Publications

Publications

In-house

Badin AS, Morrill P, Devonshire IM, Greenfield SA. (2016) (II) "Physiological profiling of an endogenous peptide in the basal forebrain: Age-related bioactivity and blockade with a novel modulator." Neuropharmacology, 105:47-60. doi: 10.1016/j.neuropharm.2016.01.012.

Badin, AS, Fermani, F and Greenfield, SA. (2017) "The features and functions of neuronal assemblies: possible dependency on mechanisms beyond synaptic transmission." Front Neural Circuits. 2017 Jan 10;10:114. doi: 10.3389/fncir.2016.00114. eCollection 2016. View PDF

Badin, S., Eraifej, J,. Greenfield, S. A. (2013) High-resolution spatio-temporal bioactivity of a novel peptide revealed by optical imaging in rat orbitofrontal cortex in vitro: possible implications for neurodegenerative diseases. Neuropharmacology. 2013 Oct;73:10-8. doi: 10.1016/j.neuropharm.2013.05.019. Epub 2013 May 24. 

Bon, C. L. M. & Greenfield, S. A. (2003) Bioactivity of a peptide derived from acetylcholinesterase: electrophysiological characterization in guinea-pig hippocampus. Eur J Neurosci 17, 1991-1995, doi:DOI 10.1046/j.1460-9568.2003.02648.x. View PDF

Bond, C. E. & Greenfield, S. A. (2007) L-type voltage-gated calcium channels regulate astroglial responses to oxidative Stress. Neuron Glia Biol 2, S71-S71.

Bond, C. E. & Greenfield, S. A. (2007) Multiple cascade effects of oxidative stress on astroglia. Glia 55, 1348-1361, doi:Doi 10.1002/Glia.20547. View PDF

Bond, C. E., Zimmermann, M. & Greenfield, S. A. (2009) Upregulation of alpha 7 Nicotinic Receptors by Acetylcholinesterase C-Terminal Peptides. Plos One 4, -, doi:Artn E4846 Doi 0.1371/Journal.Pone.0004846. View PDF

Brai E, Stuart S, Badin AS & Greenfield SA. (2017) "A novel ex-vivo model to investigate the underlying mechanism in Alzheimer’s disease." Front. Cell. Neurosci. Doi: 10.3389/fncel.2017.00291.View PDF

Day, T. & Greenfield, S. A. (2002) A non-cholinergic, trophic action of acetylcholinesterase on hippocampal neurones in vitro: Molecular mechanisms. Neuroscience 111, 649-656, doi:Pii S0306-4522(02)00031-3. View PDF

Day, T. & Greenfield, S. A. (2003) A peptide derived from acetylcholinesterase induces neuronal cell death: characterisation of possible mechanisms. Exp Brain Res 153, 334-342, doi:DOI 10.1007/s00221-003-1567-5. View PDF

Day, T. & Greenfield, S. A. (2004) Bioactivity of a peptide derived from acetylcholinesterase in hippocampal organotypic cultures. Exp Brain Res 155, 500-508, doi:DOI 10.1007/s00221-003-1757-1. View PDF

Emmett, S. R. & Greenfield, S. A. (2004) A peptide derived from the C-terminal region of acetylcholinesterase modulates extracellular concentrations of acetylcholinesterase in the rat substantia nigra. Neurosci Lett 358, 210-214, doi:DOI 10.1016/j.neulet.2003.12.078. View PDF

Garcia-Ratés, S and Greenfield SA (2017) "Cancer and neurodegeneration: two sides, same coin?" Oncotarget, 2017, Vol. 8, (No. 14), pp: 22307-22308 View PDF

Garcia-Ratés, S, Morrill, P, Tu, H, Pottiez, G, Badin, A-S, Tormo-Garcia, C, Heffner, C, Coen, CW & Greenfield, SA. (2016) (I) "Pharmacological profiling of a novel modulator of the α7 nicotinic receptor: Blockade of a toxic acetylcholinesterase-derived peptide increased in Alzheimer brains." Neuropharmacology, vol 105, pp. 487-499., 10.1016/j.neuropharm.2016.02.006. 

Garcia-Ratés, S., Lewis, M., Worral R., & Greenfield S. A. (2013) Additive Toxicity of β-Amyloid by aNovel Bioactive Peptide In Vitro: Possible Implications for Alzheimer’s Disease. PLoS ONE 8(2):e54864. doi:10.1371/journal.pone.0054864 PLOS1. 

Greenfield SA (2005) A peptide derived from acetylcholinesterase is a pivotal signaling molecule in neurodegeneration. Chemico-Biological Interactions Vol 157-158, pp 122-218. View PDF

Greenfield SA (2013) Discovering and targeting the basic mechanism of neurodegeneration: the role of peptides from the c-terminus of acetylcholinesterase Chemico-Biological Interactions. 2013 May 25;203(3):543-6. doi: 10.1016/j.cbi.2013.03.015. Epub 2013 Apr 3. View PDF

Greenfield SA, Badin AS, Ferrati G, Devonshire IA. (2017) "Optical imaging of the rat brain suggests a previously missing link between top-down and bottom-up nervous system function." Neurophoton. 4(3), 031213 (2017), doi: 10.1117/1.NPh.4.3.031213.

Greenfield SA, Zimmermann M. and Bond CE. (2008) Non-hydrolytic functions of ACHE: The significance of C-terminal peptides. Federation of European Biochemical Societies. FEBS Journal 275, pp 604-611. View PDF

Greenfield, S. & Vaux, D. J. (2002) Parkinson’s disease, Alzheimer’s disease and motor neurone disease: Identifying a common mechanism. Neuroscience 113, 485-492. View PDF

Greenfield, S. A., Day, T., Mann, E. O. & Bermudez, I. (2004) A novel peptide modulates alpha 7 nicotinic receptor responses: implications for a possible trophic-toxic mechanism within the brain. J Neurochem 90, 325-331, doi:DOI 10.1111/j.1471-4159.2004.02494.x. View PDF

Greenfield, S. A., Zimmermann, M. & Bond, C. E. (2008) Non-hydrolytic functions of acetylcholinesterase – The significance of C-terminal peptides. Febs J 275, 604-611, doi:DOI 10.1111/j.1742-4658.2007.06235.x. View PDF

Greenfield, SA (1992) Cell death in Parkinson’s disease. Essays in Biochem. 27, pp 103-118. 

Halliday, A. C. & Greenfield, S. A. (2012) From Protein to Peptides: a Spectrum of Non-Hydrolytic Functions of Acetylcholinesterase. Protein & Peptide Letters 19, 165-172, doi:10.2174/092986612799080149. 

Halliday, A. C., Kim, O., Bond, C. E. & Greenfield, S. A. (2010) Evaluation of a technique to identify acetylcholinesterase C-terminal peptides in human serum samples. Chem-Biol Interact 187, 110-114, doi:10.1016/j.cbi.2010.02.010. View PDF

Mann, E. O., Tominaga, T., Ichikawa, M. & Greenfield, S. A. (2005) Cholinergic modulation of the spatiotemporal pattern of hippocampal activity in vitro. Neuropharmacology 48, 118-133, doi:DOI 10.1016/j.neuropharm.2004.08.022. View PDF

Onganer, P. U., Djamgoz, M. B. A., Whyte, K. & Greenfield, S. A. (2006) An acetylcholinesterasederived peptide inhibits endocytic membrane activity in a human metastatic breast cancer cell line. Bba-Gen Subjects 1760, 415-420, doi:DOI 10.1016/j.bbagen.2005.12.016. View PDF

Pepper, C, Tu, H, Morrill, P, Garcia-Rates, S, Fegan, C and Greenfield, S. (2017) "Tumour cell migration is inhibited by a novel therapeutic strategy antagonising the alpha-7 receptor." Oncotarget. 2017 Feb 14;8(7):11414-11424. doi: 10.18632/oncotarget.14545. 

Small GW, Greenfield S. "Current and Future Treatments for Alzheimer Disease." Am J Geriatr Psychiatry. 2015 Nov; 23 (11):1101-5. doi: 10.1016/j.jagp.2015.08.006.

Whyte, K. A. & Greenfield, S. A. (2003) Effects of acetylcholinesterase and butyrylcholinesterase on cell survival, neurite outgrowth, and voltage-dependent calcium currents of embryonic ventral mesencephalic neurons. Exp Neurol 184, 496-509, doi:Doi 10.1016/S0014-4886(03)00386-8. View PDF

Zbarsky, V., Thomas, J. & Greenfield, S. (2004) Bioactivity of a peptide derived from acetylcholinesterase: involvement of an ivermectin-sensitive site on the alpha 7 nicotinic receptor. Neurobiology of Disease 16, 283-289, doi:10.1016/j.nbd.2004.02.009. View PDF

Zimmermann, M., Grosgen, S., Westwell, M. S. & Greenfield, S. A. (2008) Selective enhancement of the activity of C-terminally truncated, but not intact, acetylcholinesterase. J Neurochem 104, 221-232, doi:DOI 10.1111/j.1471-4159.2007.05045.x. View PDF


Supporting Publications

Arendt, T., M. K. Bruckner, M. Lange and V. Bigl (1992) “Changes in acetylcholinesterase and butyrylcholinesterase in Alzheimer’s disease resemble embryonic development–a study of molecular forms.” Neurochem Int 21(3): 381-396.

Attems et al. (2012) The relationship between subcortical tau pathology and Alzheimer’s diseaseBiochem Soc Trans. 40 (4): 711-5.

Bond, C. E. et al. (2006) Astroglia up-regulate transcription and secretion of ‘readthrough’ acetylcholinesterase following oxidative stress. Eur J Neurosci 24, 381-386, doi:DOI 10.1111/j.1460-9568.2006.04989.x. 

Bondareff et al. (1987) Neuronal degeneration in locus coreuleus and cortical correlates of Alzheimers disease. Arch Neurol 60 (3): 337-41.

Braak & Del Tredici (2011) Alzheimer’s pathogenesis: is there neuron-to-neuron propagation? Acta neuropathol. 121 (5): 589-95.

Braak & Del Tredici. (2012) Where, when, and in what form does sporadic Alzheimer’s disease begin? Curr opin Neurol. 25 (6): 708-14.

Braak et al. (2011) Stages of the Pathologic Process in Alzheimer Disease: Age Categories From 1 to 100 YearsJournal of Neuropathology & Experimental Neurology. 70(11):960-969.

Card, J. P., R. P. Meade and L. G. Davis (1988) “Immunocytochemical localization of the precursor protein for beta-amyloid in the rat central nervous system.” Neuron 1(9): 835-846.

Garcia-Ayllon, M. S., D. H. Small, J. Avila and J. Saez-Valero (2011) “Revisiting the Role of Acetylcholinesterase in Alzheimer’s Disease: Cross-Talk with P-tau and beta-Amyloid.” Front Mol Neurosci 4: 22.

Garcia-Ayllon, M. S., I. Riba-Llena, C. Serra-Basante, J. Alom, R. Boopathy and J. Saez-Valero (2010) “Altered levels of acetylcholinesterase in Alzheimer plasma.” PLoS One 5(1): e8701.

Garcia-Ayllón, M.-S., E. Llorens, J. Avila, J. Alom and J. Saez-Valero (2014) “Elevated Acetylcholinesterase Levels by Hyperphosphorylated Tau Overexpression.” Alzheimer’s & Dementia 10(4): P651.

Haglund et al. (2006) Locus coeruleus degeneration is ubiquitous in Alzheimer’s disease: possible implications for diagnosis and treatment.Neurophatology 26 (6): 528-32.

Horvath et al. (2014) Neuropathology of Parkinsonism in patients with pure Alzheimer’s disease. J Alzheimers Dis. 39 (1): 115-20.

Irwin, D. J., Lee, V. M. & Trojanowski, J. Q. Parkinson’s disease dementia: convergence of alpha synuclein, tau and amyloid-beta pathologies (2013) Nature reviews. Neuroscience 14, 626-636,

Lea Tenenholz Grinberg, Udo Rueb and Helmut Heinsen. (2011) Brainstem: Neglected Locus in Neurodegenerative Diseases. Front Neuro); 2: 42.

Mohs R. and Greig N. (2017) Drug discovery and development: Role of basic biological research: Alzheimer's & Dementia: Tranlational Research & Clinical Interventions, 3 (4) 651-657

Morgan et al. (2012) Can the flow of medicines be improved? Fundametnal pharmacokinetic and pharmacological principles towards improving Phase II survival: Drug Discovery Today. 17(9-10) 419-424

Rossor MN. (1981) Parkinson’s disease and Alzheimer’s disease as disorders of the isodendritic core. Br Med J (Clin Res Ed). 19 Dec 12;283(6306):1588-90.

Simic et al. (2009) Does Alzheimer’s disease begin in the brainstem? Neuropathol Appl Neuobiol. 35 (6): 532-54.

Szot (2012) Common factors among Alzheimer’s disease, Parkinson disease, and epilepsy: possible role of the noradrenergic nervous system. Epilepsi 53 (1): 61-6.

Trillo et al. (2013) Ascending monoaminergic systems alterations in Alzheimer’s disease, translantic basic science into clinical careNeurosci Biobehav Rev. 37 (8): 1363-79.

Weinshenker (2008) Functional consequences of locus coeruleus degeneration in Alzheimer’s disease. Curr Alzheimer Res 5 (3): 342-5.

Woolf, N. J. (1996) “Global and serial neurons form A hierarchically arranged interface proposed to underlie memory and cognition.” Neuroscience 74(3): 625-651.

Zarow et al. (2003) Neuronal loss is greater in the locus coeruleus than nucleus basalis and substantia nigra in Alzheimers and Parkinson diseasesArch Neurol 60 (30): 337-41.