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Amylin Analog Pramlintide Induces Migraine-like Attacks in Patients

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Harvard

Ghanizada, H, Al-Karagholi, MA-M, Walker, CS, Arngrim, N, Rees, T, Petersen, J, Siow, A, Mørch-Rasmussen, M, Tan, S, O'Carroll, SJ, Harris, P, Skovgaard, LT, Jørgensen, NR, Brimble, M, Waite, JS, Rea, BJ, Sowers, LP, Russo, AF, Hay, DL & Ashina, M 2021, 'Amylin Analog Pramlintide Induces Migraine-like Attacks in Patients', Annals of Neurology, bind 89, nr. 6, s. 1157-1171. https://doi.org/10.1002/ana.26072

APA

Ghanizada, H., Al-Karagholi, M. A-M., Walker, C. S., Arngrim, N., Rees, T., Petersen, J., Siow, A., Mørch-Rasmussen, M., Tan, S., O'Carroll, S. J., Harris, P., Skovgaard, L. T., Jørgensen, N. R., Brimble, M., Waite, J. S., Rea, B. J., Sowers, L. P., Russo, A. F., Hay, D. L., & Ashina, M. (2021). Amylin Analog Pramlintide Induces Migraine-like Attacks in Patients. Annals of Neurology, 89(6), 1157-1171. https://doi.org/10.1002/ana.26072

CBE

Ghanizada H, Al-Karagholi MA-M, Walker CS, Arngrim N, Rees T, Petersen J, Siow A, Mørch-Rasmussen M, Tan S, O'Carroll SJ, Harris P, Skovgaard LT, Jørgensen NR, Brimble M, Waite JS, Rea BJ, Sowers LP, Russo AF, Hay DL, Ashina M. 2021. Amylin Analog Pramlintide Induces Migraine-like Attacks in Patients. Annals of Neurology. 89(6):1157-1171. https://doi.org/10.1002/ana.26072

MLA

Vancouver

Author

Ghanizada, Hashmat ; Al-Karagholi, Mohammad Al-Mahdi ; Walker, Christopher S ; Arngrim, Nanna ; Rees, Tayla ; Petersen, Jakeb ; Siow, Andrew ; Mørch-Rasmussen, Mette ; Tan, Sheryl ; O'Carroll, Simon J ; Harris, Paul ; Skovgaard, Lene Theil ; Jørgensen, Niklas Rye ; Brimble, Margaret ; Waite, Jayme S ; Rea, Brandon J ; Sowers, Levi P ; Russo, Andrew F ; Hay, Debbie L ; Ashina, Messoud. / Amylin Analog Pramlintide Induces Migraine-like Attacks in Patients. I: Annals of Neurology. 2021 ; Bind 89, Nr. 6. s. 1157-1171.

Bibtex

@article{c75b53f2152842f8b27358b342d90df1,
title = "Amylin Analog Pramlintide Induces Migraine-like Attacks in Patients",
abstract = "OBJECTIVE: Migraine is a prevalent and disabling neurological disease. Its genesis is poorly understood, and there remains unmet clinical need. We aimed to identify mechanisms and thus novel therapeutic targets for migraine using human models of migraine and translational models in animals, with emphasis on amylin, a close relative of calcitonin gene-related peptide (CGRP).METHODS: Thirty-six migraine without aura patients were enrolled in a randomized, double-blind, 2-way, crossover, positive-controlled clinical trial study to receive infusion of an amylin analogue pramlintide or human αCGRP on 2 different experimental days. Furthermore, translational studies in cells and mouse models, and rat, mouse and human tissue samples were conducted.RESULTS: Thirty patients (88%) developed headache after pramlintide infusion, compared to 33 (97%) after CGRP (p = 0.375). Fourteen patients (41%) developed migraine-like attacks after pramlintide infusion, compared to 19 patients (56%) after CGRP (p = 0.180). The pramlintide-induced migraine-like attacks had similar clinical characteristics to those induced by CGRP. There were differences between treatments in vascular parameters. Human receptor pharmacology studies showed that an amylin receptor likely mediates these pramlintide-provoked effects, rather than the canonical CGRP receptor. Supporting this, preclinical experiments investigating symptoms associated with migraine showed that amylin treatment, like CGRP, caused cutaneous hypersensitivity and light aversion in mice.INTERPRETATION: Our findings propose amylin receptor agonism as a novel contributor to migraine pathogenesis. Greater therapeutic gains could therefore be made for migraine patients through dual amylin and CGRP receptor antagonism, rather than selectively targeting the canonical CGRP receptor. ANN NEUROL 2021.",
author = "Hashmat Ghanizada and Al-Karagholi, {Mohammad Al-Mahdi} and Walker, {Christopher S} and Nanna Arngrim and Tayla Rees and Jakeb Petersen and Andrew Siow and Mette M{\o}rch-Rasmussen and Sheryl Tan and O'Carroll, {Simon J} and Paul Harris and Skovgaard, {Lene Theil} and J{\o}rgensen, {Niklas Rye} and Margaret Brimble and Waite, {Jayme S} and Rea, {Brandon J} and Sowers, {Levi P} and Russo, {Andrew F} and Hay, {Debbie L} and Messoud Ashina",
note = "{\textcopyright} 2021 American Neurological Association.",
year = "2021",
month = jun,
doi = "10.1002/ana.26072",
language = "English",
volume = "89",
pages = "1157--1171",
journal = "Annals of Neurology",
issn = "0364-5134",
publisher = "John/Wiley & Sons, Inc. John/Wiley & Sons Ltd",
number = "6",

}

RIS

TY - JOUR

T1 - Amylin Analog Pramlintide Induces Migraine-like Attacks in Patients

AU - Ghanizada, Hashmat

AU - Al-Karagholi, Mohammad Al-Mahdi

AU - Walker, Christopher S

AU - Arngrim, Nanna

AU - Rees, Tayla

AU - Petersen, Jakeb

AU - Siow, Andrew

AU - Mørch-Rasmussen, Mette

AU - Tan, Sheryl

AU - O'Carroll, Simon J

AU - Harris, Paul

AU - Skovgaard, Lene Theil

AU - Jørgensen, Niklas Rye

AU - Brimble, Margaret

AU - Waite, Jayme S

AU - Rea, Brandon J

AU - Sowers, Levi P

AU - Russo, Andrew F

AU - Hay, Debbie L

AU - Ashina, Messoud

N1 - © 2021 American Neurological Association.

PY - 2021/6

Y1 - 2021/6

N2 - OBJECTIVE: Migraine is a prevalent and disabling neurological disease. Its genesis is poorly understood, and there remains unmet clinical need. We aimed to identify mechanisms and thus novel therapeutic targets for migraine using human models of migraine and translational models in animals, with emphasis on amylin, a close relative of calcitonin gene-related peptide (CGRP).METHODS: Thirty-six migraine without aura patients were enrolled in a randomized, double-blind, 2-way, crossover, positive-controlled clinical trial study to receive infusion of an amylin analogue pramlintide or human αCGRP on 2 different experimental days. Furthermore, translational studies in cells and mouse models, and rat, mouse and human tissue samples were conducted.RESULTS: Thirty patients (88%) developed headache after pramlintide infusion, compared to 33 (97%) after CGRP (p = 0.375). Fourteen patients (41%) developed migraine-like attacks after pramlintide infusion, compared to 19 patients (56%) after CGRP (p = 0.180). The pramlintide-induced migraine-like attacks had similar clinical characteristics to those induced by CGRP. There were differences between treatments in vascular parameters. Human receptor pharmacology studies showed that an amylin receptor likely mediates these pramlintide-provoked effects, rather than the canonical CGRP receptor. Supporting this, preclinical experiments investigating symptoms associated with migraine showed that amylin treatment, like CGRP, caused cutaneous hypersensitivity and light aversion in mice.INTERPRETATION: Our findings propose amylin receptor agonism as a novel contributor to migraine pathogenesis. Greater therapeutic gains could therefore be made for migraine patients through dual amylin and CGRP receptor antagonism, rather than selectively targeting the canonical CGRP receptor. ANN NEUROL 2021.

AB - OBJECTIVE: Migraine is a prevalent and disabling neurological disease. Its genesis is poorly understood, and there remains unmet clinical need. We aimed to identify mechanisms and thus novel therapeutic targets for migraine using human models of migraine and translational models in animals, with emphasis on amylin, a close relative of calcitonin gene-related peptide (CGRP).METHODS: Thirty-six migraine without aura patients were enrolled in a randomized, double-blind, 2-way, crossover, positive-controlled clinical trial study to receive infusion of an amylin analogue pramlintide or human αCGRP on 2 different experimental days. Furthermore, translational studies in cells and mouse models, and rat, mouse and human tissue samples were conducted.RESULTS: Thirty patients (88%) developed headache after pramlintide infusion, compared to 33 (97%) after CGRP (p = 0.375). Fourteen patients (41%) developed migraine-like attacks after pramlintide infusion, compared to 19 patients (56%) after CGRP (p = 0.180). The pramlintide-induced migraine-like attacks had similar clinical characteristics to those induced by CGRP. There were differences between treatments in vascular parameters. Human receptor pharmacology studies showed that an amylin receptor likely mediates these pramlintide-provoked effects, rather than the canonical CGRP receptor. Supporting this, preclinical experiments investigating symptoms associated with migraine showed that amylin treatment, like CGRP, caused cutaneous hypersensitivity and light aversion in mice.INTERPRETATION: Our findings propose amylin receptor agonism as a novel contributor to migraine pathogenesis. Greater therapeutic gains could therefore be made for migraine patients through dual amylin and CGRP receptor antagonism, rather than selectively targeting the canonical CGRP receptor. ANN NEUROL 2021.

UR - http://www.scopus.com/inward/record.url?scp=85104046048&partnerID=8YFLogxK

U2 - 10.1002/ana.26072

DO - 10.1002/ana.26072

M3 - Journal article

C2 - 33772845

VL - 89

SP - 1157

EP - 1171

JO - Annals of Neurology

JF - Annals of Neurology

SN - 0364-5134

IS - 6

ER -

ID: 65608616