Abstract
Many studies support the existence of an association between type 2 diabetes (T2DM) and Alzheimer’s disease (AD). In AD, in addition to brain, a number of peripheral tissues and cells are affected, including red blood cell (RBC) and because there are currently no reliable diagnostic biomarkers of AD in the blood, a gradually increasing attention has been given to the study of RBC’s alterations. Recently it has been evidenced in diabetes, RBC alterations superimposable to the ones occurring in AD RBC. Furthermore, growing evidence suggests that oxidative stress plays a pivotal role in the development of RBC’s alterations and vice versa. Once again this represents a further evidence of a shared pathway between AD and T2DM. The present review summarizes the two disorders, highlighting the role of RBC in the postulated common biochemical links, and suggests RBC as a possible target for clinical trials.
Highlights
Patients affected by Alzheimer’s disease (AD) have senile plaques in central nervous system (CNS) areas where neurodegenerative process takes place (Selkoe, 1994)
There are in literature data on impaired insulin action or production, impaired signaling pathway involving insulin receptor (IR) and insulin growth factor (IGF) defects, toxicity caused by hyperglycemia, increase of advance glycation end products, inflammation at the vascular level and others (Sjöholm and Nyström, 2006; Luchsinger, 2012; de la Monte, 2012)
Examples of this innovative idea, derive from recent literature focused on the understanding of red blood cell (RBC) abnormalities that involve the impairment of RBC morphology, deformability, and function leading to vascular dysfunctions
Summary
Patients affected by Alzheimer’s disease (AD) have senile plaques in central nervous system (CNS) areas where neurodegenerative process takes place (Selkoe, 1994). T2DM-related conditions, including obesity (Beydoun et al, 2008), hyperinsulinemia (Peila et al, 2004) and metabolic syndrome, may be risk factors for AD In this regard, there are in literature data on impaired insulin action or production, impaired signaling pathway involving insulin receptor (IR) and insulin growth factor (IGF) defects, toxicity caused by hyperglycemia, increase of advance glycation end products, inflammation at the vascular level and others (Sjöholm and Nyström, 2006; Luchsinger, 2012; de la Monte, 2012). The main important mechanisms that affect RBC structure and function in diabetes patients are given below
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