Rapid advances in public health and medicine in the past century have reduced the incidences of childhood diseases and increased the average life span of people in most countries. However, even as numbers of healthy children and average life span increases, incidences of neurological diseases are increasing too. Neurodevelopmental disorders like autism, Tuberous Sclerosis, Fragile X syndrome as well as neurodegenerative diseases like Alzheimer’s and Parkinson’s exact an emotional, intellectual and financial toll on individuals as well as on the society as a whole. Mounting evidence suggests that misregulation of synapse development and/or maintenance underlies these complex diseases. Thus, in order to develop specific and effective molecular diagnostic tools and therapies against these diseases, it is imperative to gain mechanistic insights into how perturbations in synapse development and maintenance lead to neurodevelopmental or neurodegenerative conditions. While extensive research has been conducted in these areas, research on molecular details of how synaptic dysfunction contributes specifically to each of these diseases is still not well understood. For instance, while misregulation of many important signaling pathways have been implicated in autism/neurodevelopmental conditions, precisely how these pathways cross talk and how this fine homeostatic balance gets tipped leading to neurodevelopmental defects is unclear. Similarly, identification and characterization of oligomers as a key toxic species in neurodegenerative disorders and the role of synapses in the spread of amyloid and tau pathology via prion-like mechanisms have opened up new fields of investigation. This is especially important in the light of failure of all the clinical trials that have primarily targeted large fibrillar aggregates. Thus, molecular mechanisms that investigate how the oligomers spread and mediate their toxic effects, and studies that test whether targeting these intermediate species will lead to beneficial outcomes are examples of articles that will be pertinent to this Research Topic.
In this Frontiers Research Topic, we welcome original research manuscripts, reviews or descriptions of novel methodologies that pertain to these diseases from a fundamental research perspective as well as a clinical setting. Our goal is to provide a platform to showcase emerging trends in these areas. Thus, we encourage articles ranging from basic synapse biology in various model organisms in the context of neurodevelopmental or neurodegenerative diseases to clinical studies and novel therapies for these conditions.
Rapid advances in public health and medicine in the past century have reduced the incidences of childhood diseases and increased the average life span of people in most countries. However, even as numbers of healthy children and average life span increases, incidences of neurological diseases are increasing too. Neurodevelopmental disorders like autism, Tuberous Sclerosis, Fragile X syndrome as well as neurodegenerative diseases like Alzheimer’s and Parkinson’s exact an emotional, intellectual and financial toll on individuals as well as on the society as a whole. Mounting evidence suggests that misregulation of synapse development and/or maintenance underlies these complex diseases. Thus, in order to develop specific and effective molecular diagnostic tools and therapies against these diseases, it is imperative to gain mechanistic insights into how perturbations in synapse development and maintenance lead to neurodevelopmental or neurodegenerative conditions. While extensive research has been conducted in these areas, research on molecular details of how synaptic dysfunction contributes specifically to each of these diseases is still not well understood. For instance, while misregulation of many important signaling pathways have been implicated in autism/neurodevelopmental conditions, precisely how these pathways cross talk and how this fine homeostatic balance gets tipped leading to neurodevelopmental defects is unclear. Similarly, identification and characterization of oligomers as a key toxic species in neurodegenerative disorders and the role of synapses in the spread of amyloid and tau pathology via prion-like mechanisms have opened up new fields of investigation. This is especially important in the light of failure of all the clinical trials that have primarily targeted large fibrillar aggregates. Thus, molecular mechanisms that investigate how the oligomers spread and mediate their toxic effects, and studies that test whether targeting these intermediate species will lead to beneficial outcomes are examples of articles that will be pertinent to this Research Topic.
In this Frontiers Research Topic, we welcome original research manuscripts, reviews or descriptions of novel methodologies that pertain to these diseases from a fundamental research perspective as well as a clinical setting. Our goal is to provide a platform to showcase emerging trends in these areas. Thus, we encourage articles ranging from basic synapse biology in various model organisms in the context of neurodevelopmental or neurodegenerative diseases to clinical studies and novel therapies for these conditions.