ArticleFrontiers in aging neuroscience2014
Deciphering the molecular profile of plaques, memory decline and neuron loss in two mouse models for Alzheimer's disease by deep sequencing.
Article in Frontiers in aging neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 90 citations in OpenAlex.
- Endophenotype-based in silico network medicine discovery combined with insurance record data mining identifies sildenafil as a candidate drug for Alzheimer's disease.Nature aging · 2021Trial
- Zinc-mediated lysosomal activation by 1H10 enhances autophagy and attenuates tau pathology in Alzheimer's disease models.Molecular brain · 2026Article
- Reduced CB1 Cannabinoid Receptor Expression in Alzheimer's Disease and Transgenic Mouse Models.Aging medicine (Milton (N.S.W)) · 2026Article
- Unravelling Synaptic and Metabolic Mechanisms of Cognitive Resilience in Asymptomatic Alzheimer's Disease Across Two Alzheimer's Disease Cohorts.Cellular and molecular neurobiology · 2026Article
- Relationship between CXCR4 and GNG4 in the Brain and Chronic Stress-Induced Atherosclerosis.Journal of molecular medicine (Berlin, Germany) · 2025Article
- Targeting the miR-96-5p/Cathepsin B Pathway to Alleviate Neuron-Derived Neuroinflammation in Alzheimer's Disease.MedComm · 2025Article
- The Auditory Brainstem Response Diagnoses Alzheimer-Like Disease in the 5xFAD Mouse Model.eNeuro · 2025Article
- Disrupted calcium dynamics and electrophysiological activity in the stratum pyramidale and hippocampal alveus during fear conditioning in the 5xFAD model of Alzheimer's disease.Frontiers in aging neuroscience · 2025Article
- Behaviour Hallmarks in Alzheimer's Disease 5xFAD Mouse Model.International journal of molecular sciences · 2024Review
- Single-Cell RNA-seq reveals transcriptomic modulation of Alzheimer's disease by activated protein C.Aging · 2024Article
- Interactions of Cellular Energetic Gene Clusters in the Alzheimer's Mouse Brain.Molecular neurobiology · 2024Article
- O-demethyl galantamine alters protein expression in cerebellum of 5xFAD mice.Turkish journal of biology = Turk biyoloji dergisi · 2024Article
- Neuroinflammation in a Mouse Model of Alzheimer's Disease versus Auditory Dysfunction: Machine Learning Interpretation and Analysis.Research square · 2023Article
- Inhibition of ACAT as a Therapeutic Target for Alzheimer's Disease Is Independent of ApoE4 Lipidation.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Article
- Serelaxin Alleviates Fibrosis in Thyroid-Associated Ophthalmopathy via the Notch Pathway.International journal of molecular sciences · 2023Article
- Cathepsin B Gene Knockout Improves Behavioral Deficits and Reduces Pathology in Models of Neurologic Disorders.Pharmacological reviews · 2022Review
- Visuo-spatial learning and memory impairments in the 5xFAD mouse model of Alzheimer's disease: Effects of age, sex, albinism, and motor impairments.Genes, brain, and behavior · 2022Article
- Artificial intelligence framework identifies candidate targets for drug repurposing in Alzheimer's disease.Alzheimer's research & therapy · 2022Article
- Idebenone Regulates Aβ and LPS-Induced Neurogliosis and Cognitive Function Through Inhibition of NLRP3 Inflammasome/IL-1β Axis Activation.Frontiers in immunology · 2022Article
- Association of peripheral blood DNA methylation level with Alzheimer's disease progression.Clinical epigenetics · 2021Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
One of the central research questions on the etiology of Alzheimer's disease (AD) is the elucidation of the molecular signatures triggered by the amyloid cascade of pathological events. Next-generation sequencing allows the identification of genes involved in disease processes in an unbiased manner. We have combined this technique with the analysis of two AD mouse models: (1) The 5XFAD model develops early plaque formation, intraneuronal Aβ aggregation, neuron loss, and behavioral deficits. (2) The Tg4-42 model expresses N-truncated Aβ4-42 and develops neuron loss and behavioral deficits albeit without plaque formation. Our results show that learning and memory deficits in the Morris water maze and fear conditioning tasks in Tg4-42 mice at 12 months of age are similar to the deficits in 5XFAD animals. This suggested that comparative gene expression analysis between the models would allow the dissection of plaque-related and -unrelated disease relevant factors. Using deep sequencing differentially expressed genes (DEGs) were identified and subsequently verified by quantitative PCR. Nineteen DEGs were identified in pre-symptomatic young 5XFAD mice, and none in young Tg4-42 mice. In the aged cohort, 131 DEGs were found in 5XFAD and 56 DEGs in Tg4-42 mice. Many of the DEGs specific to the 5XFAD model belong to neuroinflammatory processes typically associated with plaques. Interestingly, 36 DEGs were identified in both mouse models indicating common disease pathways associated with behavioral deficits and neuron loss.
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