Rosenberg's Molecular and Genetic Basis of Neurological and Psychiatric Disease (6^th Ed.) Volume 2

SECTION I. DEGENERATIVE DISORDERS
SECTION II. MOVEMENT DISORDERS
SECTION III. NEURO-ONCOLOGY
SECTION IV. NEUROCUTANEOUS DISORDERS
SECTION V. EPILEPSY
SECTION VI. WHITE MATTER DISEASESSECTION VII. NEUROPATHIES AND NEURONOPATHIES
SECTION VIII. MUSCLE AND NEUROMUSCULAR JUNCTION DISORDERS
SECTION IX. STROKE
Sub-Section: Psychiatric Disease
SECTION X. A NEUROLOGIC GENE MAP

Roger N. Rosenberg, MD is a graduate of Northwestern University Medical School, With Distinction, and was subsequently trained in Neurology with H. Houston Merritt, MD at the Neurological Institute, Columbia University, New York, was Chief Resident and then was a Post-Doctoral Fellow with Nobel Laureate Marshall Nirenberg at the NIH in the Laboratory of Biochemical Genetics. He is Board Certified by the American Board of Psychiatry and Neurology. He is holder of the Zale Distinguished Chair and Professor of Neurology and Neurotherapeutics at the University of Texas Southwestern Medical Center at Dallas since 1973 and developed the department for 18 years as Chair from 1973-1991.
He described for the first time in 1975 Machado Joseph disease, an autosomal dominant cerebellar degeneration, which produces imbalance and impaired coordination, and showed it was due to a unique expansion of DNA in the causal gene. It is the most common inherited form of impaired coordination in the world and his research has provided a genetic marker to eliminate it in large families in future generations.
He has served as the Founding Director of the UT Southwestern NIH funded Alzheimer’s Disease Center and Principal Investigator of the NIH Center Grant from 1987-2019.
He directs an active laboratory effort in Alzheimer’s Disease. He is developing a DNA Aß42 trimer vaccine for Alzheimer's disease for which he was awarded a US Patent "Amyloid Beta Gene Vaccines" in January 2009. It has been tested in mouse, transgenic mouse, New Zealand white rabbits and rhesus monkeys. The vaccine produces effective anti-Aß42 peptide antibody levels and is non-inflammatory in all three species. The vaccine reduces by 40% Aß42 peptide and by 50% tau and phospho-tau in the brains of 3X AD Tg mice, the two main pathologies of Alzheimer’s disease, with high levels of anti-Aß42 antibody and with a non-inflammatory immune response. He is preparing now a Phase 1 Clinical trial Grant - First in Hu