About this Research Topic
In recent years, TAU protein has become increasingly important because alterations associated with it are the basis of diseases known as tauopathies.
TAU is a microtubule-associated protein in neurons which, under pathological conditions, forms aberrant assembly into insoluble aggregates. This leads to synaptic dysfunction and neural cell death in a range of neurodegenerative disorders. Therefore, it is vital to unravel the molecular mechanisms in which TAU protein is involved and its association with various pathologies.
In addition, new evidence indicates that there are alterations in TAU in pathologies that were not classically associated with it. All this points to the high relevance of the molecular mechanism involving TAU function.
It is then essential to understand the different functions and diverse localizations of TAU in the brain and to discover its implications in cell signaling, genomic stability, and synaptic plasticity.
This Research Topic should, on one hand, emphasize the importance of TAU protein and the molecular cascades involved, such as:
• microtubules assembly and disassembly;
• inflammation;
• hyperphosphorylation;
• autophagy/proteostasis;
• TAU interaction partners;
• gene regulation;
and on the other hand, it should also highlight its possible role and involvement as a pharmacological tool for therapeutic strategies, including:
• antibodies that bound disease modified TAU;
• blocking aggregation;
• enhance autophagy;
• drugs that reduce memory loss.
In this regard, we would like to welcome review articles that address the above-mentioned issues from different perspectives. Alternatively, any original research papers contributing significantly to TAU signaling progress or advancing our understanding of biological implications, are highly welcome.
TAU is a microtubule-associated protein in neurons which, under pathological conditions, forms aberrant assembly into insoluble aggregates. This leads to synaptic dysfunction and neural cell death in a range of neurodegenerative disorders. Therefore, it is vital to unravel the molecular mechanisms in which TAU protein is involved and its association with various pathologies.
In addition, new evidence indicates that there are alterations in TAU in pathologies that were not classically associated with it. All this points to the high relevance of the molecular mechanism involving TAU function.
It is then essential to understand the different functions and diverse localizations of TAU in the brain and to discover its implications in cell signaling, genomic stability, and synaptic plasticity.
This Research Topic should, on one hand, emphasize the importance of TAU protein and the molecular cascades involved, such as:
• microtubules assembly and disassembly;
• inflammation;
• hyperphosphorylation;
• autophagy/proteostasis;
• TAU interaction partners;
• gene regulation;
and on the other hand, it should also highlight its possible role and involvement as a pharmacological tool for therapeutic strategies, including:
• antibodies that bound disease modified TAU;
• blocking aggregation;
• enhance autophagy;
• drugs that reduce memory loss.
In this regard, we would like to welcome review articles that address the above-mentioned issues from different perspectives. Alternatively, any original research papers contributing significantly to TAU signaling progress or advancing our understanding of biological implications, are highly welcome.
Keywords: TAU dysfunction, Aggregation, Transmission, Genetic Variations, Tauopathy
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.
