Research Topic

Developmental Factors as Potential Targets for Halting Neurodegeneration

About this Research Topic

Neurodegenerative diseases are characterized by the gradual decline of neuronal function, loss of neuronal projections, and death of neuronal cell bodies. The type of neurons affected, and the pattern of neuronal loss, varies depending on the disease such as Alzheimer’s, Parkinson’s, and Huntington’s disease, as well as Multiple System Atrophy and Amyotrophic Lateral Sclerosis, among others. Several symptomatic treatments have been discovered that alleviate patients’ symptoms, but fail nonetheless to halt neurodegeneration. Ways to treat neurodegeneration are desperately needed however, and all efforts in that direction, so far, have failed. Discovering neuroprotective therapies is rendered very challenging because the etiology of most neurodegenerative diseases is complex, involves several genetic and environmental factors, and is poorly understood. Finally, known influential factors can explain only a minority of cases.

In view of our insufficient understanding of the causes of neurodegenerative diseases, and the corresponding mechanisms leading to neuronal death, discovering neuroprotective strategies appears to be a very challenging task. Nevertheless, perhaps the formation of neurons may reveal important clues about factors that may promote their survival. Indeed, it has been shown that some genes active during neuronal development affect a multitude of functions, including survival. For instance, administration of the neurotrophic developmental factors GDNF, BDNF or NGF was considered as potential treatment for neurodegenerative diseases. Interestingly, several genes linked with the pathogenesis of neurodegenerative diseases have also indispensable developmental functions. Deletion of Huntingtin, or the Alzheimer's disease Amyloid Precursor Protein (APP) in mice lead to brain developmental abnormalities. Also, overexpression of the Parkinson’s disease associated alpha-synuclein affects the number of dopaminergic neurons during embryogenesis. Finally, genes such as engrailed1/2, Nurr1, Foxa1/2, Lmx1a/b, Otx2, PTX3 are not only dopaminergic neuron survival factors during embryogenesis, but exert neuroprotective functions in adults and have been proposed as neuroprotective targets. In fact, small agonists molecules modulating their function have shown promising results in preclinical disease models. Furthermore, as it was theorized, manipulating the same target with the same compound has shown encouraging results in preclinical models of different neurodegenerative diseases demonstrating neuroprotection irrespective of cause.

This Research Topic aims to shed light upon neurodevelopmental genes which, beyond development, may be involved in mechanisms and processes associated with neuroprotection in adult onset of neurodegenerative diseases.
We will welcome research articles that would provide molecular, cellular or whole organism experimental evidence that helps validate them as targets for neuroprotection. Such experimental evidence could include, but it is not limited to:
• Genetic or GWAS association with a neurodegenerative disease.
• Altered Expression level associated with a neurodegenerative disease
• Altered Expression levels during or after neuroprotective or neurodegenerative interventions
• Altered Expression levels during aging
• Expression alteration due to Pharmacological intervention
• Molecular or genetic manipulation (overexpression / knockdown) affecting neuroprotective or neurodegenerative outcome


Keywords: neuronal precursors, final differentiation, neurotransmitter, homeobox, pleiotropy


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

Neurodegenerative diseases are characterized by the gradual decline of neuronal function, loss of neuronal projections, and death of neuronal cell bodies. The type of neurons affected, and the pattern of neuronal loss, varies depending on the disease such as Alzheimer’s, Parkinson’s, and Huntington’s disease, as well as Multiple System Atrophy and Amyotrophic Lateral Sclerosis, among others. Several symptomatic treatments have been discovered that alleviate patients’ symptoms, but fail nonetheless to halt neurodegeneration. Ways to treat neurodegeneration are desperately needed however, and all efforts in that direction, so far, have failed. Discovering neuroprotective therapies is rendered very challenging because the etiology of most neurodegenerative diseases is complex, involves several genetic and environmental factors, and is poorly understood. Finally, known influential factors can explain only a minority of cases.

In view of our insufficient understanding of the causes of neurodegenerative diseases, and the corresponding mechanisms leading to neuronal death, discovering neuroprotective strategies appears to be a very challenging task. Nevertheless, perhaps the formation of neurons may reveal important clues about factors that may promote their survival. Indeed, it has been shown that some genes active during neuronal development affect a multitude of functions, including survival. For instance, administration of the neurotrophic developmental factors GDNF, BDNF or NGF was considered as potential treatment for neurodegenerative diseases. Interestingly, several genes linked with the pathogenesis of neurodegenerative diseases have also indispensable developmental functions. Deletion of Huntingtin, or the Alzheimer's disease Amyloid Precursor Protein (APP) in mice lead to brain developmental abnormalities. Also, overexpression of the Parkinson’s disease associated alpha-synuclein affects the number of dopaminergic neurons during embryogenesis. Finally, genes such as engrailed1/2, Nurr1, Foxa1/2, Lmx1a/b, Otx2, PTX3 are not only dopaminergic neuron survival factors during embryogenesis, but exert neuroprotective functions in adults and have been proposed as neuroprotective targets. In fact, small agonists molecules modulating their function have shown promising results in preclinical disease models. Furthermore, as it was theorized, manipulating the same target with the same compound has shown encouraging results in preclinical models of different neurodegenerative diseases demonstrating neuroprotection irrespective of cause.

This Research Topic aims to shed light upon neurodevelopmental genes which, beyond development, may be involved in mechanisms and processes associated with neuroprotection in adult onset of neurodegenerative diseases.
We will welcome research articles that would provide molecular, cellular or whole organism experimental evidence that helps validate them as targets for neuroprotection. Such experimental evidence could include, but it is not limited to:
• Genetic or GWAS association with a neurodegenerative disease.
• Altered Expression level associated with a neurodegenerative disease
• Altered Expression levels during or after neuroprotective or neurodegenerative interventions
• Altered Expression levels during aging
• Expression alteration due to Pharmacological intervention
• Molecular or genetic manipulation (overexpression / knockdown) affecting neuroprotective or neurodegenerative outcome


Keywords: neuronal precursors, final differentiation, neurotransmitter, homeobox, pleiotropy


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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Submission Deadlines

13 December 2020 Abstract
12 April 2021 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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Topic Editors

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Submission Deadlines

13 December 2020 Abstract
12 April 2021 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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