![]() The gas transport capacity of red blood cells is not only determined by the characteristics of hemoglobin, but also by the capacity to regulate intracellular pH, deformability, ATP production, redox status, resistance to osmotic and mechanical stress, and recognition and removal by the immune system. In addition, there are hardly any data indicating that physiological aging in vivo or in vitro during storage in the blood bank has a notable effect on oxygen supply of the tissues and carbon dioxide removal ( 3). Also, many obvious deviations of the classical discoid red blood cell shape, due to inborn errors in integral membrane proteins and cytoskeletal components, have no obvious clinical implications ( 2). There are many genetically determined, structural abnormalities in the hemoglobin chains that, in most circumstances, do not affect red blood cell integrity and do not seem to affect transport of oxygen binding and release in lungs and tissues, respectively ( 1). The statement that a healthy red blood cell is essential for organismal homeostasis may sound as a truism, but this depends on the functional definition of a healthy red blood cell. Therefore, interventions that reduce the susceptibility of red blood cells to physiological and pathological stress may reduce the extent or progress of neurodegeneration. An exploration of the literature suggests that disturbed red blood cell function may play a role in the pathophysiology of various neurodegenerative diseases. Also, susceptibility may be induced or enhanced by systemic pathological conditions such as inflammation. Through this mechanism, an increased susceptibility of already compromised red blood cells to physiological stress conditions may constitute an additional risk factor in vulnerable individuals. The underlying mutations may not only affect red cell function, but also render neurons in specific brain areas more susceptible to a concomitant reduction in oxygen supply. Our data on the misshapen red blood cells of patients with neuroacanthocytosis illustrate this general mechanism: an abnormal morphology is associated with an increase in the susceptibility of red blood cells to osmotic and mechanical stress, and alters their rheological properties. Often, functional deficits become apparent only when they are subjected to biochemical or mechanical stress in vitro, or to pathological conditions in vivo. The structure of red blood cells is affected by many inborn and acquired factors, but in most cases this does not seem to affect their function or survival in physiological conditions. ![]()
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