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G.T. Feke, F. Berisha, C.L. Trempe, J.W. McMeel, C.L. Schepens; Retinal Hemodynamics in Alzheimer's Disease . Invest. Ophthalmol. Vis. Sci. 2006;47(13):464.
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© ARVO (1962-2015); The Authors (2016-present)
Visual symptoms are often the initial complaint of patients with Alzheimer’s Disease (AD), and there has been some evidence suggesting that morphological manifestations of AD may extend to the retina. Results of electrophysiological tests have supported this conjecture. Impaired cerebral blood flow has been documented in AD, and, most recently, even in the pre–clinical stage of AD. Among the mechanisms responsible for reduced cerebral blood flow are beta–amyloid plaques on the arterial side, and collagen deposition leading to increased vessel wall thickness on the venous side of the circulation. The purpose of this study was to determine whether the retinal circulation was abnormal in AD patients.
Ten patients with a diagnosis of probable AD (age 74.9±5.0 years) and seven age–matched healthy controls (age 71.6±2.9 years) were recruited for the study. Blood column diameter, centerline blood speed, and retinal blood flow rate were measured in the major superior temporal retinal vein in one eye of each subject using the Canon CLBF 100 retinal laser Doppler blood flow instrument. The results in the two groups were compared using unpaired t–tests and Mann–Whitney U tests.
There was no significant difference in IOP between the groups, but Snellen visual acuity was decreased (p=0.027) in the AD group. Venous blood column diameter was 134±10 µm in the AD group and 149±9 µm in the control group, a statistically significant (p=0.008) difference. However, venous centerline blood speed (28.9±10.0 mm/s in the AD patients; 30.8±5.9 mm/s in the controls) was similar in both groups. The resultant blood flow rates were 12.3±4.3 µl/min in the AD patients, and 15.9±2.9 µl/min in the controls. The difference in blood flow rate did not reach the level of statistical significance (p=0.077).
The results showed a marked narrowing of the retinal venous blood column diameter in AD patients. There was also a trend toward decreased venous blood flow in the patients. It is tempting to speculate that the narrowing of the venous blood column diameter is related to thickening of the venous wall due to collagen deposition as found in cerebral veins. If confirmed in a larger study, our findings might serve as a sensitive biomarker for early detection and as a surrogate endpoint in the evaluation of pharmacological treatments for AD.
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