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Cognitive dysfunction in Alzheimer's disease (AD) correlates closely with pathology in the neuronal microtubule-associated protein tau. Tau pathology may spread via neural synapses. In a population of cognitively unimpaired elderly at elevated risk of AD, we investigated four cerebrospinal (CSF) markers of synaptic dysfunction and degeneration.
View Article and Find Full Text PDFNon-canonical Roles of Complement in the CNS: From Synaptic Organizer to Presynaptic Modulator of Glutamate Transmission.
Curr Neuropharmacol
January 2025
Department of Pharmacy, DIFAR, Pharmacology and Toxicology Section, University of Genoa, Viale Cembrano 4, 16148, Genoa, Italy.
The central nervous system (CNS) is not an immune-privileged compartment, but it is intimately intertwined with the immune system. Among the components shared by the two compartments is the complement, a main constituent of innate immunity, which is also produced centrally and controls the development and organization of synaptic connections. Complement is considered a doubled-faced system that, besides controlling the physiological development of the central network, also subserves synaptic engulfment pivotal to the progression of neurodegenerative diseases.
View Article and Find Full Text PDFThe astrocytic zinc transporter ZIP12 is a synaptic protein that contributes to synaptic zinc levels in mouse auditory cortex.
J Neurosci
January 2025
Department of Neuroscience, Rockefeller Neuroscience Institute, West Virginia University School of Medicine, Morgantown, WV, USA.
Synaptically released zinc is a neuronal signaling system that arises from the actions of the presynaptic vesicular zinc transporter protein ZnT3. Mechanisms that regulate the actions of zinc at synapses are of great importance for many aspects of synaptic signaling in the brain. Here, we identify the astrocytic zinc transporter protein ZIP12 as a candidate mechanism that contributes to zinc clearance at cortical synapses.
View Article and Find Full Text PDFChloroquine Affects Presynaptic Membrane Retrieval in Diaphragm Neuromuscular Junctions of Old Mice.
Int J Mol Sci
December 2024
Department of Anesthesiology & Perioperative Medicine, Mayo Clinic, Rochester, MN 55905, USA.
Aging disrupts multiple homeostatic processes, including autophagy, a cellular process for the recycling and degradation of defective cytoplasmic structures. Acute treatment with the autophagy inhibitor chloroquine blunts the maximal forces generated by the diaphragm muscle, but the mechanisms underlying neuromuscular dysfunction in old age remain poorly understood. We hypothesized that chloroquine treatment increases the presynaptic retention of the styryl dye FM 4-64 following high-frequency nerve stimulation, consistent with the accumulation of unprocessed bulk endosomes.
View Article and Find Full Text PDFAutism-Linked Mutations in αδ-1 and αδ-3 Reduce Protein Membrane Expression but Affect Neither Calcium Channels nor Trans-Synaptic Signaling.
Pharmaceuticals (Basel)
November 2024
Division of Physiology, Department of Pharmacology, Physiology, and Microbiology, Karl Landsteiner University of Health Sciences, 3500 Krems, Austria.
Article Synopsis
- αδ proteins play a crucial role in regulating calcium channels and synaptic functions, with missense variants in their genes linked to autism spectrum disorder (ASD), although their pathogenic effects remain unclear.
- Functional characterization of two specific mutations (p.R351T in αδ-1 and p.A275T in αδ-3) showed reduced membrane expression and synaptic localization but did not significantly affect the biophysical properties of calcium channels.
- The findings suggest that the pathogenic mechanisms related to these mutations may not be tied to traditional channel functions or trans-synaptic signaling, indicating a complex role for αδ proteins in ASD.
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