Introduction: The quest for reliable fluid biomarkers tracking synaptic disruption is supported by the evidence of a tight association between synaptic density and cognitive performance in neurodegenerative diseases (NDD), especially Alzheimer's disease (AD).
Areas Covered: Neurogranin (Ng) is a post-synaptic protein largely expressed in neurons involved in the memory networks. Currently, Ng measured in CSF is the most promising synaptic biomarker. Several studies show Ng elevated in AD dementia with a hippocampal phenotype as well as in MCI individuals who progress to AD. Ng concentrations are also increased in Creutzfeldt Jacob Disease where widespread and massive synaptic disintegration takes place. Ng does not discriminate Parkinson's disease from atypical parkinsonisms, nor is it altered in Huntington disease. CSF synaptosomal-associated protein 25 (SNAP-25) and synaptotagmin-1 (SYT-1) are emerging candidates.
Expert Opinion: CSF Ng revealed a role as a diagnostic and prognostic biomarker in NDD. Ng increase seems to be very specific for typical AD phenotype, probably for a prevalent hippocampal involvement. Synaptic biomarkers may serve different context-of-use in AD and other NDD including prognosis, diagnosis, and tracking synaptic damage - a critical pathophysiological mechanism in NDD - thus representing reliable tools for a precision medicine-oriented approach to NDD.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1080/14789450.2020.1831388 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Investigating the Therapeutic Mechanisms of Total Saikosaponins in Alzheimer's Disease: A Metabolomic and Proteomic Approach.
Pharmaceuticals (Basel)
January 2025
School of Pharmacy, Ningxia Medical University, Yinchuan 750004, China.
Alzheimer's disease (AD) is the leading cause of dementia among the elderly, yet effective treatments remain elusive. Total saikosaponins (TSS), the primary bioactive components in , have shown promising therapeutic effects against AD in previous studies. : To delve deeper into the mechanisms underlying the therapeutic role of TSS in AD, we investigated its neuroprotective effects and associated molecular mechanisms in APP/PS1 mice.
View Article and Find Full Text PDFIgG-NR2B-A Potentially Valuable Biomarker in the Management of Refractory Anti-NMDAR Encephalitis.
Int J Mol Sci
January 2025
Department of Pathology, Faculty of Health Care and Social Work, Trnava University and University Hospital, 917 02 Trnava, Slovakia.
The autoantibodies against the NR1 subunit are well known in the pathomechanism of NMDAR encephalitis. The dysfunction of the NR2 subunit could be a critical factor in this neurological disorder due to its important role in the postsynaptic pathways that direct synaptic plasticity. We report a case of paraneoplastic anti-NMDAR encephalitis presented alongside very severe illness.
View Article and Find Full Text PDFTranscriptomic Evidence Reveals the Dysfunctional Mechanism of Synaptic Plasticity Control in ASD.
Genes (Basel)
December 2024
Institute for Complex Systems and Mathematical Biology, King's College, University of Aberdeen, Old Aberdeen AB24 3UE, UK.
Background/objectives: A prominent endophenotype in Autism Spectrum Disorder (ASD) is the synaptic plasticity dysfunction, yet the molecular mechanism remains elusive. As a prototype, we investigate the postsynaptic signal transduction network in glutamatergic neurons and integrate single-cell nucleus transcriptomics data from the Prefrontal Cortex (PFC) to unveil the malfunction of translation control.
Methods: We devise an innovative and highly dependable pipeline to transform our acquired signal transduction network into an mRNA Signaling-Regulatory Network (mSiReN) and analyze it at the RNA level.
The Role of Neuroglia in the Development and Progression of Schizophrenia.
Biomolecules
December 2024
Neurochemical Research Unit and Bebensee Schizophrenia Research Unit, Department of Psychiatry and Neuroscience and Mental Health Institute, University of Alberta, Edmonton, AB T6G 2G3, Canada.
Schizophrenia is a complex heterogenous disorder thought to be caused by interactions between genetic and environmental factors. The theories developed to explain the etiology of schizophrenia have focused largely on the dysfunction of neurotransmitters such as dopamine, serotonin and glutamate with their receptors, although research in the past several decades has indicated strongly that other factors are also involved and that the role of neuroglial cells in psychotic disorders including schizophrenia should be given more attention. Although glia were originally thought to be present in the brain only to support neurons in a physical, metabolic and nutritional capacity, it has become apparent that these cells have a variety of important physiological roles and that abnormalities in their function may make significant contributions to the symptoms of schizophrenia.
View Article and Find Full Text PDFNeurofilament light chain levels in neuronal surface antibody-associated autoimmune encephalitis: a systematic review and meta-analysis.
Transl Psychiatry
January 2025
Department of Neurology, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
Background: Neuronal surface antibody-associated autoimmune encephalitis (NSAE) is a group of neuro-inflammatory disorders that is mediated by autoantibodies against the cell-surface and synaptic antigens. Studies have explored the role of neurofilament light chain (NfL) in NSAE and provided inconsistent data. We performed a systematic review and meta-analysis to evaluate the NfL levels in the serum and cerebrospinal fluid (CSF) of patients with NSAE.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!