Abstract #0616

Parametric MRI Reveals Vascular Effects of Antibodies to the &[alpha]1-Adrenergic Receptor by Demonstrating a Reduction in Relative Cerebral Blood Volume (RCBV)

Andreas Pohlmann¹, Babette Dieringer¹, Peter Karczewski², Natali Wisbrun³, Irina Palatnik¹, Christina Eichhorn⁴, Petra Hempel², Rudolf Kunze⁵, Marion Bimmler⁶, Thoralf Niendorf¹,⁷

¹Berlin Ultrahigh Field Facility (B.U.F.F.), Max-Delbrueck Center for Molecular Medicine, Berlin, Germany; ²E.R.D.E.-AAK-Diagnostik GmbH, Berlin, Germany; ³Animal Facilities, Max Delbrck Center for Molecular Medicine, Berlin, Germany; ⁴IT Department, Max-Delbrueck Center for Molecular Medicine, Berlin, Germany; ⁵E.R.D.E. e.V., Berlin, Germany; ⁶Autoimmunity and G Protein-Coupled Receptors, Max Delbrck Center for Molecular Medicine, Berlin, Germany; ⁷Experimental and Clinical Research Center, a cooperation between the Charit Medical Faculty and the Max Delbrck Center for Molecular Medicine, Berlin, Germany

Evidence suggests Alzheimers Disease (AD) may be primarily a vascular disease. Recently, agonistic autoantibodies to the &[alpha]1-adrenergic receptor (&[alpha]1-AR) were found to cause impairments of blood flow in larger vessels (TOF-MRA) in the rat brain. This work examines the long-term effects of α1-AR antibodies on relative cerebral blood volume (rCBV) in rats. Estimation of rCBV by ΔR₂*/ΔR₂ mapping in conjunction with an intravascular contrast agent demonstrated a significant reduction in rCBV for &[alpha]1-AR antibody treatment. This data underpins the pathogenic significance of autoimmunity to the &[alpha]1-AR for AD and vascular dementia.