Richard Milner, M.D., Ph.D.

Neurology & Neurological Disorders

Research Focus

Dr. Milner’s research studies focus on the design of new therapeutic approaches aimed at combating neurological disease such as multiple sclerosis (MS) and vascular dementia by increasing blood supply and reducing vascular breakdown. Blood vessels in the central nervous system (CNS) are unique in forming the blood-brain barrier (BBB), which confers low permeability properties, thus protecting neural cells such as neurons and oligodendrocytes (myelin cells) from potentially harmful blood components. A strong BBB also helps to reduce the influx of destructive inflammatory immune cells into the CNS.

Recently, the Milner lab showed that chronic mild hypoxia (CMH) accelerates clinical recovery in an animal model of MS, leading to long-term stable reductions in disease severity. Importantly, this protective effect of CMH was attributed to enhanced BBB integrity and accelerated cell death of infiltrated immune cells. Ongoing studies are exploring ways of using this information to generate new approaches for treating MS. In related projects, the Milner lab are examining how specific cell adhesion mechanisms on CNS endothelial cells (cells which line blood vessels) contribute to angiogenic remodeling (and thus increased vascularity) and BBB integrity. A more complete understanding of these mechanisms will facilitate future therapeutic strategies aimed at increasing vascularity and BBB integrity so as to combat the destructive effects of MS.

In related projects, his group are examining the impact of hypoxia on transient vascular breakdown, and in recent studies have defined a novel protective role for microglia in preventing hypoxia-associated transient vascular disruption, both in the brain and in the spinal cord. Ongoing studies are defining the age-dependence of this effect as well as the role of microglia and other protective mechanisms on vasculo-protection. An improved understanding of these mechanisms may aid in the design of new therapeutics aimed at preventing hypoxia-induced BBB disruption with implications for the prevention of vascular dementia.


M.D. in Medicine, University of Cambridge, 1998
Ph.D. in Neuroscience, University of Cambridge, 1994
B.Sc. (1st Class Honors) in Physiology, University of Leeds, 1990

Professional Experience

2018 – Present, Current Professor, San Diego BioMed
2012 – 2018 Associate Professor, Department of Molecular and Experimental Medicine, The Scripps Research Institute
2006 – 2012 Assistant Professor, Department of Molecular and Experimental Medicine, The Scripps Research Institute
2004 – 2006 Senior Research Associate, Department of Molecular and Experimental Medicine, The Scripps Research Institute
2003 – 2004 Wellcome Trust Career Development Fellow, Department of Pathology, University of Cambridge
2000 – 2002 Research Associate, Department of Neuropharmacology, The Scripps Research Institute
1994 – 1996 Postdoctoral Research Fellow, Wellcome/CRC Institute, University of Cambridge

Honors and Awards

Harry Weaver Neuroscience Scholar Award, National Multiple Sclerosis Society, 2006
Wellcome Trust Career Development Fellowship, 2003
Wellcome Trust International Prize Traveling Research Fellowship, 2000
J.E. Cunning prize in Clinical Final Examinations, University of Cambridge, 1998
Wellcome Trust Clinical Student Elective Prize, University of Cambridge, 1998
Peter Brook Award in Psychiatry, University of Cambridge, 1998
Finalist in Flaxo.MRS Young Investigator of the Year Award, United Kingdom, 1996
Wellcome Trust Prize Studentship, University of Cambridge, 1991-1994

Professional Activities

Member, American Heart Association Scientific Review Committee, Brain 4, 2016 – 2019
Member, American Heart Association Fellowship, Committee 2, 2013 – 2015
Member, National Multiple Sclerosis Society Peer Review Committee B, 2012 – 2016

Select Publications

Halder SK, Milner R. Hypoxia in multiple sclerosis; is it the chicken or the egg? Brain. 2020 Dec 22:awaa427. doi: 10.1093/brain/awaa427. Epub ahead of print. PMID: 33351069.

Halder SK, Milner R. Mild hypoxia triggers transient blood-brain barrier disruption: a fundamental protective role for microglia. Acta Neuropathol Commun. 2020 Oct 28;8(1):175. doi: 10.1186/s40478-020-01051-z. PMID: 33115539; PMCID: PMC7592567.


Halder SK, Milner R. Chronic mild hypoxia accelerates recovery from preexisting EAE by enhancing vascular integrity and apoptosis of infiltrated monocytes. Proc Natl Acad Sci U S A. 2020 May 19;117(20):11126-11135. doi: 10.1073/pnas.1920935117. Epub 2020 May 5. PMID: 32371484; PMCID: PMC7245138.


Kant R, Halder SK, Fernández JA, Griffin JH, Milner R. Activated Protein C Attenuates Experimental Autoimmune Encephalomyelitis Progression by Enhancing Vascular Integrity and Suppressing Microglial Activation. Front Neurosci. 2020 Apr 15;14:333. doi: 10.3389/fnins.2020.00333. PMID: 32351356; PMCID: PMC7174764.


Halder SK, Milner R. A critical role for microglia in maintaining vascular integrity in the hypoxic spinal cord. Proc Natl Acad Sci U S A. 2019 Dec 17;116(51):26029-26037.


Kant R, Halder SK, Bix GJ, Milner R. Absence of endothelial α5β1 integrin triggers early onset of experimental autoimmune encephalomyelitis due to reduced vascular remodeling and compromised vascular integrity. Acta Neuropathol Commun. 2019;7(1):11. Published 2019 Jan 24.


Halder, S. K., Kant, R. and Milner, R. (2018). Hypoxic pre-conditioning suppresses experimental autoimmune encephalomyelitis by modifying multiple properties of blood vessels. Acta. Neuropathologica. Communications. 6, 86.


All of Dr. Richard Milner’s Publications

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Our research programs are funded primarily by grants from the National Institutes of Health (NIH). Private donations help to accelerate the progress of research through the purchase of laboratory supplies and equipment or the recruitment of additional laboratory personnel. Thank you!

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