Petter Järemo*, Alenka Jejcic, Vesna Jelic, Tasmin Shahnaz, Homira Behbahani, Magnus Oweling and Bengt Winblad Pages 834 - 835 ( 2 )
Background: Alzheimer’s Disease (AD) features the accumulation of β-amyloid in erythrocytes. The subsequent red cell damage may well affect their oxygen-carrying capabilities. 2,3- diphosphoglycerate (2,3-DPG) binds to the hemoglobin thereby promoting oxygen release. It is theorized that 2,3-DPG is reduced in AD and that the resulting hypoxia triggers erythropoietin (EPO) release. <p></p> Methods & Objective: To explore this theory, we analyzed red cell 2,3-DPG content and EPO in AD, mild cognitive impairment, and the control group, subjective cognitive impairment. <p></p> Results: We studied (i) 2,3-DPG in red cells, and (ii) circulating EPO in AD, and both markers were unaffected by dementia. Disturbances of these oxygen-regulatory pathways do not appear to participate in brain hypoxia in AD.
Alzheimer, 2,3-diphosphoglycerate, erythrocytes, erythropoietin, β-amyloid, cognitive impairment.
Department of Internal Medicine, Vrinnevi Hospital, Norrköping, Department of Internal Medicine, Vrinnevi Hospital, Norrköping, Karolinska University Hospital, Theme Aging, Huddinge, Stockholm, Department of Internal Medicine, Vrinnevi Hospital, Norrköping, Department of Neurobiology, Care Sciences, and Society, Center for Alzheimer Research, Division of Clinical Geriatrics, Karolinska Institutet, Solna, Department of Internal Medicine, Vrinnevi Hospital, Norrköping, Department of Neurobiology, Care Sciences, and Society, Center for Alzheimer Research, Division of Clinical Geriatrics, Karolinska Institutet, Solna