Research Topic

Beta Amyloid: From Physiology to Pathogenesis

About this Research Topic

Amyloid-beta (Aβ) has been primarily studied as a pathogenetic factor in Alzheimer’s disease (AD). However, Aβ exerts multiple physiological actions, including the regulation of synaptic activity, excitability, memory formation, microtubule dynamics, glial regulation, and neuro-immune response. How the physiological actions of Aβ relate to AD pathogenesis remains to be fully elucidated. Nonetheless, a growing understanding of Aβ biology and physiology has informed the development of novel AD therapeutics.
 
Aβ is endogenously present at low levels (pM – nM) in the hippocampus and cortex, regions of the brain that undergo neurodegeneration in AD. Moreover, the levels of Aβ are dynamically regulated by synaptic activity, which in turn can regulate synaptic plasticity and process underlying memory, leading to the suggestion that Aβ functions as a neuropeptide.
 
For this Research Topic, current advances in understanding Aβ biology and physiology and their relation to AD pathogenesis will be presented. Areas to be covered include:

• Synaptic plasticity – synaptic dysfunction
• Regulation of circuit excitability - hyperexcitability
• Microtubule dynamics – altered axonal transport
• Regulation of glial function – microglia in synaptic pruning
• Regulation of glia phenotypes – glial overactivation

We primarily welcome Original Research articles, Reviews, and Mini Reviews on the above themes and other areas related to the Research Topic.


Keywords: synaptic regulation, neuronal excitability, Amyloid-beta, pathogenesis


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.

Amyloid-beta (Aβ) has been primarily studied as a pathogenetic factor in Alzheimer’s disease (AD). However, Aβ exerts multiple physiological actions, including the regulation of synaptic activity, excitability, memory formation, microtubule dynamics, glial regulation, and neuro-immune response. How the physiological actions of Aβ relate to AD pathogenesis remains to be fully elucidated. Nonetheless, a growing understanding of Aβ biology and physiology has informed the development of novel AD therapeutics.
 
Aβ is endogenously present at low levels (pM – nM) in the hippocampus and cortex, regions of the brain that undergo neurodegeneration in AD. Moreover, the levels of Aβ are dynamically regulated by synaptic activity, which in turn can regulate synaptic plasticity and process underlying memory, leading to the suggestion that Aβ functions as a neuropeptide.
 
For this Research Topic, current advances in understanding Aβ biology and physiology and their relation to AD pathogenesis will be presented. Areas to be covered include:

• Synaptic plasticity – synaptic dysfunction
• Regulation of circuit excitability - hyperexcitability
• Microtubule dynamics – altered axonal transport
• Regulation of glial function – microglia in synaptic pruning
• Regulation of glia phenotypes – glial overactivation

We primarily welcome Original Research articles, Reviews, and Mini Reviews on the above themes and other areas related to the Research Topic.


Keywords: synaptic regulation, neuronal excitability, Amyloid-beta, pathogenesis


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

01 July 2020 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

01 July 2020 Manuscript

Participating Journals

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

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