Research Topic

Unfolded Protein Response (UPR): An Impending Target for Multiple Neurological Disorders

About this Research Topic

The endoplasmic reticulum (ER) not only controls calcium homeostasis, but is also responsible for translation, folding, maturation and trafficking of proteins. Numerous environmental abuses perturb functioning of this organelle and lead to the accumulation of misfolded or unfolded protein cargo in the ER lumen, thereby developing a condition termed as ER stress. This stress in turn activates an extremely conserved pathway called ER unfolded protein response (UPR). The condition is sensed by three ER stress sensors: PERK, IRE1 and ATF6, that play a central role in initiation and regulation during UPR. Under normal conditions, the endoplasmic reticulum (ER) takes care of the damaged/misfolded protein overload by the activation of rescue pathways, that altogether involves up-regulating the expression of its resident chaperones to properly fold the misfolded proteins, putting a halt to its translational job, and appropriately diverting the unwanted cargo towards degradation pathway, the endoplasmic reticulum associated degradation (ERAD). However, a condition of prolonged stress and damage provokes UPR to succumb through apoptosis. A disturbance in the UPRER machinery, leading to the development of diverse etiologies, earmarked by an accumulation of disease-related misfolded proteins, that lead to the development of different neurodegenerative disorders like Alzheimer's disease (AD), Parkinson's disease (PD) and Huntington's disease (HD).

Identifying mechanisms linking stress responses to neuronal function may lead to new treatments for neurodegeneration-related pathologies. This Research Topic will focus on genetic mechanisms and pharmacological approaches aimed to find treatment to ameliorate neurological disorders as a strategy to extend the survival of affected individuals.

We pursue Original Research, Review, Mini-Review, Hypothesis and Theory, Perspective, Clinical Trial, Case Report and Opinion articles that cover, but are not limited to:

• Molecular mechanism of ER stress in relation with neurodegeneration-related pathologies.
• ER stress-associated transcriptional regulation in neurodegeneration.
• Therapeutic potentials by targeting ER stress response pathways.
• ER stress-mediated apoptosis
• ER stress and neuroinflammation.
• Protein misfolding/UPR/ER stress response-related neurodegenerative diseases.
• Identification of sensitive ER stress biomarkers for the therapeutic target in neurodegenerative disorder.


Keywords: UPR (Unfolded Protein Response), Endoplasmic Reticulum (ER) stress, Neurodegenerative Diseases, Dementia, Therapeutics


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.

The endoplasmic reticulum (ER) not only controls calcium homeostasis, but is also responsible for translation, folding, maturation and trafficking of proteins. Numerous environmental abuses perturb functioning of this organelle and lead to the accumulation of misfolded or unfolded protein cargo in the ER lumen, thereby developing a condition termed as ER stress. This stress in turn activates an extremely conserved pathway called ER unfolded protein response (UPR). The condition is sensed by three ER stress sensors: PERK, IRE1 and ATF6, that play a central role in initiation and regulation during UPR. Under normal conditions, the endoplasmic reticulum (ER) takes care of the damaged/misfolded protein overload by the activation of rescue pathways, that altogether involves up-regulating the expression of its resident chaperones to properly fold the misfolded proteins, putting a halt to its translational job, and appropriately diverting the unwanted cargo towards degradation pathway, the endoplasmic reticulum associated degradation (ERAD). However, a condition of prolonged stress and damage provokes UPR to succumb through apoptosis. A disturbance in the UPRER machinery, leading to the development of diverse etiologies, earmarked by an accumulation of disease-related misfolded proteins, that lead to the development of different neurodegenerative disorders like Alzheimer's disease (AD), Parkinson's disease (PD) and Huntington's disease (HD).

Identifying mechanisms linking stress responses to neuronal function may lead to new treatments for neurodegeneration-related pathologies. This Research Topic will focus on genetic mechanisms and pharmacological approaches aimed to find treatment to ameliorate neurological disorders as a strategy to extend the survival of affected individuals.

We pursue Original Research, Review, Mini-Review, Hypothesis and Theory, Perspective, Clinical Trial, Case Report and Opinion articles that cover, but are not limited to:

• Molecular mechanism of ER stress in relation with neurodegeneration-related pathologies.
• ER stress-associated transcriptional regulation in neurodegeneration.
• Therapeutic potentials by targeting ER stress response pathways.
• ER stress-mediated apoptosis
• ER stress and neuroinflammation.
• Protein misfolding/UPR/ER stress response-related neurodegenerative diseases.
• Identification of sensitive ER stress biomarkers for the therapeutic target in neurodegenerative disorder.


Keywords: UPR (Unfolded Protein Response), Endoplasmic Reticulum (ER) stress, Neurodegenerative Diseases, Dementia, Therapeutics


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

31 July 2020 Abstract
28 February 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

31 July 2020 Abstract
28 February 2021 Manuscript

Participating Journals

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

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