Synaptic Transmission with a Focus on Neural Networks of Alzheimer's Disease

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder that significantly impairs cognitive function and mental health, affecting approximately one in three individuals over the age of 65, with over 50 million people currently diagnosed worldwide. The neuropathological hallmarks of AD include the extracellular deposition of amyloid-β (Aβ) plaques, intracellular accumulation of neurofibrillary tangles composed of hyperphosphorylated tau, neuroinflammation, neuronal death, and synaptic dysfunction or loss. Synaptic dysfunction and loss are particularly critical as they are closely associated with cognitive decline in AD. Brain plasticity, which underpins memory, is defined by activity-dependent changes in synaptic efficacy, such as long-term potentiation (LTP) and long-term depression (LTD). In AD, the severity of cognitive dysfunction correlates with the disruption of neuronal network dynamics. While abnormal aggregates of Aβ and tau proteins have been shown to impact synaptic physiology in animal and cellular models, the role of non-neuronal cells like astrocytes and microglia in synaptic dysfunction remains underexplored. Addressing these gaps is essential for developing therapeutics aimed at delaying cognitive deficits in AD.

This research topic aims to elucidate the mechanisms underlying synaptic transmission and dysfunction within the neural networks of Alzheimer’s disease. Specifically, it seeks to answer how synaptic structure, type, and markers are altered in AD, how LTP, LTD, and receptor signaling pathways are affected, and how neuronal networks are disrupted due to synaptic transmission issues. Additionally, the research will explore the contributions of non-neuronal cells such as astrocytes and microglia to synaptic changes and the impact of Aβ and tau on synaptic function. The ultimate goal is to identify potential innovative therapies to mitigate synapse loss and dysfunction and to understand synaptic resilience in maintaining cognitive function in AD.

To gather further insights into the boundaries of synaptic transmission in AD, we welcome articles addressing, but not limited to, the following themes:

- How synaptic structure, type, and markers are affected and changed in AD.

- How LTP, LTD, and GABA and glutamate receptor signaling pathways are affected in AD.

- How neuronal networks are affected in AD due to disruption of synaptic transmission.

- Contributions of other cell types such as microglia, astrocytes, and oligodendrocytes to synaptic changes in AD.

- Impact of Aβ or tau on synaptic transmission/function.

- Cellular and animal models of AD that show functional changes in synapses.

- Potential innovative therapies aimed at mitigating synapse loss and dysfunction.

- Synaptic resilience to maintain cognitive function in AD.

Article types and fees

This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:

• Brief Research Report
• Data Report
• Editorial
• FAIR² Data
• General Commentary
• Hypothesis and Theory
• Methods
• Mini Review
• Opinion
• ... View all formats

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Article types

This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:

• Brief Research Report
• Data Report
• Editorial
• FAIR² Data
• General Commentary
• Hypothesis and Theory
• Methods
• Mini Review
• Opinion
• Original Research
• Perspective
• Review
• Study Protocol
• Systematic Review
• Technology and Code

Keywords: Alzheimer’s disease, synaptic transmission, neural network dysfunction, glia–neuron interactions, innovative 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.