About this Research Topic
Over the past years, findings demonstrate Alzheimer disease (AD) pathology as a consequence of variable protein expression that differs according to regional localization as well as due to post-translational modifications (PTM). Deciphering the role of PTM proteins identified under conditions as AD is a complex task. The phospho, nitrosoproteome etc., profile along with differentially aberrant proteins, established a preliminary database for further clarification of mechanistic alterations associated with AD. Abnormal phosphorylation has crucial role in disease pathology that significantly contributes in AD progression by facilitating protein dysfunctions like altered energy metabolism, synaptic loss, protein misfolding, enzymatic activity, subcellular localization, ligand binding, protein-protein interactions and several other functions.
Functional interactions between metabolic enzymes have been demonstrated to exert combined effects in regulating metabolic pathways by formation of enzyme-enzyme complex and directly transfer the metabolic intermediates from one to another enzyme. Post-translational modifications can engage in extensive crosstalk, with the potential to either positively or negatively modulate signalling networks.
Expression patterns of several proteins which are crucial for the regulation of various cellular and molecular processes have been found to be altered in AD. It is now widely accepted that protein expression alterations are mainly a consequence of dysregulated post-translational modifications (PTMs) resulting in protein dysfunction via changes in the protein structure and dynamics. However, the mechanism leading to the stage and region-specific selective neurodegeneration of nerve cells and synaptic connections preceding the emergence of dementia in patients remains elusive.
At the system level, a convergence in both the expression level of proteins and their modification alterations in functions associated with cognitive decline, neuronal cell death and signal transduction is highlighting the importance of other drivers in AD pathogenesis. Limitations so far is the lack of depth of PTMed proteome hampering the reflection of gene activity in the protein expression. The integrated view of protein-protein interaction networks would reflect the importance of PTM and their regulators and could potentially provide new insights into the pathways underlying changes in AD proteome and the risk of progression.
In this Research Topic, we welcome submissions focused on the emerging trends in AD proteomics with innovative approaches. Perspective articles on the important areas incorporating proteomics and linking it to advance the knowledge of protein interactions for deciphering molecular mechanisms that will likely emerge in the future as therapeutic interventions. We also welcome articles that analyze proteomics combinatorially with lipidomics to give a broader perspective for understanding AD pathogenesis. We especially invite articles on related areas relevant to AD proteomics, their PTMs and PPIs, depicting identification of target molecules within brain tissue/CSF/blood tissue of patients that promised to give a new insight to this area.
Functional interactions between metabolic enzymes have been demonstrated to exert combined effects in regulating metabolic pathways by formation of enzyme-enzyme complex and directly transfer the metabolic intermediates from one to another enzyme. Post-translational modifications can engage in extensive crosstalk, with the potential to either positively or negatively modulate signalling networks.
Expression patterns of several proteins which are crucial for the regulation of various cellular and molecular processes have been found to be altered in AD. It is now widely accepted that protein expression alterations are mainly a consequence of dysregulated post-translational modifications (PTMs) resulting in protein dysfunction via changes in the protein structure and dynamics. However, the mechanism leading to the stage and region-specific selective neurodegeneration of nerve cells and synaptic connections preceding the emergence of dementia in patients remains elusive.
At the system level, a convergence in both the expression level of proteins and their modification alterations in functions associated with cognitive decline, neuronal cell death and signal transduction is highlighting the importance of other drivers in AD pathogenesis. Limitations so far is the lack of depth of PTMed proteome hampering the reflection of gene activity in the protein expression. The integrated view of protein-protein interaction networks would reflect the importance of PTM and their regulators and could potentially provide new insights into the pathways underlying changes in AD proteome and the risk of progression.
In this Research Topic, we welcome submissions focused on the emerging trends in AD proteomics with innovative approaches. Perspective articles on the important areas incorporating proteomics and linking it to advance the knowledge of protein interactions for deciphering molecular mechanisms that will likely emerge in the future as therapeutic interventions. We also welcome articles that analyze proteomics combinatorially with lipidomics to give a broader perspective for understanding AD pathogenesis. We especially invite articles on related areas relevant to AD proteomics, their PTMs and PPIs, depicting identification of target molecules within brain tissue/CSF/blood tissue of patients that promised to give a new insight to this area.
Keywords: Alzheimer’s disease, post translation modifications, PPI, proteomics, lipidomics
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