Life Sciences Research for Lifelong Health

Jemeen Sreedharan

Dr 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.

Latest Publications

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)

PMID: 26923397

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)

PMID: 26459111

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)

PMID: 26037249

Absence of SARM1 rescues development and survival of NMNAT2-deficient axons.

Gilley J, Orsomando G, Nascimento-Ferreira I

Cell reports
10 2211-1247:1974-81 (2015)

PMID: 25818290

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
1558-1497: (2014)

PMID: 25443288

The Axon-Protective WLD(S) Protein Partially Rescues Mitochondrial Respiration and Glycolysis After Axonal Injury.

Godzik K, Coleman MP

Journal of molecular neuroscience : MN
1559-1166: (2014)

PMID: 25352062

A rise in NAD precursor nicotinamide mononucleotide (NMN) after injury promotes axon degeneration.

Di Stefano M, Nascimento-Ferreira I, Orsomando G

Cell death and differentiation
1476-5403: (2014)

PMID: 25323584