The University of Southampton
University of Southampton Institutional Repository

Calcium channel antagonists as disease-modifying therapy for Parkinson's disease: Therapeutic rationale and current status

Calcium channel antagonists as disease-modifying therapy for Parkinson's disease: Therapeutic rationale and current status
Calcium channel antagonists as disease-modifying therapy for Parkinson's disease: Therapeutic rationale and current status

Parkinson's disease is a disabling hypokinetic neurological movement disorder in which the aetiology is unknown in the majority of cases. Current pharmacological treatments, though effective at restoring movement, are only symptomatic and do nothing to slow disease progression. Electrophysiological, epidemiological and neuropathological studies have implicated CaV1.3 subtype calcium channels in the pathogenesis of the disorder, and drugs with some selectivity for this ion channel (brain-penetrant dihydropyridine calcium channel blockers) are neuroprotective in animal models of the disease. Dihydropyridines have been safely used for decades to treat hypertension and other cardiovascular disorders. A phase II clinical trial found that isradipine was safely tolerated by patients with Parkinson's disease, and a phase III trial is currently underway to determine whether treatment with isradipine is neuroprotective and therefore able to slow the progression of Parkinson's disease. This manuscript reviews the current information about the use of dihydropyridines as therapy for Parkinson's disease and discusses the possible mechanism of action of these drugs, highlighting CaV1.3 calcium channels as a potential therapeutic target for neuroprotection in Parkinson's disease.

Journal Article
1172-7047
1127-1135
Swart, Tara
3925c5e7-e729-4b8c-b5bc-0db7637cb157
Hurley, Michael J.
07b0180f-8e32-4ce1-8185-e046a42ef15a
Swart, Tara
3925c5e7-e729-4b8c-b5bc-0db7637cb157
Hurley, Michael J.
07b0180f-8e32-4ce1-8185-e046a42ef15a

Swart, Tara and Hurley, Michael J. (2016) Calcium channel antagonists as disease-modifying therapy for Parkinson's disease: Therapeutic rationale and current status. CNS drugs, 30 (12), 1127-1135. (doi:10.1007/s40263-016-0393-9).

Record type: Article

Abstract

Parkinson's disease is a disabling hypokinetic neurological movement disorder in which the aetiology is unknown in the majority of cases. Current pharmacological treatments, though effective at restoring movement, are only symptomatic and do nothing to slow disease progression. Electrophysiological, epidemiological and neuropathological studies have implicated CaV1.3 subtype calcium channels in the pathogenesis of the disorder, and drugs with some selectivity for this ion channel (brain-penetrant dihydropyridine calcium channel blockers) are neuroprotective in animal models of the disease. Dihydropyridines have been safely used for decades to treat hypertension and other cardiovascular disorders. A phase II clinical trial found that isradipine was safely tolerated by patients with Parkinson's disease, and a phase III trial is currently underway to determine whether treatment with isradipine is neuroprotective and therefore able to slow the progression of Parkinson's disease. This manuscript reviews the current information about the use of dihydropyridines as therapy for Parkinson's disease and discusses the possible mechanism of action of these drugs, highlighting CaV1.3 calcium channels as a potential therapeutic target for neuroprotection in Parkinson's disease.

Full text not available from this repository.

More information

e-pub ahead of print date: 8 November 2016
Published date: December 2016
Keywords: Journal Article

Identifiers

Local EPrints ID: 416278
URI: http://eprints.soton.ac.uk/id/eprint/416278
ISSN: 1172-7047
PURE UUID: 42312534-b5c0-4d00-80d2-b2eb8d275a10

Catalogue record

Date deposited: 11 Dec 2017 17:30
Last modified: 07 Aug 2018 16:32

Export record

Altmetrics

Download statistics

Downloads from ePrints over the past year. Other digital versions may also be available to download e.g. from the publisher's website.

View more statistics

Atom RSS 1.0 RSS 2.0

Contact ePrints Soton: eprints@soton.ac.uk

ePrints Soton supports OAI 2.0 with a base URL of http://eprints.soton.ac.uk/cgi/oai2

This repository has been built using EPrints software, developed at the University of Southampton, but available to everyone to use.

We use cookies to ensure that we give you the best experience on our website. If you continue without changing your settings, we will assume that you are happy to receive cookies on the University of Southampton website.

×