Ronald E. van Kesteren
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View article: Progressive remote memory decline coincides with parvalbumin interneuron hyperexcitability and enhanced inhibition of cortical engram cells in a mouse model of Alzheimer’s disease
Progressive remote memory decline coincides with parvalbumin interneuron hyperexcitability and enhanced inhibition of cortical engram cells in a mouse model of Alzheimer’s disease Open
Patients with Alzheimer’s disease (AD) initially show temporally-graded retrograde amnesia, which gradually progresses into more severe retrograde amnesia. Although mouse models of AD have provided insight into neurobiological mechanisms c…
View article: Author response: Progressive remote memory decline coincides with parvalbumin interneuron hyperexcitability and enhanced inhibition of cortical engram cells in a mouse model of Alzheimer’s disease
Author response: Progressive remote memory decline coincides with parvalbumin interneuron hyperexcitability and enhanced inhibition of cortical engram cells in a mouse model of Alzheimer’s disease Open
View article: One-step induction of human GABAergic neurons promotes presynaptic development & synapse maturation
One-step induction of human GABAergic neurons promotes presynaptic development & synapse maturation Open
Human induced pluripotent stem cells (iPSCs) present a powerful approach to study human brain physiology and disease, yet robust, pure GABAergic induction has remained difficult. Here we present improved, single-step, transposon-based GABA…
View article: Progressive remote memory decline coincides with parvalbumin interneuron hyperexcitability and enhanced inhibition of cortical engram cells in a mouse model of Alzheimer’s disease
Progressive remote memory decline coincides with parvalbumin interneuron hyperexcitability and enhanced inhibition of cortical engram cells in a mouse model of Alzheimer’s disease Open
Patients with Alzheimer’s disease (AD) initially show temporally graded retrograde amnesia, which gradually progresses into more severe retrograde amnesia. Although mouse models of AD have provided insight into neurobiological mechanisms c…
View article: Progressive remote memory decline coincides with parvalbumin interneuron hyperexcitability and enhanced inhibition of cortical engram cells in a mouse model of Alzheimer’s disease
Progressive remote memory decline coincides with parvalbumin interneuron hyperexcitability and enhanced inhibition of cortical engram cells in a mouse model of Alzheimer’s disease Open
Patients with Alzheimer’s disease (AD) initially show temporally-graded retrograde amnesia, which gradually progresses into more severe retrograde amnesia. Although mouse models of AD have provided insight into neurobiological mechanisms c…
View article: Progressive remote memory decline coincides with parvalbumin interneuron hyperexcitability and enhanced inhibition of cortical engram cells in a mouse model of Alzheimer’s disease
Progressive remote memory decline coincides with parvalbumin interneuron hyperexcitability and enhanced inhibition of cortical engram cells in a mouse model of Alzheimer’s disease Open
Patients with Alzheimer’s disease (AD) initially show temporally-graded retrograde amnesia, which gradually progresses into more severe retrograde amnesia. Although mouse models of AD have provided insight into neurobiological mechanisms c…
View article: The transcription factor combination MEF2 and KLF7 promotes axonal sprouting in the injured spinal cord with functional improvement and regeneration-associated gene expression
The transcription factor combination MEF2 and KLF7 promotes axonal sprouting in the injured spinal cord with functional improvement and regeneration-associated gene expression Open
Background Axon regeneration after injury to the central nervous system (CNS) is limited by an inhibitory environment but also because injured neurons fail to initiate expression of regeneration associated genes (RAGs). The potential of st…
View article: Hippocampal and cortical activities reflect early hyperexcitability in an Alzheimer's mouse model
Hippocampal and cortical activities reflect early hyperexcitability in an Alzheimer's mouse model Open
Early stages of Alzheimer's disease are marked by brain hyperexcitability, evidenced by subclinical epileptiform features suggesting an excitation–inhibition imbalance. Clinically translatable biomarkers for early detection of excitation–i…
View article: How Can Early Stress Influence Later Alzheimer's Disease Risk? Possible Mediators and Underlying Mechanisms
How Can Early Stress Influence Later Alzheimer's Disease Risk? Possible Mediators and Underlying Mechanisms Open
View article: Continuous locomotor activity monitoring to assess animal welfare following intracranial surgery in mice
Continuous locomotor activity monitoring to assess animal welfare following intracranial surgery in mice Open
Locomotor activity can serve as a readout to identify discomfort and pain. Therefore, monitoring locomotor activity following interventions that induce potential discomfort may serve as a reliable method for evaluating animal health, compl…
View article: Torpor induces reversible tau hyperphosphorylation and accumulation in mice expressing human tau
Torpor induces reversible tau hyperphosphorylation and accumulation in mice expressing human tau Open
View article: Functional network disruption in cognitively unimpaired autosomal dominant Alzheimer’s disease: a magnetoencephalography study
Functional network disruption in cognitively unimpaired autosomal dominant Alzheimer’s disease: a magnetoencephalography study Open
Understanding the nature and onset of neurophysiological changes, and the selective vulnerability of central hub regions in the functional network, may aid in managing the growing impact of Alzheimer’s disease on society. However, the prec…
View article: Mitochondrial Targeting against Alzheimer’s Disease: Lessons from Hibernation
Mitochondrial Targeting against Alzheimer’s Disease: Lessons from Hibernation Open
Alzheimer’s disease (AD) is the most common cause of dementia worldwide and yet remains without effective therapy. Amongst the many proposed causes of AD, the mitochondrial cascade hypothesis is gaining attention. Accumulating evidence sho…
View article: Neurophysiological alterations in mice and humans carrying mutations in <i>APP</i> and <i>PSEN1</i> genes
Neurophysiological alterations in mice and humans carrying mutations in <i>APP</i> and <i>PSEN1</i> genes Open
Background Studies in animal models of Alzheimer’s disease (AD) have provided valuable insights into the molecular and cellular processes underlying neuronal network dysfunction, but whether and how AD‐related neurophysiological alteration…
View article: Interneuron hyperexcitability in an APP/PS1 mouse model of Alzheimer’s disease
Interneuron hyperexcitability in an APP/PS1 mouse model of Alzheimer’s disease Open
Background Neuronal hyperexcitability is commonly observed in Alzheimer’s disease (AD) patients and in mouse models of AD. What is not clear yet is whether hyperexcitability occurs in all neurons or whether certain types of neurons are sel…
View article: Neurophysiological alterations in mice and humans carrying mutations in APP and PSEN1 genes
Neurophysiological alterations in mice and humans carrying mutations in APP and PSEN1 genes Open
View article: Fast-spiking parvalbumin-positive interneurons in brain physiology and Alzheimer’s disease
Fast-spiking parvalbumin-positive interneurons in brain physiology and Alzheimer’s disease Open
View article: Single-cell RNA sequencing data reveals rewiring of transcriptional relationships in Alzheimer’s Disease associated with risk variants
Single-cell RNA sequencing data reveals rewiring of transcriptional relationships in Alzheimer’s Disease associated with risk variants Open
Understanding how genetic risk variants contribute to Alzheimer’s Disease etiology remains a challenge. Single-cell RNA sequencing (scRNAseq) allows for the investigation of cell type specific effects of genomic risk loci on gene expressio…
View article: Resting-state oscillations reveal disturbed excitation–inhibition ratio in Alzheimer’s disease patients
Resting-state oscillations reveal disturbed excitation–inhibition ratio in Alzheimer’s disease patients Open
View article: Additional file 14 of The hibernation-derived compound SUL-138 shifts the mitochondrial proteome towards fatty acid metabolism and prevents cognitive decline and amyloid plaque formation in an Alzheimer’s disease mouse model
Additional file 14 of The hibernation-derived compound SUL-138 shifts the mitochondrial proteome towards fatty acid metabolism and prevents cognitive decline and amyloid plaque formation in an Alzheimer’s disease mouse model Open
Additional file 14: Supplementary dataset 3. GO analysis of protein dysregulation in the hippocampus due to disease (APP/PS1 mice compared to wildtype controls - APP VEH vs. WT VEH); significantly up regulated group.
View article: Additional file 20 of The hibernation-derived compound SUL-138 shifts the mitochondrial proteome towards fatty acid metabolism and prevents cognitive decline and amyloid plaque formation in an Alzheimer’s disease mouse model
Additional file 20 of The hibernation-derived compound SUL-138 shifts the mitochondrial proteome towards fatty acid metabolism and prevents cognitive decline and amyloid plaque formation in an Alzheimer’s disease mouse model Open
Additional file 20: Supplementary dataset 9. SynGO annotation of significantly regulated proteins in the WT VEH vs. APP VEH comparison.
View article: Additional file 19 of The hibernation-derived compound SUL-138 shifts the mitochondrial proteome towards fatty acid metabolism and prevents cognitive decline and amyloid plaque formation in an Alzheimer’s disease mouse model
Additional file 19 of The hibernation-derived compound SUL-138 shifts the mitochondrial proteome towards fatty acid metabolism and prevents cognitive decline and amyloid plaque formation in an Alzheimer’s disease mouse model Open
Additional file 19: Supplementary dataset 8. GO analysis of SUL-138-regulated proteins overlapping with proteins affected in APP/PS1 mice; significantly up regulated group.
View article: Additional file 16 of The hibernation-derived compound SUL-138 shifts the mitochondrial proteome towards fatty acid metabolism and prevents cognitive decline and amyloid plaque formation in an Alzheimer’s disease mouse model
Additional file 16 of The hibernation-derived compound SUL-138 shifts the mitochondrial proteome towards fatty acid metabolism and prevents cognitive decline and amyloid plaque formation in an Alzheimer’s disease mouse model Open
Additional file 16: Supplementary dataset 5. GO analysis of hippocampal protein regulation as a result of 3 months of SUL-138 treatment in APP/PS1 mice (APP SUL vs. APP VEH); significantly up regulated group.
View article: Additional file 21 of The hibernation-derived compound SUL-138 shifts the mitochondrial proteome towards fatty acid metabolism and prevents cognitive decline and amyloid plaque formation in an Alzheimer’s disease mouse model
Additional file 21 of The hibernation-derived compound SUL-138 shifts the mitochondrial proteome towards fatty acid metabolism and prevents cognitive decline and amyloid plaque formation in an Alzheimer’s disease mouse model Open
Additional file 21: Supplementary dataset 10. SynGO annotation of significantly regulated proteins in the APP VEH vs. APP SUL comparison.
View article: Additional file 17 of The hibernation-derived compound SUL-138 shifts the mitochondrial proteome towards fatty acid metabolism and prevents cognitive decline and amyloid plaque formation in an Alzheimer’s disease mouse model
Additional file 17 of The hibernation-derived compound SUL-138 shifts the mitochondrial proteome towards fatty acid metabolism and prevents cognitive decline and amyloid plaque formation in an Alzheimer’s disease mouse model Open
Additional file 17: Supplementary dataset 6. GO analysis of SUL-138-regulated proteins overlapping with proteins affected in APP/PS1 mice.
View article: Additional file 18 of The hibernation-derived compound SUL-138 shifts the mitochondrial proteome towards fatty acid metabolism and prevents cognitive decline and amyloid plaque formation in an Alzheimer’s disease mouse model
Additional file 18 of The hibernation-derived compound SUL-138 shifts the mitochondrial proteome towards fatty acid metabolism and prevents cognitive decline and amyloid plaque formation in an Alzheimer’s disease mouse model Open
Additional file 18: Supplementary dataset 7. GO analysis of SUL-138-regulated proteins overlap with proteins affected in APP/PS1 mice; significantly down regulated group.
View article: Additional file 23 of The hibernation-derived compound SUL-138 shifts the mitochondrial proteome towards fatty acid metabolism and prevents cognitive decline and amyloid plaque formation in an Alzheimer’s disease mouse model
Additional file 23 of The hibernation-derived compound SUL-138 shifts the mitochondrial proteome towards fatty acid metabolism and prevents cognitive decline and amyloid plaque formation in an Alzheimer’s disease mouse model Open
Additional file 23: Supplementary dataset 12. Mitocarta and mitoXplorer data analysis.
View article: Additional file 12 of The hibernation-derived compound SUL-138 shifts the mitochondrial proteome towards fatty acid metabolism and prevents cognitive decline and amyloid plaque formation in an Alzheimer’s disease mouse model
Additional file 12 of The hibernation-derived compound SUL-138 shifts the mitochondrial proteome towards fatty acid metabolism and prevents cognitive decline and amyloid plaque formation in an Alzheimer’s disease mouse model Open
Additional file 12: Supplementary dataset 1. differential expression analysis (DEA).
View article: Additional file 15 of The hibernation-derived compound SUL-138 shifts the mitochondrial proteome towards fatty acid metabolism and prevents cognitive decline and amyloid plaque formation in an Alzheimer’s disease mouse model
Additional file 15 of The hibernation-derived compound SUL-138 shifts the mitochondrial proteome towards fatty acid metabolism and prevents cognitive decline and amyloid plaque formation in an Alzheimer’s disease mouse model Open
Additional file 15: Supplementary dataset 4. GO analysis of hippocampal protein regulation as a result of 3 months of SUL-138 treatment in APP/PS1 mice (APP SUL vs. APP VEH); significantly down regulated group.
View article: Additional file 13 of The hibernation-derived compound SUL-138 shifts the mitochondrial proteome towards fatty acid metabolism and prevents cognitive decline and amyloid plaque formation in an Alzheimer’s disease mouse model
Additional file 13 of The hibernation-derived compound SUL-138 shifts the mitochondrial proteome towards fatty acid metabolism and prevents cognitive decline and amyloid plaque formation in an Alzheimer’s disease mouse model Open
Additional file 13: Supplementary dataset 2. GO analysis of protein dysregulation in the hippocampus due to disease (APP/PS1 mice compared to wildtype controls - APP VEH vs. WT VEH); significantly down regulated group.