Abstract
Fifteen Alzheimer (AD) and fifteen normative (NM) age-matched autopsy brains were analyzed in superior temporal cortex, hippocampal and brainstem samples. Vascular endothelial growth factor (VEGF) positive capillaries were quantitatively analyzed in all three sites in the 30 cases. Amyloid β42 senile plaques and VEGF positive capillaries were counted and statistically analyzed using Mann-Whitney, Kruskal–Wallis and the non-parametric Spearman’s test. There is a significantly different expression of capillary VEGF between normative and Alzheimer brains. Within Alzheimer’s superior temporal, hippocampus and brainstem sites there was reduced VEGF expression, with the P value being less than 0.05 in all three sites (superior temporal less than 0.035, hippocampus less than 0.001, brainstem less than 0.006). As VEGF is an important endothelial growth factor involved in vascular remodeling, angiogenesis, and endothelial/blood brain barrier maintenance, its reduced expression in Alzheimer’s disease is evidence for altered capillary function in this disease, which may be contributory to its pathogenesis by altering beta amyloid handling and efflux.
Keywords: Alzheimer's disease, blood-brain barrier, senile plaques, VEGF.
Current Neurovascular Research
Title:Reduction in Vascular Endothelial Growth Factor Expression in the Superior Temporal, Hippocampal, and Brainstem Regions in Alzheimer`s Disease
Volume: 11 Issue: 3
Author(s): John Provias and Brian Jeynes
Affiliation:
Keywords: Alzheimer's disease, blood-brain barrier, senile plaques, VEGF.
Abstract: Fifteen Alzheimer (AD) and fifteen normative (NM) age-matched autopsy brains were analyzed in superior temporal cortex, hippocampal and brainstem samples. Vascular endothelial growth factor (VEGF) positive capillaries were quantitatively analyzed in all three sites in the 30 cases. Amyloid β42 senile plaques and VEGF positive capillaries were counted and statistically analyzed using Mann-Whitney, Kruskal–Wallis and the non-parametric Spearman’s test. There is a significantly different expression of capillary VEGF between normative and Alzheimer brains. Within Alzheimer’s superior temporal, hippocampus and brainstem sites there was reduced VEGF expression, with the P value being less than 0.05 in all three sites (superior temporal less than 0.035, hippocampus less than 0.001, brainstem less than 0.006). As VEGF is an important endothelial growth factor involved in vascular remodeling, angiogenesis, and endothelial/blood brain barrier maintenance, its reduced expression in Alzheimer’s disease is evidence for altered capillary function in this disease, which may be contributory to its pathogenesis by altering beta amyloid handling and efflux.
Export Options
About this article
Cite this article as:
Provias John and Jeynes Brian, Reduction in Vascular Endothelial Growth Factor Expression in the Superior Temporal, Hippocampal, and Brainstem Regions in Alzheimer`s Disease, Current Neurovascular Research 2014; 11 (3) . https://dx.doi.org/10.2174/1567202611666140520122316
DOI https://dx.doi.org/10.2174/1567202611666140520122316 |
Print ISSN 1567-2026 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5739 |
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
Related Articles
-
Intracompartmental Delivery of CNTF as Therapy for Huntingtons Disease and Retinitis Pigmentosa
Current Gene Therapy Pathologically-Activated Therapeutics for Neuroprotection: Mechanism of NMDA Receptor Block by Memantine and S-Nitrosylation
Current Drug Targets Shear Stress-sensitive Carriers for Localized Drug Delivery
Current Pharmaceutical Design Pharmacologic Targeting of Endothelial Progenitor Cells
Cardiovascular & Hematological Disorders-Drug Targets From Presenilinase to γ-Secretase, Cleave to Capacitate
Current Alzheimer Research Neuronal Response of Peroxisomal and Peroxisome-Related Proteins to Chronic and Acute Aβ Injury
Current Alzheimer Research Haptoglobin Phenotype May Alter Endothelial Progenitor Cell Cluster Formation in Cerebral Small Vessel Disease
Current Neurovascular Research Rosiglitazone Does Not Improve Cognition or Global Function when Used as Adjunctive Therapy to AChE Inhibitors in Mild-to-Moderate Alzheimers Disease: Two Phase 3 Studies
Current Alzheimer Research Lithium, a Therapy for AD: Current Evidence from Clinical Trials of Neurodegenerative Disorders
Current Alzheimer Research Homocysteine: A Risk Factor in Patietns with Cardiovascular Disorders in Pakistan
Current Bioactive Compounds The Role of Microglial Cells on Neuroinflammation: Possible Therapeutic Applications
Recent Patents on Regenerative Medicine Toward The Rational Design of Cell Fate Modifiers Notch Signaling as a Target for Novel Biopharmaceuticals
Current Pharmaceutical Biotechnology Treating Schizophrenia: Novel Targets for the Cholinergic System
CNS & Neurological Disorders - Drug Targets Pharmacological Effects of Turmeric on Learning, Memory and Expression of Muscarinic Receptor Genes (M1, M3 and M5) in Stress-induced Mouse Model
Current Drug Targets Biological Roles of the Eclectic Chromogranin-A-derived Peptide Catestatin
Current Medicinal Chemistry Insight into the Epigenetics of Alzheimer's Disease: A Computational Study from Human Interactome
Current Alzheimer Research The Mechanism of Memory Impairment Induced by Aβ Chronic Administration Involves Imbalance between Cytokines and Neurotrophins in the Rat Hippocampus
Current Alzheimer Research Hypothermia and Alzheimer's Disease Neuropathogenic Pathways
Current Alzheimer Research Recent Studies on Design and Development of Drugs Against Alzheimer’s Disease (AD) Based on Inhibition of BACE-1 and Other AD-causative Agents
Current Topics in Medicinal Chemistry A Cyclooxygenase-2 Inhibitor Reduces Vascular Wall Thickness and Ameliorates Cognitive Impairment in a Cerebral Small Vessel Diseases Rat Model
Current Alzheimer Research