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Background Temporal interference (TI) stimulation is a novel method of electrical brain stimulation that is capable of non‐invasively and selectively targeting deep brain structures. Previously, we demonstrated that TI stimulation could modulate hippocampal activity and improve performance on an episodic memory task in healthy young adults. In this study, we investigated the effects of multi‐session TI stimulation of the hippocampus in patients with early‐stage Alzheimer's disease (AD). Method Twenty‐one AD patients received 50 minutes of TI stimulation to the left hippocampus daily, over 10 consecutive days. The effects of the intervention were assessed using a battery of neurocognitive assessments and neuroimaging measures, including positron emission tomography (PET) of mitochondrial complex‐1, blood‐oxygen level‐dependent functional magnetic resonance imaging (BOLD fMRI), arterial spin labelling (ASL) and diffusion tensor imaging (DTI). Result We demonstrate that multi‐session TI stimulation of the hippocampus is safe and well‐tolerated. Following TI stimulation, AD patients showed selective improvements in hippocampal‐dependent episodic memory tasks. Conclusion We report the main outcomes in terms of safety, neurocognitive assessments and neuroimaging measures from the first study of TI stimulation in patients with early‐stage AD.

Temporal interference (TI) stimulation is a novel method of electrical brain stimulation that is capable of non-invasively and selectively targeting deep brain structures. Previously, we demonstrated that TI stimulation could modulate hippocampal activity and improve performance on an episodic memory task in healthy young adults. In this study, we investigated the effects of multi-session TI stimulation of the hippocampus in patients with early-stage Alzheimer's disease (AD). Twenty-one AD patients received 50 minutes of TI stimulation to the left hippocampus daily, over 10 consecutive days. The effects of the intervention were assessed using a battery of neurocognitive assessments and neuroimaging measures, including positron emission tomography (PET) of mitochondrial complex-1, blood-oxygen level-dependent functional magnetic resonance imaging (BOLD fMRI), arterial spin labelling (ASL) and diffusion tensor imaging (DTI). We demonstrate that multi-session TI stimulation of the hippocampus is safe and well-tolerated. Following TI stimulation, AD patients showed selective improvements in hippocampal-dependent episodic memory tasks. We report the main outcomes in terms of safety, neurocognitive assessments and neuroimaging measures from the first study of TI stimulation in patients with early-stage AD.

BackgroundIntravenous drug administration is essential in intensive care treatment. However, the risk of particulate contamination in infusion solutions during treatment is often underestimated.MethodsResidual amounts of infusion solutions prepared and administered at the adult intensive care unit were examined for visible and subvisible particles according to the recommendations of the European Pharmacopoeia monographs 2.9.19 and 2.9.20.ResultsSamples from 169 infusion solutions were collected, 149 of which could be analysed. The Pharmacopoeia requirements for visible particles were not fulfilled in 42.9% (n=64/149) of the samples, while the requirements for subvisible particles were not met in 4.7% (n=7/149). A specific correlation between the pharmaceutical drugs or within the infusion set (bottle vs connected infusion line) and particulate contamination was not possible as the sample was too small for a correlation analysis. A Spearman rho analysis showed no correlation between particle contamination and administration mode (subvisible (10 µm): p=0.969, r=−0.005; subvisible (25 µm): p=0.834, r=−0.026; visible: p=0.711, r=−0.047) and particle contamination and dosage form (subvisible (10 µm): p=0.291, r=−0.092; subvisible (25 µm): p=0.513, r=0.057; visible: p=0.415, r=0.071).ConclusionsThis study showed that residuals of intravenously administered solutions have particulate contaminations. A specific causal factor was not identified.

Synapse loss correlates with cognitive decline in Alzheimer’s disease (AD). Data from mouse models suggests microglia are important for synapse degeneration, but direct human evidence for any glial involvement in synapse removal in human AD remains to be established. Here we observe astrocytes and microglia from human brains contain greater amounts of synaptic protein in AD compared to non-disease controls, and that proximity to amyloid-β plaques and the APOE4 risk gene exacerbate this effect. In culture, mouse and human astrocytes and primary mouse and human microglia phagocytose AD patient-derived synapses more than synapses from controls. Inhibiting MFG-E8 function rescued the elevated engulfment of AD synapses by astrocytes and microglia without affecting control synapse uptake. Thus, AD promotes increased synapse ingestion by human glial cells via an MFG-E8 opsonophagocytic mechanism with potential for targeted therapeutic manipulation. Glial cells ingest synapses in Alzheimer’s disease and antibody treatment reduces this ingestion in cultured human cells.