ReviewNeuromolecular medicine2011
APP transgenic mice: their use and limitations.
Review in Neuromolecular medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
34 citing papers in PubMed, 81 citations in OpenAlex.
- Olive Oil Industry By-Products as a Novel Source of Biophenols with a Promising Role in Alzheimer Disease Prevention.Molecules (Basel, Switzerland) · 2024Review
- Alzheimer's Disease Puzzle: Delving into Pathogenesis Hypotheses.Aging and disease · 2024Review
- β-amyloid accumulation enhances microtubule associated protein tau pathology in an APPFrontiers in neuroscience · 2024Article
- Sheep as a large animal model for hearing research: comparison to common laboratory animals and humans.Laboratory animal research · 2023Review
- Spatial Memory Training Counteracts Hippocampal GIRK Channel Decrease in the Transgenic APPInternational journal of molecular sciences · 2022Article
- Emerging roles of dysregulated adenosine homeostasis in brain disorders with a specific focus on neurodegenerative diseases.Journal of biomedical science · 2021Review
- Comparison of memory, affective behavior, and neuropathology in APPBehavioural brain research · 2021Article
- Enrichment of Neurodegenerative Microglia Signature in Brain-Derived Extracellular Vesicles Isolated from Alzheimer's Disease Mouse Models.Journal of proteome research · 2021Article
- Chronic Memantine Treatment Ameliorates Behavioral Deficits, Neuron Loss, and Impaired Neurogenesis in a Model of Alzheimer's Disease.Molecular neurobiology · 2021Article
- An Overview of Astrocyte Responses in Genetically Induced Alzheimer's Disease Mouse Models.Cells · 2020Review
- Mechanisms of NLRP3 Inflammasome Activation: Its Role in the Treatment of Alzheimer's Disease.Neurochemical research · 2020Review
- Studying the Relationship of Intermittent Fasting and β-Amyloid in Animal Model of Alzheimer's Disease: A Scoping Review.Nutrients · 2020Article
- Can mouse models mimic sporadic Alzheimer's disease?Neural regeneration research · 2020Review
- X-ray Phase Contrast Tomography Serves Preclinical Investigation of Neurodegenerative Diseases.Frontiers in neuroscience · 2020Article
- Alzheimer's disease: from basic science to precision medicine approach.BMJ neurology open · 2020Review
- Amyloid-β plaque formation and reactive gliosis are required for induction of cognitive deficits in App knock-in mouse models of Alzheimer's disease.BMC neuroscience · 2019Article
- Cognitive and emotional alterations in App knock-in mouse models of Aβ amyloidosis.BMC neuroscience · 2018Article
- Chemical exchange saturation transfer MRI shows low cerebral 2-deoxy-D-glucose uptake in a model of Alzheimer's Disease.Scientific reports · 2018Article
- Toxin-Induced Experimental Models of Learning and Memory Impairment.International journal of molecular sciences · 2016Review
- A genetic cause of Alzheimer disease: mechanistic insights from Down syndrome.Nature reviews. Neuroscience · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease is the most widespread form of dementia. Its histopathological hallmarks include vascular and extracellular β-amyloid (Aβ) deposition and intraneuronal neurofibrillary tangles (NFTs). Gradual decline of cognitive functions linked to progressive synaptic loss makes patients unable to store new information in the earlier stages of the pathology, later becoming completely dependent because they are unable to do even elementary daily life actions. Although more than a hundred years have passed since Alois Alzheimer described the first case of AD, and despite many years of intense research, there are still many crucial points to be discovered in the neuropathological pathway. The development of transgenic mouse models engineered with overexpression of the amyloid precursor protein carrying familial AD mutations has been extremely useful. Transgenic mice present the hallmarks of the pathology, and histological and behavioural examination supports the amyloid hypothesis. As in human AD, extracellular Aβ deposits surrounded by activated astrocytes and microglia are typical features, together with synaptic and cognitive defects. Although animal models have been widely used, they are still being continuously developed in order to recapitulate some missing aspects of the disease. For instance, AD therapeutic agents tested in transgenic mice gave encouraging results which, however, were very disappointing in clinical trials. Neuronal cell death and NFTs typical of AD are much harder to replicate in these mice, which thus offer a fundamental but still imperfect tool for understanding and solving dementia pathology.
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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.