Affiliations: Department of Pathology and Laboratory Medicine, University of California, Davis School of Medicine, Sacramento, CA, USA
Note: [] Dr. Stanley Chew is a board-certified physician with an internal medicine practice in Sacramento, CA, USA. He is a physician-scientist collaborating with Dr. Tomic and Dr. Cheung in this report.
Note: [] Corresponding author: Dr. Anthony T.W. Cheung, Department of Pathology and Laboratory Medicine, University of California, Davis School of Medicine, Research III Building, Suite 3400 4645, Second Avenue, Sacramento, CA 95817, USA. Tel.: +1 916 734 3855; Fax: +1 916 734 2698; E-mail: Anthony.cheung@ucdmc.ucdavis.edu
Abstract: Context: The etiology of Alzheimer’s disease (AD) is inconclusive. Treatments targeting amyloid have largely been unsuccessful. There is increasing evidence that vasculopathy may play an important pathogenic role in AD. Objective: Longitudinal measurements of whole blood viscosity (WBV) using a computer-assisted hemorheologic protocol and characterization of microvascular abnormalities using computer-assisted intravital microscopy (CAIM) are two objective methods adopted in this laboratory to noninvasively quantify vasculopathy in AD patients. A correlation of increased disease severity with worsened vasculopathy would further bolster a cause and effect relationship. A case report (Case 1) is presented to illustrate the usefulness of following an AD patient with these noninvasive techniques to correlate disease progression with vasculopathy. Design: Patients were selected from a private practice setting who met the Diagnostic and Statistical Manual of Mental Disorders criteria for AD. The Rheolog™, a computer-assisted scanning rheometer, was used to obtain longitudinal measurements of WBV. The microvascular abnormalities in the bulbar conjunctiva were quantified using a severity index (SI, scale 0–15). The patient was observed over a 4 year period from 2005 to 2008. Conclusion: This case study shows a correlation of disease progression in an AD patient with worsened vasculopathy. It illustrates the usefulness of WBV and CAIM as tools to quantify vasculopathy in AD patients and additionally suggests a pathogenetic role vasculopathy may play in concert with the amyloid hypothesis.
