ArticleNeuron2016
Loss of Aβ43 Production Caused by Presenilin-1 Mutations in the Knockin Mouse Brain.
Article in Neuron, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06869941 (Adipose Tissue Gene Expression and Metabolomics Links to the Gut Microbiome-brain Axis), which is not on this map. Cited by 28 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.
The trial behind it
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.
Adipose Tissue Gene Expression and Metabolomics Links to the Gut Microbiome-brain Axis (POINSETTIA Study)
Who cites it
28 citing papers in PubMed, 32 citations in OpenAlex.
- Cortical neurodegeneration caused byProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Lipophorin receptors genetically modulate neurodegeneration caused by reduction of Psn expression in the aging Drosophila brain.Genetics · 2024Article
- Towards a Unitary Hypothesis of Alzheimer's Disease Pathogenesis.Journal of Alzheimer's disease : JAD · 2024Article
- Article
- 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
- Developing a Gene Therapy for the Treatment of Autosomal Dominant Alzheimer's Disease.Human gene therapy · 2023Article
- Selective ferroptosis vulnerability due to familial Alzheimer's disease presenilin mutations.Cell death and differentiation · 2022Article
- PSEN2 Thr421Met Mutation in a Patient with Early Onset Alzheimer's Disease.International journal of molecular sciences · 2022Article
- Genetics, Functions, and Clinical Impact of Presenilin-1 (PSEN1) Gene.International journal of molecular sciences · 2022Review
- NeuroProtect, a Candidate Formula From Traditional Chinese Medicine, Attenuates Amyloid-Frontiers in pharmacology · 2022Article
- Exploring the Role of PSEN Mutations in the Pathogenesis of Alzheimer's Disease.Neurotoxicity research · 2020Review
- [Progress on loss-of-function hypothesis of presenilin-1 mutations in Alzheimer diseases].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2020Article
- The Alzheimer Disease-Causing Presenilin-1 L435F Mutation Causes Increased Production of Soluble Aβ43 Species in Patient-Derived iPSC-Neurons, Closely Mimicking Matched Patient Brain Tissue.Journal of neuropathology and experimental neurology · 2020Article
- Pathogenic PSEN1 Glu184Gly Mutation in a Family from Thailand with Probable Autosomal Dominant Early Onset Alzheimer's Disease.Diagnostics (Basel, Switzerland) · 2020Article
- Amyloid precursor protein processing in human neurons with an allelic series of theBrain communications · 2019Article
- Dysregulation of Intracellular Calcium Signaling in Alzheimer's Disease.Antioxidants & redox signaling · 2018Review
- Autophagy in Age-Associated Neurodegeneration.Cells · 2018Review
- The genes associated with early-onset Alzheimer's disease.Oncotarget · 2018Review
- Integration of Drosophila and Human Genetics to Understand Notch Signaling Related Diseases.Advances in experimental medicine and biology · 2018Review
- The role of astrocytes in amyloid production and Alzheimer's disease.Open biology · 2017Review
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Authors and funding
3 authors at 2 institutions in 1 country.
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Abstract
We recently reported that homozygous Presenilin-1 (Psen1) knockin (KI) mice carrying the familial Alzheimer's disease (FAD) mutation L435F or C410Y recapitulate the phenotypes of Psen1(-/-) mice. Production and steady-state levels of Aβ40 and Aβ42 are undetectable in KI/KI brains and reduced in KI/+ brains, though the Aβ42/Aβ40 ratio is slightly increased in KI/+ brains. Moreover, the FAD mutation impairs synaptic function, learning and memory, and age-dependent neuronal survival in the adult brain. Here we extend our analysis of the effects of the L435F and C410Y mutations to the generation of Aβ43. Similar to Aβ40 and Aβ42, production of Aβ43 is undetectable in KI/KI brains and reduced in KI/+ brains. These results support our previous conclusions that the L435F and C410Y mutations cause loss of Presenilin function and γ-secretase activity, including impaired Aβ production in the brain. This Matters Arising Response paper addresses the Veugelen et al. (2016) Matters Arising paper, published concurrently in Neuron.
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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.