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.