ArticleMolecular neurodegeneration2008
Molecular signatures of neurodegeneration in the cortex of PS1/PS2 double knockout mice.
Article in Molecular neurodegeneration, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- Role of Tau Protein in Neurodegenerative Diseases and Development of Its Targeted Drugs: A Literature Review.Molecules (Basel, Switzerland) · 2024Review
- The Neuroepigenetic Landscape of Vertebrate and Invertebrate Models of Neurodegenerative Diseases.Epigenetics insights · 2022Review
- Patient-Derived Fibroblasts With Presenilin-1 Mutations, That Model Aspects of Alzheimer's Disease Pathology, Constitute a Potential Object for Early Diagnosis.Frontiers in aging neuroscience · 2022Article
- Genes and pathways associated with pregnancy loss in dairy cattle.Scientific reports · 2021Article
- Synthesis of α-Ketoamide-Based Stereoselective Calpain-1 Inhibitors as Neuroprotective Agents.ChemMedChem · 2020Article
- MicroRNA Profiling in Aging Brain of PSEN1/PSEN2 Double Knockout Mice.Molecular neurobiology · 2018Article
- Autophagy and Alzheimer's Disease: From Molecular Mechanisms to Therapeutic Implications.Frontiers in aging neuroscience · 2018Review
- Complement C3 deficiency protects against neurodegeneration in aged plaque-rich APP/PS1 mice.Science translational medicine · 2017Article
- Pyramidal cell selective ablation of N-methyl-D-aspartate receptor 1 causes increase in cellular and network excitability.Biological psychiatry · 2015Article
- Genes and pathways underlying regional and cell type changes in Alzheimer's disease.Genome medicine · 2013Article
- A role for presenilins in autophagy revisited: normal acidification of lysosomes in cells lacking PSEN1 and PSEN2.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Functional genomics of brain aging and Alzheimer's disease: focus on selective neuronal vulnerability.Current genomics · 2010Article
- Analysis of chaperone mRNA expression in the adult mouse brain by meta analysis of the Allen Brain Atlas.PloS one · 2010Article
- Amyloid precursor protein transgenic mouse models and Alzheimer's disease: understanding the paradigms, limitations, and contributions.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2009Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundFamilial Alzheimer's disease-linked variants of presenilin (PSEN1 and PSEN2) contribute to the pathophysiology of disease by both gain-of-function and loss-of-function mechanisms. Deletions of PSEN1 and PSEN2 in the mouse forebrain result in a strong and progressive neurodegenerative phenotype which is characterized by both anatomical and behavioral changes.
resultsTo better understand the molecular changes associated with these morphological and behavioral phenotypes, we performed a DNA microarray transcriptome profiling of the hippocampus and the frontal cortex of the PSEN1/PSEN2 double knock-out mice and littermate controls at five different ages ranging from 2-8 months. Our data suggest that combined deficiencies of PSEN1 and PSEN2 results in a progressive, age-dependent transcriptome signature related to neurodegeneration and neuroinflammation. While these events may progress differently in the hippocampus and frontal cortex, the most critical expression signatures are common across the two brain regions, and involve a strong upregulation of cathepsin and complement system transcripts.
conclusionThe observed neuroinflammatory expression changes are likely to be causally linked to the neurodegenerative phenotype observed in mice with compound deletions of PSEN1 and PSEN2. Furthermore, our results suggest that the evaluation of inhibitors of PS/gamma-secretase activity for treatment of Alzheimer's Disease must include close monitoring for signs of calpain-cathepsin system activation.
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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.