Synaptic dysfunction in Alzheimer's disease and related dementias represents a critical area of research, given the profound impact of these conditions on cognitive function. The deposition of senile plaques and neurofibrillary tangles in the brain is a hallmark of Alzheimer's disease, yet evidence increasingly suggests that cognitive decline is more closely associated with synaptic dysfunction and loss. Notably, some individuals exhibit significant neuropathological features of Alzheimer's disease without manifesting cognitive symptoms, a phenomenon linked to preserved synaptic integrity. This underscores the importance of synaptic health as an early indicator of disease progression. Recent studies have highlighted the role of NMDA receptor overstimulation in synaptic dysfunction, leading to a cascade of events culminating in synaptic loss and neuronal apoptosis. Despite advances in identifying potential synaptic biomarkers, such as neurogranin, SNAP-25, synaptotagmin-1, and GAP-43, there remains a lack of consensus on their clinical utility, necessitating further research.
Goal
This Research Topic aims to elucidate the relevance of synaptic biomarkers in Alzheimer's disease and related dementias, with the ultimate goal of enhancing our understanding of the early pathophysiological events that characterize these conditions. By spotlighting recent discoveries from both preclinical and clinical research, we seek to identify synaptic biomarkers that hold diagnostic and prognostic value. Key questions include the mechanisms underlying synaptic disruption, the identification of novel biomarkers, and the validation of existing ones in clinical settings. This endeavor aims to bridge the gap between current knowledge and the need for reliable biomarkers to improve early diagnosis and treatment outcomes.
Scope and information for authors
To gather further insights into the boundaries of synaptic dysfunction in Alzheimer's disease and related dementias, we welcome articles addressing, but not limited to, the following themes:
- The study of the pathophysiology of synaptic disruption in Alzheimer's disease and related dementias
- Preclinical models of Alzheimer's disease investigating synaptic dysfunction
- Clinical studies aimed at defining the role of synaptic biomarkers in Alzheimer's disease and related dementias
- Clinical studies aiming to identify novel synaptic biomarkers in cerebrospinal fluid
- Clinical studies aiming to identify novel synaptic biomarkers in blood
Synaptic dysfunction in Alzheimer's disease and related dementias represents a critical area of research, given the profound impact of these conditions on cognitive function. The deposition of senile plaques and neurofibrillary tangles in the brain is a hallmark of Alzheimer's disease, yet evidence increasingly suggests that cognitive decline is more closely associated with synaptic dysfunction and loss. Notably, some individuals exhibit significant neuropathological features of Alzheimer's disease without manifesting cognitive symptoms, a phenomenon linked to preserved synaptic integrity. This underscores the importance of synaptic health as an early indicator of disease progression. Recent studies have highlighted the role of NMDA receptor overstimulation in synaptic dysfunction, leading to a cascade of events culminating in synaptic loss and neuronal apoptosis. Despite advances in identifying potential synaptic biomarkers, such as neurogranin, SNAP-25, synaptotagmin-1, and GAP-43, there remains a lack of consensus on their clinical utility, necessitating further research.
Goal
This Research Topic aims to elucidate the relevance of synaptic biomarkers in Alzheimer's disease and related dementias, with the ultimate goal of enhancing our understanding of the early pathophysiological events that characterize these conditions. By spotlighting recent discoveries from both preclinical and clinical research, we seek to identify synaptic biomarkers that hold diagnostic and prognostic value. Key questions include the mechanisms underlying synaptic disruption, the identification of novel biomarkers, and the validation of existing ones in clinical settings. This endeavor aims to bridge the gap between current knowledge and the need for reliable biomarkers to improve early diagnosis and treatment outcomes.
Scope and information for authors
To gather further insights into the boundaries of synaptic dysfunction in Alzheimer's disease and related dementias, we welcome articles addressing, but not limited to, the following themes:
- The study of the pathophysiology of synaptic disruption in Alzheimer's disease and related dementias
- Preclinical models of Alzheimer's disease investigating synaptic dysfunction
- Clinical studies aimed at defining the role of synaptic biomarkers in Alzheimer's disease and related dementias
- Clinical studies aiming to identify novel synaptic biomarkers in cerebrospinal fluid
- Clinical studies aiming to identify novel synaptic biomarkers in blood
