ArticleProceedings of the National Academy of Sciences of the United States of America2004
Forebrain degeneration and ventricle enlargement caused by double knockout of Alzheimer's presenilin-1 and presenilin-2.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 123 citations in OpenAlex.
- Targeting the PDK1/c-Myc/SOX10 Signaling in Oligodendrocytes Alleviates Neuropathic Pain.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Presenilin Loss Impairs Synaptic Transmission and Causes Axonal Degeneration through Ryanodine Receptor Dysfunction, Independent of γ-Secretase Activity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Kv1.1 channel dysfunction in parvalbumin-positive interneurons contributes to anxiety-like behaviors in young adult presenilin 1/2 conditional double knockout mice.Cell & bioscience · 2025Article
- Cortical neurodegeneration caused byProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Age- and Genotype-Dependent Effects of Chronic Nicotine on Presenilin1/2 Double Knockout Mice: From Behavior to Molecular Pathways.Current Alzheimer research · 2024Article
- Human Presenilin-1 delivered by AAV9 rescues impaired γ-secretase activity, memory deficits, and neurodegeneration inProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Spatiotemporal patterns of gliosis and neuroinflammation in presenilin 1/2 conditional double knockout mice.Frontiers in aging neuroscience · 2022Article
- TM2D genes regulate Notch signaling and neuronal function in Drosophila.PLoS genetics · 2021Article
- Urinary metabolomic changes and microbiotic alterations in presenilin1/2 conditional double knockout mice.Journal of translational medicine · 2021Article
- Neuron-specific deletion of presenilin enhancer2 causes progressive astrogliosis and age-related neurodegeneration in the cortex independent of the Notch signaling.CNS neuroscience & therapeutics · 2021Article
- Electroacupuncture Ameliorates Neuroinflammation-Mediated Cognitive Deficits through Inhibition of NLRP3 in Presenilin1/2 Conditional Double Knockout Mice.Neural plasticity · 2021Article
- Cell-autonomous role of Presenilin in age-dependent survival of cortical interneurons.Molecular neurodegeneration · 2020Article
- Dexamethasone does not ameliorate gliosis in a mouse model of neurodegenerative disease.Biochemistry and biophysics reports · 2020Article
- Bayesian Scalar on Image Regression With Nonignorable Nonresponse.Journal of the American Statistical Association · 2020Article
- Rodent models for Alzheimer disease.Nature reviews. Neuroscience · 2018Review
- The genes associated with early-onset Alzheimer's disease.Oncotarget · 2018Review
- Unraveling Novel Mechanisms of Neurodegeneration Through a Large-Scale Forward Genetic Screen inFrontiers in genetics · 2018Review
- Histone Deacetylase Inhibitor Alleviates the Neurodegenerative Phenotypes and Histone Dysregulation in Presenilins-Deficient Mice.Frontiers in aging neuroscience · 2018Article
- Dominant negative mechanism ofProceedings of the National Academy of Sciences of the United States of America · 2017Article
- Increased adult neurogenesis associated with reactive astrocytosis occurs prior to neuron loss in a mouse model of neurodegenerative disease.CNS neuroscience & therapeutics · 2017Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Early-onset familial Alzheimer's disease is the most aggressive form of Alzheimer's, striking patients as early as their 30s; those patients typically carry mutations in presenilin-1 and presenilin-2. To investigate the coordinated functions of presenilin in the adult brain, we generated double knockout mice, in which both presenilins were deleted in the forebrain. We found that concurrent loss of presenilins in adulthood resulted in massive cortical shrinkage, atrophy of hippocampal molecular layers and corpus callosum, and enlargement of the lateral and third ventricles. We further revealed that deficiency of presenilins caused a series of biochemical alterations, including neuronal atrophy, astrogliosis, caspase-3-mediated apoptosis, and tau hyperphosphorylation. Thus, our study demonstrates that presenilins are essential for the ongoing maintenance of cortical structures and function.
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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.