration.
• Impact of aging on metabolism and neurodegeneration.
• Signaling pathways that regulate metabolisms and are shared with neurodegeneration.
• Metabolic manipulations as therapeutic approaches for neurodegenerative diseases.
• Gut brain communication: how does it work.
• Interaction between gut dysbiosis and neurodegenerative diseases.
• Exosomes in aging and neurodegeneration as vehicles of communication.
