ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2013
Increased amyloid-β peptide-induced memory deficits in phospholipid transfer protein (PLTP) gene knockout mice.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 46 citations in OpenAlex.
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- Repercussion of Primary Nucleation Pathway: Dementia and Cognitive Impairment.Current aging science · 2024Review
- Vitamin E and Its Molecular Effects in Experimental Models of Neurodegenerative Diseases.International journal of molecular sciences · 2023Review
- The Role of Dietary Antioxidants and Their Potential Mechanisms in Alzheimer's Disease Treatment.Metabolites · 2023Review
- Arc Regulates Transcription of Genes for Plasticity, Excitability and Alzheimer's Disease.Biomedicines · 2022Article
- Chronic Stress and Oxidative Stress as Common Factors of the Pathogenesis of Depression and Alzheimer's Disease: The Role of Antioxidants in Prevention and Treatment.Antioxidants (Basel, Switzerland) · 2021Review
- The Role of Phospholipid Transfer Protein in the Development of Atherosclerosis.Current atherosclerosis reports · 2021Review
- Impact of Phospholipid Transfer Protein in Lipid Metabolism and Cardiovascular Diseases.Advances in experimental medicine and biology · 2020Review
- Phospholipid transfer protein: its impact on lipoprotein homeostasis and atherosclerosis.Journal of lipid research · 2018Review
- Deletion of plasmaOncotarget · 2018Article
- Altered Insulin/Insulin-Like Growth Factor Signaling in a Comorbid Rat model of Ischemia and β-Amyloid Toxicity.Scientific reports · 2018Article
- Role of Vitamin E in the Treatment of Alzheimer's Disease: Evidence from Animal Models.International journal of molecular sciences · 2017Review
- Plasma cholesterol level determines in vivo prion propagation.Journal of lipid research · 2017Article
- Toxin-Induced Experimental Models of Learning and Memory Impairment.International journal of molecular sciences · 2016Review
- Overnutrition Determines LPS Regulation of Mycotoxin Induced Neurotoxicity in Neurodegenerative Diseases.International journal of molecular sciences · 2015Review
- Epidemic spreading model to characterize misfolded proteins propagation in aging and associated neurodegenerative disorders.PLoS computational biology · 2014Article
- Vitamin E inadequacy in humans: causes and consequences.Advances in nutrition (Bethesda, Md.) · 2014Review
- Phospholipid transfer protein is expressed in cerebrovascular endothelial cells and involved in high density lipoprotein biogenesis and remodeling at the blood-brain barrier.The Journal of biological chemistry · 2014Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidative stress is recognized as one of the earliest and most intense pathological processes in Alzheimer's disease (AD), and the antioxidant vitamin E has been shown to efficiently prevent amyloid plaque formation and neurodegeneration. Plasma phospholipid transfer protein (PLTP) has a major role in vitamin E transfers in vivo, and PLTP deficiency in mice is associated with reduced brain vitamin E levels. To determine the impact of PLTP on amyloid pathology in vivo, we analyzed the vulnerability of PLTP-deficient (PLTP-KO) mice to the toxic effects induced by intracerebroventricular injection of oligomeric amyloid-β 25-35 (Aβ 25-35) peptide, a non-transgenic model of AD. Under basal conditions, PLTP-KO mice showed increased cerebral oxidative stress, increased brain Aβ 1-42 levels, and a lower expression of the synaptic function marker synaptophysin, as compared with wild-type mice. This PLTP-KO phenotype was associated with increased memory impairment 1 week after Aβ25-35 peptide injection. Restoration of brain vitamin E levels in PLTP-KO mice through a chronic dietary supplementation prevented Aβ 25-35-induced memory deficits and reduced cerebral oxidative stress and toxicity. We conclude that PLTP, through its ability to deliver vitamin E to the brain, constitutes an endogenous neuroprotective agent. Increasing PLTP activity may offer a new way to develop neuroprotective therapies.
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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.