ArticleScientific reports2019
BACE1 partial deletion induces synaptic plasticity deficit in adult mice.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 29 citations in OpenAlex.
- 3D multi-omics tumour atlases: from technology to biology and clinical translation.Nature reviews. Cancer · 2026Review
- Intranasal administration of neural stem cell-derived extracellular vesicles prevents cognitive decline in both male and female 3×Tg-AD mice by dampening neuroinflammation and epigenetically regulating amyloid β metabolism.Alzheimer's research & therapy · 2026Article
- Convergence and divergence of molecular mechanisms in Hebbian and homeostatic plasticity.Frontiers in synaptic neuroscience · 2026Review
- BACE1 Expression Is Required for Proper Synaptic Vesicle Dynamics in the Hippocampus.Journal of neurochemistry · 2025Article
- Contribution of amyloid deposition from oligodendrocytes in a mouse model of Alzheimer's disease.Molecular neurodegeneration · 2024Article
- Taming microglia: the promise of engineered microglia in treating neurological diseases.Journal of neuroinflammation · 2024Review
- Physiological Roles of β-amyloid in Regulating Synaptic Function: Implications for AD Pathophysiology.Neuroscience bulletin · 2023Review
- Cytosolic calcium: Judge, jury and executioner of neurodegeneration in Alzheimer's disease and beyond.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023Review
- BACE1 regulates expression of Clusterin in astrocytes for enhancing clearance of β-amyloid peptides.Molecular neurodegeneration · 2023Article
- Postnatal neuronal Bace1 deletion impairs neuroblast and oligodendrocyte maturation.Human molecular genetics · 2023Article
- Amyloid-β in Alzheimer's disease - front and centre after all?Neuronal signaling · 2023Review
- The BACE1-generated C-terminal fragment of the neural cell adhesion molecule 2 (NCAM2) promotes BACE1 targeting to Rab11-positive endosomes.Cellular and molecular life sciences : CMLS · 2022Article
- miR-212-3p attenuates neuroinflammation of rats with Alzheimer's disease via regulating the SP1/BACE1/NLRP3/Caspase-1 signaling pathway.Bosnian journal of basic medical sciences · 2022Article
- Targeted BACE-1 inhibition in microglia enhances amyloid clearance and improved cognitive performance.Science advances · 2022Article
- Neuronal KCNQ2/3 channels are recruited to lipid raft microdomains by palmitoylation of BACE1.The Journal of general physiology · 2022Article
- Meprin β knockout reduces brain Aβ levels and rescues learning and memory impairments in the APP/lon mouse model for Alzheimer's disease.Cellular and molecular life sciences : CMLS · 2022Article
- The case for low-level BACE1 inhibition for the prevention of Alzheimer disease.Nature reviews. Neurology · 2021Review
- BACE1 controls synaptic function through modulating release of synaptic vesicles.Molecular psychiatry · 2021Article
- BACE inhibitor treatment of mice induces hyperactivity in a Seizure-related gene 6 family dependent manner without altering learning and memory.Scientific reports · 2021Article
- The physiological roles of tau and Aβ: implications for Alzheimer's disease pathology and therapeutics.Acta neuropathologica · 2020Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
BACE1 is the first enzyme involved in APP processing, thus it is a strong therapeutic target candidate for Alzheimer's disease. The observation of deleterious phenotypes in BACE1 Knock-out (KO) mouse models (germline and conditional) raised some concerns on the safety and tolerability of BACE1 inhibition. Here, we have employed a tamoxifen inducible BACE1 conditional Knock-out (cKO) mouse model to achieve a controlled partial depletion of BACE1 in adult mice. Biochemical and behavioural characterization was performed at two time points: 4-5 months (young mice) and 12-13 months (aged mice). A ~50% to ~70% BACE1 protein reduction in hippocampus and cortex, respectively, induced a significant reduction of BACE1 substrates processing and decrease of Aβx-40 levels at both ages. Hippocampal axonal guidance and peripheral nerve myelination were not affected. Aged mice displayed a CA1 long-term potentiation (LTP) deficit that was not associated with memory impairment. Our findings indicate that numerous phenotypes observed in germline BACE1 KO reflect a fundamental role of BACE1 during development while other phenotypes, observed in adult cKO, may be absent when partially rather than completely deleting BACE1. However, we demonstrated that partial depletion of BACE1 still induces CA1 LTP impairment, supporting a role of BACE1 in synaptic plasticity in adulthood.
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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.