Motor and Cognitive Advantages Persist 12 Months after Exenatide Exposure in Parkinson's Disease

Journal of Parkinson's Disease

Volumn 4, Issue 3, 2015, Pages 337-344

  Aviles Olmos, Iciar ^a   Dickson, John ^b   Kefalopoulou, Zinovia ^a   Djamshidian, Atbin ^c   Kahan, Joshua ^a   Ell, Peter ^b   Whitton, Peter ^d   Wyse, Richard ^e   Isaacs, Tom ^e   Lees, Andrew ^c   Limousin, Patricia ^a   Foltynie, Thomas ^a  

^a UNIVERSITY COLLEGE LONDON   (United Kingdom)

^b UNIVERSITY COLLEGE LONDON HOSPITALS   (United Kingdom)

^c UNIVERSITY COLLEGE LONDON   (United Kingdom)

^d UNIVERSITY OF LONDON   (United Kingdom)

^e UK   (United Kingdom)

Author keywords

Clinical trial; Diabetes mellitus; Disease modifying treatment; Exenatide; Parkinson's disease; UPDRS

Indexed keywords

EXENDIN 4; LEVODOPA; ANTIPARKINSON AGENT; PEPTIDE; VENOM;

ADULT; ARTICLE; CLINICAL ARTICLE; COGNITION; COGNITIVE DEFECT; CONTROLLED STUDY; DEMENTIA ASSESSMENT; DISEASE SEVERITY; DRUG EXPOSURE; DRUG SELF ADMINISTRATION; DRUG WITHDRAWAL; DYSGEUSIA; FOLLOW UP; GASTROINTESTINAL SYMPTOM; HUMAN; MATTIS DEMENTIA RATING SCALE; MIDDLE AGED; MONTGOMERY ASBERG DEPRESSION RATING SCALE; MOTOR DYSFUNCTION; MOTOR PERFORMANCE; MOVEMENT DISORDERS SOCIETY UNIFIED PARKINSON DISEASE RATING SCALE; NEUROLOGIC DISEASE ASSESSMENT; NEUROPROTECTION; OPEN STUDY; ORAL GLUCOSE TOLERANCE TEST; OUTCOME ASSESSMENT; PARKINSON DISEASE; PDQ39; PRIORITY JOURNAL; RANDOMIZED CONTROLLED TRIAL; SIDE EFFECT; WEIGHT REDUCTION; TREATMENT OUTCOME;

ANTIPARKINSON AGENTS; COGNITION; FOLLOW-UP STUDIES; HUMANS; MIDDLE AGED; PARKINSON DISEASE; PEPTIDES; TREATMENT OUTCOME; VENOMS;

EID: 84904126994     PISSN: 18777171     EISSN: 1877718X     Source Type: Journal    
DOI: 10.3233/JPD-140364     Document Type: Article

References (18)

1. Aviles-Olmos I, Limousin P, Lees A, & Foltynie T (2013) Parkinson's disease, insulin resistance and novel agents of neuroprotection. Brain, 136, 374-384.
2. Santiago JA, & Potashkin JA (2013) Shared dysregulated pathways lead to Parkinson's disease and diabetes. Trends Mol Med, 19, 176-186.
3. Perry T, Haughey NJ, Mattson MP, Egan JM, & Greig NH (2002) Protectionand reversalofexcitotoxic neuronal damage by glucagon-like peptide-1 and exendin-4. J Pharmacol Exp Ther, 302, 881-888.
4. Perry T, Lahiri DK, Chen D, Zhou J, Shaw KT, Egan JM, & Greig NH (2002) A novel neurotrophic property of glucagon-like peptide 1: A promoter of nerve growth factor-mediated differentiation in PC12 cells. J Pharmacol Exp Ther, 300, 958-966.
5. During MJ, Cao L, Zuzga DS, Francis JS, Fitzsimons HL, Jiao X, Bland RJ, Klugmann M, Banks WA, Drucker DJ, & Haile CN (2003) Glucagon-like peptide-1 receptor is involved in learning and neuroprotection. Nat Med, 9, 1173-1179.
6. Harkavyi A, Abuirmeileh A, Lever R, Kingsbury AE, Biggs CS, & Whitton PS (2008) Glucagon-like peptide 1 receptor stimulation reverses key deficits in distinct rodent models of Parkinson's disease. J Neuroinflammation, 5, 19.
7. Bertilsson G, Patrone C, Zachrisson O, Andersson A, Dan-naeus K, Heidrich J, Kortesmaa J, Mercer A, Nielsen E, Rönnholm H, & Wikström L (2008) Peptide hormone exendin-4 stimulates subventricular zone neurogenesis in the adult rodent brain and induces recovery in an animal model of Parkinson's disease. J Neurosci Res, 86, 326-338.
8. Li Y, Perry T, Kindy MS, Harvey BK, Tweedie D, Holloway HW, Powers K, Shen H, Egan JM, Sambamurti K, Brossi A, Lahiri DK, Mattson MP, Hoffer BJ, Wang Y, & Greig NH (2009) GLP-1 receptor stimulation preserves primary cortical and dopaminergic neurons in cellular and rodent models of stroke and Parkinsonism. Proc Natl Acad Sci U S A, 106, 1285-1290.
9. Kim S, Moon M, & Park S (2009) Exendin-4 protects dopaminergic neurons by inhibition of microglial activation and matrix metalloproteinase-3 expressioninananimal model of Parkinson's disease. J Endocrinol, 202, 431-439.
10. Aviles-Olmos I, Dickson J, Kefalopoulou Z, Djamshidian A, Ell P, Soderlund T, Whitton P, Wyse R, Isaacs T, Lees A, Limousin P, & Foltynie T (2013) Exenatide and the treatment of patients with Parkinson's disease. J Clin Invest, 2730-2736.
11. Barker RA, Stacy M, & Brundin P (2013) A new approach to disease-modifying drug trials in Parkinson's disease. J Clin Invest, 123, 2364-2365.
12. Schrag A, Quinn NP, & Ben-Shlomo Y (2006) Heterogeneity of Parkinson's disease. J Neurol Neurosurg Psychiatry, 77, 275-276.
13. Fearnley JM, & Lees AJ (1991) Ageing and Parkinson's disease: Substantia nigra regional selectivity. Brain, 114, 2283-2301.
14. Hilker R, Schweitzer K, Coburger S, Ghaemi M, Weisenbach S, Jacobs AH, Rudolf J, Herholz K, & Heiss WD (2005) Nonlinear progression of Parkinson disease as determined by serial positron emission tomographic imaging of striatal fluorodopa F 18 activity. Arch Neurol, 62, 378-382.
15. Schrag A, Dodel R, Spottke A, Bornschein B, Siebert U, & Quinn NP (2007) Rate of clinical progression in Parkinson's disease. A prospective study. Mov Disord, 22, 938-945.
16. Olanow CW, RascolO,HauserR,Feigin PD, JankovicJ,Lang A, Langston W, Melamed E, Poewe W, Stocchi F, & Tolosa E (2009) A double-blind, delayed-start trial of rasagiline in Parkinson's disease. N Engl J Med, 361, 1268-1278.
17. Evans JR, Mason SL, Williams-Gray CH, Foltynie T, Brayne C, Robbins TW, & Barker RA (2011) The natural history of treated Parkinson's disease in an incident, community based cohort. J Neurol Neurosurg Psychiatry, 82, 1112-1118.
18. Piboolnurak P, Lang AE, Lozano AM, et al. (2007) Levodopa response in long-term bilateral subthalamic stimulation for Parkinson's disease. Mov Disord, 22(7), 990-997.