About this Research Topic
Alzheimer’s disease (AD) is a progressive neurodegenerative disease leading to a decline in cognitive function and mental health, which affects approximately 1 in 3 people over the age of 65, currently over 50 million people in the world. Neuropathological hallmarks of AD include extracellular deposition of amyloid-β (Aβ) plaques, intracellular accumulation of neurofibrillary tangles composed of hyperphosphorylated tau, neuroinflammation, neuronal death and synaptic dysfunction/loss.
The synapse has been regarded as a critical target for AD, and synapse dysfunction and loss is one of the main biological correlates of cognitive decline within AD. Brain plasticity is the core neurophysiological basis of memory and is generally defined by activity-dependent changes in synaptic efficacy, such as long-term potentiation (LTP) and long-term depression (LTD). In AD, the severity of the cognitive dysfunction also correlates with the level of disruption of neuronal network dynamics.
Abnormal aggregates of Aβ or tau proteins have been demonstrated to impact on synaptic physiology in animal and cellular models of AD. Meanwhile, how non-neuronal cell types such as astrocytes and microglia, and their related mechanisms of dysfunction independent of amyloid and tau contribute to synaptic dysfunction in AD still needs to be further explored.
Therefore, we believe that this Research Topic will be critical for the development of therapeutics aiming at delaying the onset of cognitive deficits.
This Research Topic welcomes all original articles, reviews, and reports related, but not limited to, the following sub-topics.
- 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.
- How do other cell types such as microglia, astrocytes and oligodendrocytes contribute to the synaptic changes in AD?
- How does Aβ or tau affect 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.
The synapse has been regarded as a critical target for AD, and synapse dysfunction and loss is one of the main biological correlates of cognitive decline within AD. Brain plasticity is the core neurophysiological basis of memory and is generally defined by activity-dependent changes in synaptic efficacy, such as long-term potentiation (LTP) and long-term depression (LTD). In AD, the severity of the cognitive dysfunction also correlates with the level of disruption of neuronal network dynamics.
Abnormal aggregates of Aβ or tau proteins have been demonstrated to impact on synaptic physiology in animal and cellular models of AD. Meanwhile, how non-neuronal cell types such as astrocytes and microglia, and their related mechanisms of dysfunction independent of amyloid and tau contribute to synaptic dysfunction in AD still needs to be further explored.
Therefore, we believe that this Research Topic will be critical for the development of therapeutics aiming at delaying the onset of cognitive deficits.
This Research Topic welcomes all original articles, reviews, and reports related, but not limited to, the following sub-topics.
- 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.
- How do other cell types such as microglia, astrocytes and oligodendrocytes contribute to the synaptic changes in AD?
- How does Aβ or tau affect 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.
Keywords: Glutamate Receptors, Alzheimer's Disease, microglia, oligodendrocytes, astrocytes, synaptic transmission, amyloid-β, tau
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.
