Imperial College London

Dr Tony Goldstone

Faculty of MedicineDepartment of Medicine

Senior Clinical Research Fellow
 
 
 
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Contact

 

+44 (0)20 7594 5989tony.goldstone Website

 
 
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Location

 

E313Burlington DanesHammersmith Campus

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Summary

 

Publications

Publication Type
Year
to

93 results found

Azor AM, Cole JH, Holland AJ, Dumba M, Patel MC, Sadlon A, Goldstone AP, Manning KEet al., 2019, Increased brain age in adults with Prader-Willi syndrome., Neuroimage Clin, Vol: 21

Prader-Willi syndrome (PWS) is the most common genetic obesity syndrome, with associated learning difficulties, neuroendocrine deficits, and behavioural and psychiatric problems. As the life expectancy of individuals with PWS increases, there is concern that alterations in brain structure associated with the syndrome, as a direct result of absent expression of PWS genes, and its metabolic complications and hormonal deficits, might cause early onset of physiological and brain aging. In this study, a machine learning approach was used to predict brain age based on grey matter (GM) and white matter (WM) maps derived from structural neuroimaging data using T1-weighted magnetic resonance imaging (MRI) scans. Brain-predicted age difference (brain-PAD) scores, calculated as the difference between chronological age and brain-predicted age, are designed to reflect deviations from healthy brain aging, with higher brain-PAD scores indicating premature aging. Two separate adult cohorts underwent brain-predicted age calculation. The main cohort consisted of adults with PWS (n = 20; age mean 23.1 years, range 19.8-27.7; 70.0% male; body mass index (BMI) mean 30.1 kg/m2, 21.5-47.7; n = 19 paternal chromosome 15q11-13 deletion) and age- and sex-matched controls (n = 40; age 22.9 years, 19.6-29.0; 65.0% male; BMI 24.1 kg/m2, 19.2-34.2) adults (BMI PWS vs. control P = .002). Brain-PAD was significantly greater in PWS than controls (effect size mean ± SEM +7.24 ± 2.20 years [95% CI 2.83, 11.63], P = .002). Brain-PAD remained significantly greater in PWS than controls when restricting analysis to a sub-cohort matched for BMI consisting of n = 15 with PWS with BMI range 21.5-33.7 kg/m2, and n = 29 controls with BMI 21.7-34.2 kg/m2 (effect size +5.51 ± 2.56 years [95% CI 3.44, 10.38], P = .037). In the PWS group, brain-PAD scores were not associated with intelligence quotient (IQ), use of hormonal and psychotropic medications, nor severity of repetitive or disruptive

JOURNAL ARTICLE

Scott G, Zetterberg H, Jolly A, Cole JH, De Simoni S, Jenkins PO, Feeney C, Owen DR, Lingford-Hughes A, Howes O, Patel MC, Goldstone AP, Gunn RN, Blennow K, Matthews PM, Sharp DJet al., 2018, Minocycline reduces chronic microglial activation after brain trauma but increases neurodegeneration, BRAIN, Vol: 141, Pages: 459-471, ISSN: 0006-8950

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Glaysher MA, Mohanaruban A, Prechtl CG, Goldstone AP, Miras AD, Lord J, Chhina N, Falaschetti E, Johnson NA, Al-Najim W, Smith C, Li JV, Patel M, Ahmed AR, Moore M, Poulter N, Bloom S, Darzi A, Le Roux C, Byrne JP, Teare JPet al., 2017, A randomised controlled trial of a duodenal-jejunal bypass sleeve device (EndoBarrier) compared with standard medical therapy for the management of obese subjects with type 2 diabetes mellitus, BMJ OPEN, Vol: 7, ISSN: 2044-6055

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Tan CL, Alavi SA, Baldeweg SE, Belli A, Carson A, Feeney C, Goldstone AP, Greenwood R, Menon DK, Simpson HL, Toogood AA, Gurnell M, Hutchinson PJet al., 2017, The screening and management of pituitary dysfunction following traumatic brain injury in adults: British Neurotrauma Group guidance, JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY, Vol: 88, Pages: 971-981, ISSN: 0022-3050

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Feeney C, Sharp DJ, Hellyer PJ, Jolly AE, Cole JH, Scott G, Baxter D, Jilka S, Ross E, Ham TE, Jenkins PO, Li LM, Gorgoraptis N, Midwinter M, Goldstone APet al., 2017, Serum IGF-I levels are associated with improved white matter recovery after TBI., Annals of Neurology, Vol: 82, Pages: 30-43, ISSN: 0364-5134

OBJECTIVE: Traumatic brain injury (TBI) is a common disabling condition with limited treatment options. Diffusion tensor imaging (DTI) measures recovery of axonal injury in white matter (WM) tracts after TBI. Growth hormone deficiency (GHD) after TBI may impair axonal and neuropsychological recovery, and serum IGF-I may mediate this effect. We conducted a longitudinal study to determine the effects of baseline serum IGF-I concentrations on WM tract and neuropsychological recovery after TBI. METHODS: Thirty-nine adults after TBI (84.6% male; age median 30.5y; 87.2% moderate-severe; time since TBI median 16.3 months, n=4 with GHD) were scanned twice, 13.3 months (12.1-14.9) apart, and 35 healthy controls scanned once. Symptom and quality of life questionnaires and cognitive assessments were completed at both visits (n=33). Our main outcome measure was fractional anisotropy (FA), a measure of WM tract integrity, in a priori regions of interest: splenium of corpus callosum (SPCC), and posterior limb of internal capsule (PLIC). RESULTS: At baseline, FA was reduced in many WM tracts including SPCC and PLIC following TBI compared to controls, indicating axonal injury, with longitudinal increases indicating axonal recovery. There was a significantly greater increase in SPCC FA over time in patients with serum IGF-I above vs. below the median-for-age. Only the higher IGF-I group had significant improvements in immediate verbal memory recall over time. INTERPRETATION: WM recovery and memory improvements after TBI were greater in patients with higher serum IGF-I at baseline. These findings suggest that GH/IGF-I system may be a potential therapeutic target following TBI. This article is protected by copyright. All rights reserved.

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Miras AD, Herring R, Vusirikala A, Shojaee-Moradi F, Jackson NC, Chandaria S, Jackson SN, Goldstone AP, Hakim N, Patel AG, Umpleby AM, Le Roux CWet al., 2017, Measurement of hepatic insulin sensitivity early after the bypass of the proximal small bowel in humans, OBESITY SCIENCE & PRACTICE, Vol: 3, Pages: 95-98, ISSN: 2055-2238

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Limbrick-Oldfield EH, Mick I, Cocks RE, McGonigle J, Sharman SP, Goldstone AP, Stokes PRA, Waldman A, Erritzoe D, Bowden-Jones H, Nutt D, Lingford-Hughes A, Clark Let al., 2017, Neural substrates of cue reactivity and craving in gambling disorder, TRANSLATIONAL PSYCHIATRY, Vol: 7, ISSN: 2158-3188

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Feeney C, Scott G, Raffel J, Roberts S, Coello C, Jolly A, Searle G, Goldstone AP, Brooks DJ, Nicholas RS, Trigg W, Gunn RN, Sharp DJet al., 2016, Kinetic analysis of the translocator protein positron emission tomography ligand [F-18]GE-180 in the human brain, EUROPEAN JOURNAL OF NUCLEAR MEDICINE AND MOLECULAR IMAGING, Vol: 43, Pages: 2201-2210, ISSN: 1619-7070

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Jamall OA, Feeney C, Zaw-Linn J, Malik A, Niemi MEK, Tenorio-Jimenez C, Ham TE, Jilka SR, Jenkins PO, Scott G, Li LM, Gorgoraptis N, Baxter D, Sharp DJ, Goldstone APet al., 2016, Prevalence and correlates of vitamin D deficiency in adults after traumatic brain injury, CLINICAL ENDOCRINOLOGY, Vol: 85, Pages: 636-644, ISSN: 0300-0664

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Feeney C, Scott GP, Cole JH, Sastre M, Goldstone AP, Leech Ret al., 2016, Seeds of neuroendocrine doubt, NATURE, Vol: 535, Pages: E1-E2, ISSN: 0028-0836

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Byrne CS, Chambers ES, Alhabeeb H, Chhina N, Morrison DJ, Preston T, Tedford C, Fitzpatrick J, Irani C, Busza A, Garcia-Perez I, Fountana S, Holmes E, Goldstone AP, Frost GSet al., 2016, Increased colonic propionate reduces anticipatory reward responses in the human striatum to high-energy foods, AMERICAN JOURNAL OF CLINICAL NUTRITION, Vol: 104, Pages: 5-14, ISSN: 0002-9165

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Iacovazzo D, Caswell R, Bunce B, Jose S, Yuan B, Hernandez-Ramirez LC, Kapur S, Caimari F, Evanson J, Ferrau F, Dang MN, Gabrovska P, Larkin SJ, Ansorge O, Rodd C, Vance ML, Ramirez-Renteria C, Mercado M, Goldstone AP, Buchfelder M, Burren CP, Gurlek A, Dutta P, Choong CS, Cheetham T, Trivellin G, Stratakis CA, Lopes M-B, Grossman AB, Trouillas J, Lupski JR, Ellard S, Sampson JR, Roncaroli F, Korbonits Met al., 2016, Germline or somatic GPR101 duplication leads to X-linked acrogigantism: a clinico-pathological and genetic study, ACTA NEUROPATHOLOGICA COMMUNICATIONS, Vol: 4, ISSN: 2051-5960

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Goldstone AP, Miras AD, Scholtz S, Jackson S, Neff KJ, Penicaud L, Geoghegan J, Chhina N, Durighel G, Bell JD, Meillon S, le Roux CWet al., 2016, Link Between Increased Satiety Gut Hormones and Reduced Food Reward After Gastric Bypass Surgery for Obesity, JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, Vol: 101, Pages: 599-609, ISSN: 0021-972X

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Scholtz S, Goldstone AP, le Roux CW, 2015, Changes in Reward after Gastric Bypass: the Advantages and Disadvantages, CURRENT ATHEROSCLEROSIS REPORTS, Vol: 17, ISSN: 1523-3804

JOURNAL ARTICLE

Alsters SIM, Goldstone AP, Buxton JL, Zekavati A, Sosinsky A, Yiorkas AM, Holder S, Klaber RE, Bridges N, van Haelst MM, le Roux CW, Walley AJ, Walters RG, Mueller M, Blakemore AIFet al., 2015, Truncating Homozygous Mutation of Carboxypeptidase E (CPE) in a Morbidly Obese Female with Type 2 Diabetes Mellitus, Intellectual Disability and Hypogonadotrophic Hypogonadism, PLOS ONE, Vol: 10, ISSN: 1932-6203

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Scheimann AO, Nadler EE, Driscoll DJ, Butler MG, Miller JL, Markovic TP, Goldstone APet al., 2015, Laparoscopic Sleeve Gastrectomy in 108 Obese Children and Adolescents Ages 5 to 21 Years by Alqahtani AR, Antonisamy B, Alamri H, Elahmedi M, Zimmerman VA, ANNALS OF SURGERY, Vol: 261, Pages: E118-E118, ISSN: 0003-4932

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Sam AH, Sleeth ML, Thomas EL, Ismail NA, Daud NM, Chambers E, Shojaee-Moradie F, Umpleby M, Goldstone AP, Le Roux CW, Bech P, Busbridge M, Laurie R, Cuthbertson DJ, Buckley A, Ghatei MA, Bloom SR, Frost GS, Bell JD, Murphy KGet al., 2015, Circulating Pancreatic Polypeptide Concentrations Predict Visceral and Liver Fat Content, JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, Vol: 100, Pages: 1048-1052, ISSN: 0021-972X

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Bereket A, Kiess W, Lustig RH, Muller HL, Goldstone AP, Weiss R, Yavuz Y, Hochberg Zet al., 2015, Hypothalamic obesity in children

© 2015 S. Karger AG, Basel. Hypothalamic obesity (HyOb) is a severe and rapidly developing form of obesity that was initially described in patients with hypothalamic tumours and surgical damage. However, this definition has now expanded to include obesity developing after a variety of insults to hypothalamic centres, such as infections, infiltrations, trauma, vascular problems, and hydrocephalus in addition to acquired or congenital functional defects in central energy homeostasis. The pathogenetic mechanisms underlying HyOb are complex and multifactorial. Weight gain results from damage to the ventromedial hypothalamus, which may lead to hyperphagia, a low resting metabolic rate, autonomic imbalance, growth hormone, gonadotropin and thyroid-stimulating hormone deficiencies, hypomobility and insomnia. Disruption of leptin signalling and decreased central sympathetic output seem to have a critical role in the development of HyOb. Surgical strategies to preserve hypothalamic integrity are mandatory for the prevention of HyOb in patients with craniopharyngioma or other hypothalamic tumours. At present, there is no standard pharmacological intervention that has been shown to consistently help these complicated patients. In select cases, octreotide seems to be effective when introduced early after the cranial insult. The safety and effectiveness of bariatric surgery in the management of HyOb has also not been well established. A general overview on HyOb with special emphasis on craniopharyngioma and Prader-Willi syndrome is provided in this chapter.

BOOK

Kweh FA, Miller JL, Sulsona CR, Wasserfall C, Atkinson M, Shuster JJ, Goldstone AP, Driscoll DJet al., 2015, Hyperghrelinemia in Prader-Willi Syndrome Begins in Early Infancy Long Before the Onset of Hyperphagia, AMERICAN JOURNAL OF MEDICAL GENETICS PART A, Vol: 167, Pages: 69-79, ISSN: 1552-4825

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Daud NM, Ismail NA, Thomas EL, Fitzpatrick JA, Bell JD, Swann JR, Costabile A, Childs CE, Pedersen C, Goldstone AP, Frost GSet al., 2014, The Impact of Oligofructose on Stimulation of Gut Hormones, Appetite Regulation and Adiposity, OBESITY, Vol: 22, Pages: 1430-1438, ISSN: 1930-7381

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Miras AD, Scholtz S, Chhina N, Durighel G, Bell JD, Le Roux C, Goldstone APet al., 2014, Role for Increased Plasma PYY and GLP-1 in Reducing Anticipatory Food Reward after Gastric Bypass Surgery, ENDOCRINE REVIEWS, Vol: 35, ISSN: 0163-769X

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Scholtz S, Miras AD, Chhina N, Prechtl CG, Sleeth ML, Daud NM, Ismail NA, Durighel G, Ahmed AR, Olbers T, Vincent RP, Alaghband-Zadeh J, Ghatei MA, Waldman AD, Frost GS, Bell JD, le Roux CW, Goldstone APet al., 2014, Obese patients after gastric bypass surgery have lower brain-hedonic responses to food than after gastric banding, GUT, Vol: 63, Pages: 891-902, ISSN: 0017-5749

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Goldstone AP, Prechtl CG, Scholtz S, Miras AD, Chhina N, Durighel G, Deliran SS, Beckmann C, Ghatei MA, Ashby DR, Waldman AD, Gaylinn BD, Thorner MO, Frost GS, Bloom SR, Bell JDet al., 2014, Ghrelin mimics fasting to enhance human hedonic, orbitofrontal cortex, and hippocampal responses to food, AMERICAN JOURNAL OF CLINICAL NUTRITION, Vol: 99, Pages: 1319-1330, ISSN: 0002-9165

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Heymsfield SB, Avena NM, Baier L, Brantley P, Bray GA, Burnett LC, Butler MG, Driscoll DJ, Egli D, Elmquist J, Forster JL, Goldstone AP, Gourash LM, Greenway FL, Han JC, Kane JG, Leibel RL, Loos RJF, Scheimann AO, Roth CL, Seeley RJ, Sheffield V, Tauber M, Vaisse C, Wang L, Waterland RA, Wevrick R, Yanovski JA, Zinn ARet al., 2014, Hyperphagia: Current Concepts and Future Directions Proceedings of the 2nd International Conference on Hyperphagia, OBESITY, Vol: 22, Pages: S1-S17, ISSN: 1930-7381

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Baxter D, Sharp DJ, Feeney C, Papadopoulou D, Ham TE, Jilka S, Hellyer PJ, Patel MC, Bennett AN, Mistlin A, McGilloway E, Midwinter M, Goldstone APet al., 2013, Pituitary Dysfunction after Blast Traumatic Brain Injury: The UK BIOSAP Study, ANNALS OF NEUROLOGY, Vol: 74, Pages: 527-536, ISSN: 0364-5134

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Bonnefond A, Raimondo A, Stutzmann F, Ghoussaini M, Ramachandrappa S, Bersten DC, Durand E, Vatin V, Balkau B, Lantieri O, Raverdy V, Pattou F, Van Hul W, Van Gaal L, Peet DJ, Weill J, Miller JL, Horber F, Goldstone AP, Driscoll DJ, Bruning JB, Meyre D, Whitelaw ML, Froguel Pet al., 2013, Loss-of-function mutations in SIM1 contribute to obesity and Prader-Willi-like features, JOURNAL OF CLINICAL INVESTIGATION, Vol: 123, Pages: 3037-3041, ISSN: 0021-9738

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Deal CL, Tony M, Hoybye C, Allen DB, Tauber M, Christiansen JSet al., 2013, Growth Hormone Research Society Workshop Summary: Consensus Guidelines for Recombinant Human Growth Hormone Therapy in Prader-Willi Syndrome, JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, Vol: 98, Pages: E1072-E1087, ISSN: 0021-972X

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Cegla J, Jones B, Seyani L, Papadoulou D, Wynne K, Martin NM, Meeran K, Chapman R, Donaldson M, Goldstone AP, Tan Tet al., 2013, Comparison of the overnight metyrapone and glucagon stimulation tests in the assessment of secondary hypoadrenalism, CLINICAL ENDOCRINOLOGY, Vol: 78, Pages: 738-742, ISSN: 0300-0664

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Goldstone AP, Holland AJ, Butler JV, Whittington JEet al., 2012, Appetite hormones and the transition to hyperphagia in children with Prader-Willi syndrome, INTERNATIONAL JOURNAL OF OBESITY, Vol: 36, Pages: 1564-1570, ISSN: 0307-0565

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Martin JL, Tedeschi M, Jackson JE, Spalding D, Goldstone AP, Cohen P, Frilling Aet al., 2012, Primary lymph node gastrinoma or metastatic gastrinoma with unidentified primary tumor site?, World Journal of Endocrine Surgery, Vol: 4, Pages: 66-70, ISSN: 0975-5039

Gastrinomas are neuroendocrine tumors that secrete gastrin and result in a clinical syndrome of peptic ulcer disease first described by Zollinger and Ellison in 1955.1 They present either sporadically or as a component of a hereditary determined syndrome, multiple endocrine neoplasia type 1. They are usually located in the pancreas and duodenum but have been reported to occur in both abdominal and extraabdominal sites.2 Reports of clinical and biochemical cure following resection of lymph nodes found to contain gastrinomas, in patients without a localized primary tumor, led investigators to cite the existence of the primary lymph node gastrinoma. Whether these cases represent metastatic disease from an, as yet, unidentified primary tumor, or de novo occurrence of a gastrinoma in a lymph node remains controversial. While some authors report that primary lymph node gastrinomas account for up to 10% of sporadic gastrinomas3,4 others question this theory, hypothesizing that their presentation represents an undetected microgastrinoma with metastatic lymph node involvement.5 Herewith, we report on a patient with Zollinger-Ellison syndrome in whom a peripancreatic lymph node with evidence of gastrinoma is the only apparent morphologic manifestation of the disease.

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