ArticleNeurobiology of aging2015
L-type calcium channel blockers and substance P induce angiogenesis of cortical vessels associated with beta-amyloid plaques in an Alzheimer mouse model.
Article in Neurobiology of aging, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- Amyloid β alters vascular CaThe Journal of physiology · 2025Article
- Hypertension and cellular senescence.Biogerontology · 2023Review
- Modulation of L-type calcium channels in Alzheimer's disease: A potential therapeutic target.Computational and structural biotechnology journal · 2023Review
- Functionally linked potassium channel activity in cerebral endothelial and smooth muscle cells is compromised in Alzheimer's disease.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Review
- Spreading of Beta-Amyloid in Organotypic Mouse Brain Slices and Microglial Elimination and Effects on Cholinergic Neurons.Biomolecules · 2021Article
- Cerebral Amyloid Angiopathy in a Mouse Model of Alzheimer's Disease Associates with Upregulated Angiopoietin and Downregulated Hypoxia-Inducible Factor.Journal of Alzheimer's disease : JAD · 2021Article
- Restoration of Olfactory Memory inFrontiers in cellular neuroscience · 2019Article
- Research Progress in the Pathogenesis of Alzheimer's Disease.Chinese medical journal · 2018Review
- Oleanolic Acid Ameliorates Aβ25-35 Injection-induced Memory Deficit in Alzheimer's Disease Model Rats by Maintaining Synaptic Plasticity.CNS & neurological disorders drug targets · 2018Article
- Organotypic Cultures from the Adult CNS: A Novel Model to Study Demyelination and Remyelination Ex Vivo.Cellular and molecular neurobiology · 2018Review
- Three-Dimensional Models of the Human Brain Development and Diseases.Advanced healthcare materials · 2018Review
- From Gene to Behavior: L-Type Calcium Channel Mechanisms Underlying Neuropsychiatric Symptoms.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2017Review
- Amyloid β-induced astrogliosis is mediated by β1-integrin via NADPH oxidase 2 in Alzheimer's disease.Aging cell · 2016Article
- Cholinergic neurodegeneration in an Alzheimer mouse model overexpressing amyloid-precursor protein with the Swedish-Dutch-Iowa mutations.Neurobiology of learning and memory · 2016Article
- Relationship Between Antihypertensive Medications and Cognitive Impairment: Part II. Review of Physiology and Animal Studies.Current hypertension reports · 2016Review
- Green-Fluorescent Protein(+) Astrocytes Attach to Beta-Amyloid Plaques in an Alzheimer Mouse Model and Are Sensitive for Clasmatodendrosis.Frontiers in aging neuroscience · 2016Article
- Alpha-Smooth Muscle Actin mRNA and Protein Are Increased in Isolated Brain Vessel Extracts of Alzheimer Mice.Pharmacology · 2016Article
- Organotypic brain slice cultures: A review.Neuroscience · 2015Review
- Organotypic brain slice cultures as a model to study angiogenesis of brain vessels.Frontiers in cell and developmental biology · 2015Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
It is well established that L-type calcium channels (LTCCs) are expressed in astroglia. However, their functional role is still speculative, especially under pathologic conditions. We recently showed that the α1 subunit-like immunoreactivity of the CaV1.2 channel is strongly expressed in reactive astrocytes around beta-amyloid plaques in 11-month-old Alzheimer transgenic (tg) mice with the amyloid precursor protein London and Swedish mutations. The aim of the present study was to examine the cellular expression of all LTCC subunits around beta-amyloid plaques by in situ hybridization using (35)S-labeled oligonucleotides. Our data show that messenger RNAs (mRNAs) of the LTCC CaV1.2 α1 subunit as well as all auxiliary β and α2δ subunits, except α2δ-4, were expressed in the hippocampus of age-matched wild-type mice. It was unexpected to see, that cells directly located in the plaque core in the cortex expressed mRNAs for CaV1.2 α1, β2, β4, and α2δ-1, whereas no expression was detected in the halo. Furthermore, cells in the plaque core also expressed preprotachykinin-A mRNA, the precursor for substance P. By means of confocal microscopy, we demonstrated that collagen-IV-stained brain vessels in the cortex were associated with the plaque core and were immunoreactive for substance P. In cortical organotypic brain slices of adult Alzheimer mice, we could demonstrate that LTCC blockers increased angiogenesis, which was further potentiated by substance P. In conclusion, our data show that brain vessels associated with beta-amyloid plaques express substance P and an LTCC and may play a role in angiogenesis.
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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.