ArticlePloS one2018
Memory deficiency, cerebral amyloid angiopathy, and amyloid-β plaques in APP+PS1 double transgenic rat model of Alzheimer's disease.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 41 citations in OpenAlex.
- Increased circulating TREM2Brain, behavior, & immunity - health · 2026Article
- Amyloidosis of bridging veins is a pathologic feature of Alzheimer's disease.The Journal of experimental medicine · 2026Article
- The integrity of perivascular spaces is absolutely essential for proper function of the glymphatic system waste and excess water removal from the brain.Histology and histopathology · 2025Review
- tRFAlzheimer's research & therapy · 2025Article
- Structural changes in cerebral microvasculature induced by ferroptosis contribute to blood-brain barrier disruption in Alzheimer's disease: an autopsy study.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Brain endothelial cell activation and dysfunction associate with and contribute to the development of enlarged perivascular spaces and cerebral small vessel disease.Histology and histopathology · 2024Review
- Shine and darkle the blood vessels: Multiparameter hypersensitive MR angiography for diagnosis of panvascular diseases.Science advances · 2024Article
- Rodent Models of Alzheimer's Disease: Past Misconceptions and Future Prospects.International journal of molecular sciences · 2024Review
- A Closer Look at the Perivascular Unit in the Development of Enlarged Perivascular Spaces in Obesity, Metabolic Syndrome, and Type 2 Diabetes Mellitus.Biomedicines · 2024Review
- The Venular Side of Cerebral Amyloid Angiopathy: Proof of Concept of a Neglected Issue.Biomedicines · 2023Review
- Zebrafish as a Potential Model for Neurodegenerative Diseases: A Focus on Toxic Metals Implications.International journal of molecular sciences · 2023Review
- Venular amyloid accumulation in transgenic Fischer 344 Alzheimer's disease rats.Scientific reports · 2022Article
- Proteomics-based investigation of cerebrovascular molecular mechanisms in cerebral amyloid angiopathy by the FFPE-LMD-PCT-SWATH method.Fluids and barriers of the CNS · 2022Article
- Blood-brain barrier leakage in Alzheimer's disease: From discovery to clinical relevance.Pharmacology & therapeutics · 2022Review
- An App knock-in rat model for Alzheimer's disease exhibiting Aβ and tau pathologies, neuronal death and cognitive impairments.Cell research · 2022Article
- Immunoreactivity and a new staining method of monocarboxylate transporter 1 located in endothelial cells of cerebral vessels of human brain in distinguishing cerebral venules from arterioles.European journal of histochemistry : EJH · 2021Article
- mTOR Attenuation with Rapamycin Reverses Neurovascular Uncoupling and Memory Deficits in Mice Modeling Alzheimer's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Rodent Models of Amyloid-Beta Feature of Alzheimer's Disease: Development and Potential Treatment Implications.Aging and disease · 2020Review
- Potential Role of Venular Amyloid in Alzheimer's Disease Pathogenesis.International journal of molecular sciences · 2020Review
- White matter inflammation and cognitive function in a co-morbid metabolic syndrome and prodromal Alzheimer's disease rat model.Journal of neuroinflammation · 2020Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Transgenic rat models of Alzheimer's disease were used to examine differences in memory and brain histology. Double transgenic female rats (APP+PS1) over-expressing human amyloid precursor protein (APP) and presenilin 1 (PS1) and single transgenic rats (APP21) over-expressing human APP were compared with wild type Fischer rats (WT). The Barnes maze assessed learning and memory and showed that both APP21 and APP+PS1 rats made significantly more errors than the WT rats during the acquisition phase, signifying slower learning. Additionally, the APP+PS1 rats made significantly more errors following a retention interval, indicating impaired memory compared to both the APP21 and WT rats. Immunohistochemistry using an antibody against amyloid-β (Aβ) showed extensive and mostly diffuse Aβ plaques in the hippocampus and dense plaques that contained tau in the cortex of the brains of the APP+PS1 rats. Furthermore, the APP+PS1 rats also showed vascular changes, including cerebral amyloid angiopathy with extensive Aβ deposits in cortical and leptomeningeal blood vessel walls and venous collagenosis. In addition to the Aβ accumulation observed in arterial, venous, and capillary walls, APP+PS1 rats also displayed enlarged blood vessels and perivascular space. Overall, the brain histopathology and behavioral assessment showed that the APP+PS1 rats demonstrated behavioral characteristics and vascular changes similar to those commonly observed in patients with Alzheimer's disease.
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