ArticleNeurobiology of disease2009
X11alpha haploinsufficiency enhances Abeta amyloid deposition in Alzheimer's disease transgenic mice.
Article in Neurobiology of disease, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 18 citations in OpenAlex.
- Haploinsufficiency and Alzheimer's Disease: The Possible Pathogenic and Protective Genetic Factors.International journal of molecular sciences · 2024Review
- Interrogation and validation of the interactome of neuronal Munc18-interacting Mint proteins with AlphaFold2.The Journal of biological chemistry · 2024Article
- Amyloid precursor protein and its interacting proteins in neurodevelopment.Biochemical Society transactions · 2023Review
- Targeting the APP-Mint2 Protein-Protein Interaction with a Peptide-Based Inhibitor Reduces Amyloid-β Formation.Journal of the American Chemical Society · 2021Article
- Genome-wide association study of rate of cognitive decline in Alzheimer's disease patients identifies novel genes and pathways.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2020Article
- Attenuation of amyloid-β generation by atypical protein kinase C-mediated phosphorylation of engulfment adaptor PTB domain containing 1 threonine 35.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- GULP1/CED-6 ameliorates amyloid-β toxicity in a Drosophila model of Alzheimer's disease.Oncotarget · 2017Article
- Amyloid-beta Alzheimer targets - protein processing, lipid rafts, and amyloid-beta pores.The Yale journal of biology and medicine · 2016Review
- Cytoplasmic fragment of Alcadein α generated by regulated intramembrane proteolysis enhances amyloid β-protein precursor (APP) transport into the late secretory pathway and facilitates APP cleavage.The Journal of biological chemistry · 2015Article
- Synergistic effects of hypertension and aging on cognitive function and hippocampal expression of genes involved in β-amyloid generation and Alzheimer's disease.American journal of physiology. Heart and circulatory physiology · 2013Article
- X11/Mint genes control polarized localization of axonal membrane proteins in vivo.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- A new Mint1 isoform, but not the conventional Mint1, interacts with the small GTPase Rab6.PloS one · 2013Article
- Activation of liver X receptor decreases BACE1 expression and activity by reducing membrane cholesterol levels.Neurochemical research · 2011Article
- Amyloid precursor protein processing and Alzheimer's disease.Annual review of neuroscience · 2011Review
- Increased amyloidogenic processing of transgenic human APP in X11-like deficient mouse brain.Molecular neurodegeneration · 2010Article
- Expression of the neuronal adaptor protein X11alpha protects against memory dysfunction in a transgenic mouse model of Alzheimer's disease.Journal of Alzheimer's disease : JAD · 2010Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The neuronal adaptor protein X11alpha/mint-1/APBA-1 binds to the cytoplasmic domain of the amyloid precursor protein (APP) to modulate its trafficking and metabolism. We investigated the consequences of reducing X11alpha in a mouse model of Alzheimer's disease (AD). We crossed hAPPswe/PS-1DeltaE9 transgenic (AD tg) mice with X11alpha heterozygous knockout mice in which X11alpha expression is reduced by approximately 50%. The APP C-terminal fragments C99 and C83, as well as soluble Abeta40 and Abeta42, were increased significantly in brain of X11alpha haploinsufficient mice. Abeta/amyloid plaque burden also increased significantly in the hippocampus and cortex of one year old AD tg/X11alpha (+/-) mice compared to AD tg mice. In contrast, the levels of sAPPalpha and sAPPbeta were not altered significantly in AD tg/X11alpha (+/-) mice. The increased neuropathological indices of AD in mice expressing reduced X11alpha suggest a normal suppressor role for X11alpha on CNS Abeta/amyloid deposition.
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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.