ArticleThe American journal of pathology2010
Age-related vascular pathology in transgenic mice expressing presenilin 1-associated familial Alzheimer's disease mutations.
Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 90 citations in OpenAlex.
- Article
- Glycocalyx and basal lamina in neurological disorders.Matrix biology : journal of the International Society for Matrix Biology · 2026Review
- Mutations associated with Alzheimer's disease and aged serum synergistically elicit blood-brain barrier dysfunction in a tissue-engineered model.Fluids and barriers of the CNS · 2026Article
- Intramural hematomas and astrocytic infiltration precede perivascular inflammation in a rat model of repetitive low-level blast injury.Journal of neuropathology and experimental neurology · 2025Article
- Exercise-mediated cerebrovascular repair in Alzheimer's disease: from pathophysiology to therapeutic precision.Frontiers in aging neuroscience · 2025Review
- Is the Relationship Between Cardiovascular Disease and Alzheimer's Disease Genetic? A Scoping Review.Genes · 2024Article
- The Neurovascular Unit as a Locus of Injury in Low-Level Blast-Induced Neurotrauma.International journal of molecular sciences · 2024Review
- Late chronic local inflammation, synaptic alterations, vascular remodeling and arteriovenous malformations in the brains of male rats exposed to repetitive low-level blast overpressures.Acta neuropathologica communications · 2023Article
- Evidence of beta amyloid independent small vessel disease in familial Alzheimer's disease.Brain pathology (Zurich, Switzerland) · 2022Article
- Peripheral Pathways to Neurovascular Unit Dysfunction, Cognitive Impairment, and Alzheimer's Disease.Frontiers in aging neuroscience · 2022Review
- Basal lamina changes in neurodegenerative disorders.Molecular neurodegeneration · 2021Review
- Low-level blast exposure induces chronic vascular remodeling, perivascular astrocytic degeneration and vascular-associated neuroinflammation.Acta neuropathologica communications · 2021Article
- The pathogenic role of c-Kit+ mast cells in the spinal motor neuron-vascular niche in ALS.Acta neuropathologica communications · 2021Article
- Repetitive transcranial magnetic stimulation increases the brain's drainage efficiency in a mouse model of Alzheimer's disease.Acta neuropathologica communications · 2021Article
- PS1 FAD mutants decrease ephrinB2-regulated angiogenic functions, ischemia-induced brain neovascularization and neuronal survival.Molecular psychiatry · 2021Article
- No observed effect on brain vasculature of Alzheimer's disease-related mutations in the zebrafish presenilin 1 gene.Molecular brain · 2021Article
- Neurovascular Alterations in Vascular Dementia: Emphasis on Risk Factors.Frontiers in aging neuroscience · 2021Article
- Stereological Changes in Microvascular Parameters in Hippocampus of a Transgenic Rat Model of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2021Article
- Altered Brain Endothelial Cell Phenotype from a Familial Alzheimer Mutation and Its Potential Implications for Amyloid Clearance and Drug Delivery.Stem cell reports · 2020Article
- Pericytic Laminin Maintains Blood-Brain Barrier Integrity in an Age-Dependent Manner.Translational stroke research · 2020Article
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Authors and funding
11 authors at 4 institutions in 1 country.
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Abstract
Mutations in the presenilin 1 (PS1) gene are the most commonly recognized cause of familial Alzheimer's disease (FAD). Besides senile plaques, neurofibrillary tangles, and neuronal loss, Alzheimer's disease (AD) is also accompanied by vascular pathology. Here we describe an age-related vascular pathology in two lines of PS1 FAD-mutant transgenic mice that mimics many features of the vascular pathology seen in AD. The pathology was especially prominent in the microvasculature whose vessels became thinned and irregular with the appearance of many abnormally looped vessels as well as string vessels. Stereologic assessments revealed a reduction of the microvasculature in the hippocampus that was accompanied by hippocampal atrophy. The vascular changes were not congophilic. Yet, despite the lack of congophilia, penetrating vessels at the cortical surface were often abnormal morphologically and microhemorrhages sometimes occurred. Altered immunostaining of blood vessels with basement membrane-associated antigens was an early feature of the microangiopathy and was associated with thickening of the vascular basal laminae and endothelial cell alterations that were visible ultrastructurally. Interestingly, although the FAD-mutant transgene was expressed in neurons in both lines of mice, there was no detectable expression in vascular endothelial cells or glial cells. These studies thus have implications for the role of neuronal to vascular signaling in the pathogenesis of the vascular pathology associated with AD.
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