Research at Leeds Beckett
Dr Nathaniel Milton
About Dr Nathaniel Milton
Nat has an international reputation in the Alzheimer's Drug Discovery and Diagnostics research field. He is a Fellow of the Royal Society of Biology and part of the Biomedical Sciences team in the School of Clinical & Applied Sciences.
For the past 20 years Nat has led the Neuroaptamer research group, which conducts research into identification of target protein binding molecules. The focus of his research has been biochemical interactions of amyloid peptides and their role in Alzheimer's disease, Diabetes, Creutzfeldt-Jakob disease and oxidative stress responses. Nat discovered the neuroprotective actions of cannabinoids in an Alzheimer's disease cell culture model.
He has used aptamer, molecular biology, biochemical and cell biology techniques to discover and characterize the mechanisms of neuroprotection of a number of compounds. He has teaching experience, at both undergraduate and postgraduate levels, in the areas of Physiology, Pharmacology, Clinical Biochemistry, Neuroscience and Entrepreneurship.
Nat is an entrepreneur and has filed a number of patent applications, one of which was granted in the UK and others which were taken to the intention to grant stage in Europe. He has founded an in silico based company, Neurodelta Ltd and raised government funding for commercial research in the Alzheimer’s Drug Discovery and Diagnostic area.
- BSc and MSc Biomedical Sciences courses
The Neuroaptamer research group is currently focused on the roles of endogenous cannabinoid plus opioid compounds in neuroprotection against toxic amyloid peptides. The group discovered neuroprotective properties of endocannabinoids against amyloid-ß in cell based models of Alzheimer's disease and has recently identified novel mechanisms of neuroprotection by endogenous opioids.
The group has also shown that products of the KiSS-1 metastasis-suppressor gene, the Kisspeptin and Kissorphin peptides, specifically bind amyloid-ß, amylin plus prion protein peptides and are neuroprotective in vitro. KiSS-1 overexpression is also neuroprotective in vitro and acts via oxytocin/vasopressin and cyclooxygenase dependent mechanisms. A patent has been granted for the use of Kissorphin peptides in Alzheimer's disease, Type 2 Diabetes and Creutzfeldt-Jakob disease. The co-localization of Kisspeptin with amyloid-ß deposits in the pons region of Alzheimer's brain has recently been demonstrated. Co-localization of corticotropin-releasing hormone with amyloid-ß deposits and also co-localization of catalase with amyloid-ß deposits in the pons region of Alzheimer's brain has also been demonstrated.
Journal articles (11)
- Chilumuri A; Markiv A; Milton NGN (2014), Immunocytochemical staining of endogenous nuclear proteins with the HIS-1 anti-poly-histidine monoclonal antibody: A potential source of error in His-tagged protein detection.
- Chilumuri A; Odell M; Milton NGN (2013), Benzothiazole Aniline Tetra(ethylene glycol) and 3-Amino-1,2,4-triazole Inhibit Neuroprotection against Amyloid Peptides by Catalase Overexpression in Vitro.
- Chilumuri A; Milton NGN (2013), The role of neurotransmitters in protection against amyloid-β toxicity by KiSS-1 overexpression in SH-SY5Y neurons
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- Chilumuri A; Ashioti M; Nercessian AN; Milton NGN (2013), Immunolocalization of kisspeptin associated with amyloid-ß deposits in the pons of an Alzheimer's disease patient
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- Milton NGN; Harris JR (2013), Fibril formation and toxicity of the non-amyloidogenic rat amylin peptide.
- Milton NGN; Chilumuri A; Rocha-Ferreira E; Nercessian AN; Ashioti M (2012), Kisspeptin Prevention of Amyloid-β Peptide Neurotoxicity in Vitro.
- Milton N (2012), Kissorphin, a hexapeptide derivative of Kisspeptin, acts via Neuropeptide FF receptors to inhibit cyclic adenosine monophosphate release but has no Gonadotrophin-Releasing-Hormone releasing activity
- Milton NGN; Harris JR (2009), Polymorphism of amyloid-beta fibrils and its effects on human erythrocyte catalase binding.
- Milton NGN (2002), Anandamide and noladin ether prevent neurotoxicity of the human amyloid-beta peptide.
- Milton NGN (2001), Inhibition of catalase activity with 3-amino-triazole enhances the cytotoxicity of the Alzheimer's amyloid-beta peptide
- Milton NGN (1999), Amyloid-beta binds catalase with high affinity and inhibits hydrogen peroxide breakdown