Jeremy Marks, MD PhD

Dr Marks focuses on the mechanisms and treatment of hypoxic-ischemic brain injury. A Neonatologist with a PhD in Neuroscience, his primary interest is in acute brain injury of the newborn.

Currently, Dr. Marks's research focuses on A) the role of decreased cerebral autoregulation in newborns at risk hypoxic-ischemic brain injury, and B) mechanisms underlying the generation of abnormal spontaneous motor behavior in survivors of Hypoxic-Ischemic encephalopathy using functional MRI.

Previously, his research focus in the laboratory was in mitochondrial mechanisms of acute neuronal degeneration and the mechanisms of membrane-targeted neuronal rescue by tri-block co-polymers of poly[ethylene oxide] and poly[propylene oxide].

Yale University
New Haven CT
Post-doctoral fellowship (4 years) - . Developmental regulation of vulnerability to hypoxic-ischemic brain injury in hippocampal neurons
1994

Yale University
New Haven, CT
Clinical fellowship (3 years) - . Neonatal-Perinatal Medicine
1993

Boston University
Boston, MA
Residency - . Pediatrics
1990

University of California, Los Angeles
Los Angeles, CA
PhD - . Neuroscience: Sleep state regulation of upper airway control of breathing
1987

McMaster University
Hamilton, Ontario, Canada
MD - . Medicine
1987

University of Toronto
Toronto, Ontario, Canada
MA - . Linguistics
1980

University of Toronto
Toronto, Ontario, Canada
BA - . Linguistics
1979

Poloxamer 188 decreases membrane toxicity of mutant SOD1 and ameliorates pathology observed in SOD1 mouse model for ALS.
Poloxamer 188 decreases membrane toxicity of mutant SOD1 and ameliorates pathology observed in SOD1 mouse model for ALS. Neurobiol Dis. 2018 07; 115:115-126.
PMID: 29627580

Noninvasive Ventilation in the Premature Newborn - Is Less Always More?
Noninvasive Ventilation in the Premature Newborn - Is Less Always More? N Engl J Med. 2017 07 27; 377(4):386-388.
PMID: 28745997

Mitochondrial mechanisms of neuronal rescue by F-68, a hydrophilic Pluronic block co-polymer, following acute substrate deprivation.
Mitochondrial mechanisms of neuronal rescue by F-68, a hydrophilic Pluronic block co-polymer, following acute substrate deprivation. Neurochem Int. 2017 Oct; 109:126-140.
PMID: 28433663

SUMOylation of NaV1.2 channels mediates the early response to acute hypoxia in central neurons.
SUMOylation of NaV1.2 channels mediates the early response to acute hypoxia in central neurons. Elife. 2016 12 28; 5.
PMID: 28029095

Secreted protein acidic and rich in cysteine (SPARC) induces lipotoxicity in neuroblastoma by regulating transport of albumin complexed with fatty acids.
Secreted protein acidic and rich in cysteine (SPARC) induces lipotoxicity in neuroblastoma by regulating transport of albumin complexed with fatty acids. Oncotarget. 2016 Nov 22; 7(47):77696-77706.
PMID: 27776337

White Matter Injury and General Movements in High-Risk Preterm Infants.
White Matter Injury and General Movements in High-Risk Preterm Infants. AJNR Am J Neuroradiol. 2017 Jan; 38(1):162-169.
PMID: 27789448

Network burst activity in hippocampal neuronal cultures: the role of synaptic and intrinsic currents.
Network burst activity in hippocampal neuronal cultures: the role of synaptic and intrinsic currents. J Neurophysiol. 2016 06 01; 115(6):3073-89.
PMID: 26984425

Hypoxic ischemic brain injury: Potential therapeutic interventions for the future.
Hypoxic ischemic brain injury: Potential therapeutic interventions for the future. Neoreviews. 2014 May 01; 15(5):e177-e186.
PMID: 25177211

Peroxiredoxin-5 targeted to the mitochondrial intermembrane space attenuates hypoxia-induced reactive oxygen species signalling.
Peroxiredoxin-5 targeted to the mitochondrial intermembrane space attenuates hypoxia-induced reactive oxygen species signalling. Biochem J. 2013 Dec 15; 456(3):337-46.
PMID: 24044889

Sirtuin 3 deficiency does not augment hypoxia-induced pulmonary hypertension.
Sirtuin 3 deficiency does not augment hypoxia-induced pulmonary hypertension. Am J Respir Cell Mol Biol. 2013 Dec; 49(6):885-91.
PMID: 24047466

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