Synaptic plasticity provides a physiological substrate in the central nervous system for individual to achieve cognitive and emotional functions, including learning, memory, forgetting, anxiety and depression et al. Impairments of synaptic plasticity is found in many brain injuries and neurodegenerative diseases, including Alzheimer’s disease (AD). In the past decades, with the development of high throughput genomic and proteomic sequencing technologies, high-resolution imaging technology, new neurotransmitter detection systems and precise neuronal activity manipulation and recording systems, intensive research efforts in AD have greatly expanded our understanding of this devastating disease. Numerous molecular mechanisms linking the progressive synaptic dysfunction with the pathological factors, including intracellular accumulated-tau-formed neurofibrillary tangles (NFTs) and extracellular deposited amyloid ß, have been identified.
However, many questions in this rapidly evolving field remain open. Synaptic plasticity is manifested in two main forms, long-term depression (LTD) and long-term potentiation (LTP). Compelling evidences have identified impaired hippocampal LTP as the signature in early stage of AD. Is this impairment caused by directly reduced synapse numbers or decreased synaptic transmission efficiency? Does reduced formation of new synapses or disappearances or silencing of pre-existing synapses synergistically or separately contribute to synapse loss? What’re the inherent molecular mechanisms underlying this aberrant number loss (synaptic-associated protein loss, microglia-mediated synapse elimination, neuroinflammation, neuron apoptosis or death)? What are the causes for synaptic transmission reduction? Such as the neurotransmitter synthesis, secretion, receptor binding and recovery pathways, post-synaptic signaling transduction (Glutamate receptors, cholinergic receptors and GABA receptors) and neuronal activity homeostasis, and so on.
Understanding the molecular mechanisms of synaptic dysfunctions could efficiently help to develop new molecular strategies directly targeting to promote synaptic plasticity. This could be a promising therapeutic direction of blocking or delaying disease progression under multiple AD-related risk factors, including aging, oxidative stress, calcium signal dysregulation, misfolded protein aggregation, neuroinflammation, genetic and environmental factors.
The aim of this Research Topic is to cover the recent progresses in the field of AD synaptic plasticity, as well as related mechanistic studies and technological advancements. We will welcome Original Research and Review related, but are not limited to the following areas:
- Genetic and epigenetic changes relating to synaptic plasticity deficits;
- Risk factors (such as free radical, hyperglycemia etc) relating to synaptic plasticity deficits;
- Mechanistic studies relating to synaptic plasticity impairments;
- Therapeutic strategies.
Synaptic plasticity provides a physiological substrate in the central nervous system for individual to achieve cognitive and emotional functions, including learning, memory, forgetting, anxiety and depression et al. Impairments of synaptic plasticity is found in many brain injuries and neurodegenerative diseases, including Alzheimer’s disease (AD). In the past decades, with the development of high throughput genomic and proteomic sequencing technologies, high-resolution imaging technology, new neurotransmitter detection systems and precise neuronal activity manipulation and recording systems, intensive research efforts in AD have greatly expanded our understanding of this devastating disease. Numerous molecular mechanisms linking the progressive synaptic dysfunction with the pathological factors, including intracellular accumulated-tau-formed neurofibrillary tangles (NFTs) and extracellular deposited amyloid ß, have been identified.
However, many questions in this rapidly evolving field remain open. Synaptic plasticity is manifested in two main forms, long-term depression (LTD) and long-term potentiation (LTP). Compelling evidences have identified impaired hippocampal LTP as the signature in early stage of AD. Is this impairment caused by directly reduced synapse numbers or decreased synaptic transmission efficiency? Does reduced formation of new synapses or disappearances or silencing of pre-existing synapses synergistically or separately contribute to synapse loss? What’re the inherent molecular mechanisms underlying this aberrant number loss (synaptic-associated protein loss, microglia-mediated synapse elimination, neuroinflammation, neuron apoptosis or death)? What are the causes for synaptic transmission reduction? Such as the neurotransmitter synthesis, secretion, receptor binding and recovery pathways, post-synaptic signaling transduction (Glutamate receptors, cholinergic receptors and GABA receptors) and neuronal activity homeostasis, and so on.
Understanding the molecular mechanisms of synaptic dysfunctions could efficiently help to develop new molecular strategies directly targeting to promote synaptic plasticity. This could be a promising therapeutic direction of blocking or delaying disease progression under multiple AD-related risk factors, including aging, oxidative stress, calcium signal dysregulation, misfolded protein aggregation, neuroinflammation, genetic and environmental factors.
The aim of this Research Topic is to cover the recent progresses in the field of AD synaptic plasticity, as well as related mechanistic studies and technological advancements. We will welcome Original Research and Review related, but are not limited to the following areas:
- Genetic and epigenetic changes relating to synaptic plasticity deficits;
- Risk factors (such as free radical, hyperglycemia etc) relating to synaptic plasticity deficits;
- Mechanistic studies relating to synaptic plasticity impairments;
- Therapeutic strategies.
