Jemeen SreedharanDr Jemeen Sreedharan studied medicine at King’s College London, intercalating a BSc in Neurosciences and developing an early interest in neurodegeneration. After general medical training in London and Cambridge he conducted doctoral studies at the Institute of Psychiatry at King’s College London. Under the supervision of Prof Christopher Shaw he identified mutations in TDP-43 as a cause of amyotrophic lateral sclerosis (ALS, or motor neuron disease, MND).
He then completed general neurology training in London before obtaining a Clinician Scientist Fellowship award from the MRC to allow him to develop novel TDP-43-based animal models of ALS. He spent the first two years of the Fellowship at the University of Massachusetts Medical School working in the laboratories of Prof Marc Freeman and Prof Robert H Brown Jr in the departments of Neurobiology and Neurology respectively. Using a unique mosaic approach to study aged adult motor neurons in fruitflies he identified three genetic suppressors of TDP-43 toxicity. In parallel he also generated a novel mouse model of ALS, which is designed to more closely mimic the human condition than existing models.
He returned to the UK in October 2014 to continue his work under the mentorship of Dr Michael Coleman.
NMN Deamidase Delays Wallerian Degeneration and Rescues Axonal Defects Caused by NMNAT2 Deficiency In Vivo.
Di Stefano M, Loreto A, Orsomando G
Current biology : CB
KIF1A mediates axonal transport of BACE1 and identification of independently moving cargoes in living SCG neurons.
Hung CO, Coleman MP
Traffic (Copenhagen, Denmark)
Synaptophysin depletion and intraneuronal Aβ in organotypic hippocampal slice cultures from huAPP transgenic mice.
Harwell CS, Coleman MP
11 1750-1326:44 (2016)
Application of virtual screening to the discovery of novel nicotinamide phosphoribosyltransferase (NAMPT) inhibitors with potential for the treatment of cancer and axonopathies.
Clark DE, Waszkowycz B, Wong M
Bioorganic & medicinal chemistry letters
Mislocalization of neuronal tau in the absence of tangle pathology in phosphomutant tau knockin mice.
Gilley J, Ando K, Seereeram A
Neurobiology of aging
39 1558-1497:1-18 (2016)
Reduced number of axonal mitochondria and tau hypophosphorylation in mouse P301L tau knockin neurons.
Rodríguez-Martín T, Pooler AM, Lau DH
Neurobiology of disease
85 1095-953X:1-10 (2015)
Short-term diabetic hyperglycemia suppresses celiac ganglia neurotransmission, thereby impairing sympathetically mediated glucagon responses.
Mundinger TO, Cooper E, Coleman MP
American journal of physiology. Endocrinology and metabolism
309 1522-1555:E246-55 (2015)
Gilley J, Orsomando G, Nascimento-Ferreira I
10 2211-1247:1974-81 (2015)
Axonal transport declines with age in two distinct phases separated by a period of relative stability.
Milde S, Adalbert R, Elaman MH
Neurobiology of aging
The Axon-Protective WLD(S) Protein Partially Rescues Mitochondrial Respiration and Glycolysis After Axonal Injury.
Godzik K, Coleman MP
Journal of molecular neuroscience : MN
Di Stefano M, Nascimento-Ferreira I, Orsomando G
Cell death and differentiation
Identification of palmitoyltransferase and thioesterase enzymes that control the subcellular localization of axon survival factor nicotinamide mononucleotide adenylyltransferase 2 (NMNAT2).
Milde S, Coleman MP
The Journal of biological chemistry
289 1083-351X:32858-70 (2014)