Abstract
Introduction: Unliganded iron both contributes to the pathology of Alzheimer's disease (AD) and also changes the morphology of erythrocytes (RBCs). We tested the hypothesis that these two facts might be linked, i.e., that the RBCs of AD individuals have a variant morphology, that might have diagnostic or prognostic value.Methods: We included a literature survey of AD and its relationships to the vascular system, followed by a laboratory study. Four different microscopy techniques were used and results statistically compared to analyze trends between high and normal serum ferritin (SF) AD individuals.Results: Light and scanning electron microscopies showed little difference between the morphologies of RBCs taken from healthy individuals and from normal SF AD individuals. By contrast, there were substantial changes in the morphology of RBCs taken from high SF AD individuals. These differences were also observed using confocal microscopy and as a significantly greater membrane stiffness (measured using force-distance curves).Conclusion: We argue that high ferritin levels may contribute to an accelerated pathology in AD. Our findings reinforce the importance of (unliganded) iron in AD, and suggest the possibility both of an early diagnosis and some means of treating or slowing down the progress of this disease.
Highlights
Unliganded iron both contributes to the pathology of Alzheimer’s disease (AD) and changes the morphology of erythrocytes (RBCs)
We argue that high ferritin levels may contribute to an accelerated pathology in AD
We have shown in the introductory paragraphs that there is extensive literature suggesting that iron levels have been closely associated with AD pathology and might exacerbate pathology in these patients, iron levels in AD patients are not seen as a compulsory pathology test, notwithstanding literature indicating the relevance of ferritin dysregulation to AD [e.g., (Connor et al, 1992; Quintana et al, 2006; Friedman et al, 2011; Giambattistelli et al, 2012; De Sole et al, 2013)]
Summary
Unliganded iron both contributes to the pathology of Alzheimer’s disease (AD) and changes the morphology of erythrocytes (RBCs). Mohanty and co-workers in 2010 noted that there is a potential link between alterations in the RBC membrane proteome in AD subjects and AD pathology (Mohanty et al, 2010). These authors showed that 15% of RBCs in AD patients were elongated, and that there were alterations in the RBC membrane architecture. They suggested that this might be due to RBC-beta-amyloid interactions and/or changes in the expression of membrane proteins. Fibrinogen, a plasma precursor of fibrin has been found in the brains of AD patients (Choi et al, 2002) and it was shown that fibrin interacted with beta-amyloid protein (Merkle et al, 1996)
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