ArticleMolecular psychiatry2014
Chronic γ-secretase inhibition reduces amyloid plaque-associated instability of pre- and postsynaptic structures.
Article in Molecular psychiatry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 37 citations in OpenAlex.
- Direct evidence for dendritic spine compensation and regeneration in Alzheimer's disease models.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Repetitive transcranial magnetic stimulation increases synaptic plasticity of cortical axons in the APP/PS1 amyloidosis mouse model.Neurophotonics · 2025Article
- Synaptic Compensatory Plasticity in Alzheimer's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Review
- Selective plasticity of callosal neurons in the adult contralesional cortex following murine traumatic brain injury.Nature communications · 2022Article
- Long-term dynamics of aberrant neuronal activity in awake Alzheimer's disease transgenic mice.Communications biology · 2021Article
- The synapse in traumatic brain injury.Brain : a journal of neurology · 2021Review
- Anti-Inflammatory Treatment with FTY720 Starting after Onset of Symptoms Reverses Synaptic Deficits in an AD Mouse Model.International journal of molecular sciences · 2020Article
- Chronic Presence of Oligomeric Aβ Differentially Modulates Spine Parameters in the Hippocampus and Cortex of Mice With Low APP Transgene Expression.Frontiers in synaptic neuroscience · 2020Article
- Hippocampal Deficits in Amyloid-β-Related Rodent Models of Alzheimer's Disease.Frontiers in neuroscience · 2020Review
- Synaptic Loss in Alzheimer's Disease: Mechanistic Insights Provided by Two-PhotonFrontiers in cellular neuroscience · 2020Review
- EphA4 loss improves social memory performance and alters dendritic spine morphology without changes in amyloid pathology in a mouse model of Alzheimer's disease.Alzheimer's research & therapy · 2019Article
- Bispecific Antibody Fragment Targeting APP and Inducing α-Site Cleavage Restores Neuronal Health in an Alzheimer's Mouse Model.Molecular neurobiology · 2019Article
- Imbalance in the response of pre- and post-synaptic components to amyloidopathy.Scientific reports · 2019Article
- Disruption of NOTCH signaling by a small molecule inhibitor of the transcription factor RBPJ.Scientific reports · 2019Article
- The Role of Glial Cells and Synapse Loss in Mouse Models of Alzheimer's Disease.Frontiers in cellular neuroscience · 2018Review
- Early Activation of Experience-Independent Dendritic Spine Turnover in a Mouse Model of Alzheimer's Disease.Cerebral cortex (New York, N.Y. : 1991) · 2017Article
- Substrate recruitment of γ-secretase and mechanism of clinical presenilin mutations revealed by photoaffinity mapping.The EMBO journal · 2016Article
- EPBscore: a Novel Method for Computer-Assisted Analysis of Axonal Structure and Dynamics.Neuroinformatics · 2016Article
- Amyloid-PET predicts inhibition of de novo plaque formation upon chronic γ-secretase modulator treatment.Molecular psychiatry · 2015Article
- A conformation-specific antibody against oligomeric β-amyloid restores neuronal integrity in a mouse model of Alzheimer's disease.The Journal of biological chemistryArticle
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 2 countries.
Funding
Abstract
The loss of synapses is a strong histological correlate of the cognitive decline in Alzheimer's disease (AD). Amyloid β-peptide (Aβ), a cleavage product of the amyloid precursor protein (APP), exerts detrimental effects on synapses, a process thought to be causally related to the cognitive deficits in AD. Here, we used in vivo two-photon microscopy to characterize the dynamics of axonal boutons and dendritic spines in APP/Presenilin 1 (APP(swe)/PS1(L166P))-green fluorescent protein (GFP) transgenic mice. Time-lapse imaging over 4 weeks revealed a pronounced, concerted instability of pre- and postsynaptic structures within the vicinity of amyloid plaques. Treatment with a novel sulfonamide-type γ-secretase inhibitor (GSI) attenuated the formation and growth of new plaques and, most importantly, led to a normalization of the enhanced dynamics of synaptic structures close to plaques. GSI treatment did neither affect spines and boutons distant from plaques in amyloid precursor protein/presenilin 1-GFP (APPPS1-GFP) nor those in GFP-control mice, suggesting no obvious neuropathological side effects of the drug.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.