ArticleNeurobiology of aging2010
Differential cerebral deposition of IDE and NEP in sporadic and familial Alzheimer's disease.
Article in Neurobiology of aging, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.
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Who cites it
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 91 citations in OpenAlex.
- Systematic review of human post-mortem immunohistochemical studies and bioinformatics analyses unveil the complexity of astrocyte reaction in Alzheimer's disease.Neuropathology and applied neurobiology · 2022Pooled it
- Anxiolytic and Memory Protective Effects of Withanolide D Isolated From Acnistus arborescens in Adult Zebrafish.Chemistry & biodiversity · 2026Article
- Amyloid-Frontiers in neuroscience · 2026Review
- Potential Mitochondria-Related Key Genes in Post-Traumatic Stress Disorder Analyzed by Machine Learning Methods.Neuropsychiatric disease and treatment · 2025Article
- Clearing Amyloid-Beta by Astrocytes: The Role of Rho GTPases Signaling Pathways as Potential Therapeutic Targets.Brain sciences · 2024Review
- Pharmacological inhibition of receptor protein tyrosine phosphatase β/ζ decreases Aβ plaques and neuroinflammation in the hippocampus of APP/PS1 mice.Frontiers in pharmacology · 2024Article
- Inhibition of insulin-degrading enzyme in human neurons promotes amyloid-β deposition.Neuronal signaling · 2023Article
- Article
- Insulin-degrading enzyme (IDE) as a modulator of microglial phenotypes in the context of Alzheimer's disease and brain aging.Journal of neuroinflammation · 2023Article
- Ferulic Acid Improves Synaptic Plasticity and Cognitive Impairments by Alleviating the PP2B/DARPP-32/PP1 Axis-Mediated STEP Increase and Aβ Burden in Alzheimer's Disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Article
- BACE1 regulates expression of Clusterin in astrocytes for enhancing clearance of β-amyloid peptides.Molecular neurodegeneration · 2023Article
- Astrocytes deficient in circadian clock gene Bmal1 show enhanced activation responses to amyloid-beta pathology without changing plaque burden.Scientific reports · 2022Article
- Ginsenoside F1 Protects the Brain against Amyloid Beta-Induced Toxicity by Regulating IDE and NEP.Life (Basel, Switzerland) · 2022Article
- A Comprehensive Machine Learning Framework for the Exact Prediction of the Age of Onset in Familial and Sporadic Alzheimer's Disease.Diagnostics (Basel, Switzerland) · 2021Article
- Rho-kinase inhibitor hydroxyfasudil protects against HIV-1 Tat-induced dysfunction of tight junction and neprilysin/Aβ transfer receptor expression in mouse brain microvessels.Molecular and cellular biochemistry · 2021Article
- Altered expression of insulin-degrading enzyme and regulator of calcineurin in the rat intracerebral streptozotocin model and human apolipoprotein E-ε4-associated Alzheimer's disease.Alzheimer's & dementia (Amsterdam, Netherlands) · 2019Article
- Oxidative inactivation of amyloid beta-degrading proteases by cholesterol-enhanced mitochondrial stress.Redox biology · 2019Article
- Activation of microglia and astrocytes: a roadway to neuroinflammation and Alzheimer's disease.Inflammopharmacology · 2019Review
- CIP2A-promoted astrogliosis induces AD-like synaptic degeneration and cognitive deficits.Neurobiology of aging · 2019Article
- Astroglia in Alzheimer's Disease.Advances in experimental medicine and biology · 2019Review
Corrections and comments
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Authors and funding
9 authors at 7 institutions in 3 countries.
Funding
Abstract
Alzheimer's disease (AD) is characterized by amyloid beta (A beta) accumulation in the brain and is classified as familial early-onset (FAD) or sporadic late-onset (SAD). Evidences suggest that deficits in the brain expression of insulin degrading enzyme (IDE) and neprilysin (NEP), both proteases involved in amyloid degradation, may promote A beta deposition in SAD. We studied by immunohistochemistry IDE and NEP cortical expression in SAD and FAD samples carrying the E280A presenilin-1 missense mutation. We showed that IDE, a soluble peptidase, is linked with aggregated A beta 40 isoform while NEP, a membrane-bound protease, negatively correlates with amyloid angiopathy and its expression in the senile plaques is independent of aggregated amyloid and restricted to SAD cases. NEP, but not IDE, is over-expressed in dystrophic neurites, both proteases are immunoreactive in activated astrocytes but not in microglia and IDE was the only one detected in astrocytes of white matter from FAD cases. Collectively, our results support the notion that gross conformational changes involved in the modification from "natively folded-active" to "aggregated-inactive" IDE and NEP may be a relevant pathogenic mechanism in SAD.
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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.