Background: The use of dihydropyridine calcium channel blockers (DCCBs) was proposed to reduce the risk of Parkinson's disease (PD). This study aimed to evaluate the association between DCCB and its dose effect and the risk of PD in patients with newly diagnosed hypertension.

Methods: This population-based retrospective cohort study enrolled 107,207 patients with newly diagnosed hypertension, between 2001 and 2013, from Taiwan's National Health Insurance Research Database. Patients who had PD before hypertension or were taking antipsychotics for more than 30 days in the 6 months prior to the end of the observation period were excluded. A Cox proportional hazard model was used to estimate the risk of PD in different groups. The dose-related effects of DCCB on the risk of PD were evaluated according to the cumulative defined daily dose (DDD).

Results: We observed 832 (1.2%) PD cases in patients treated with DCCB as compared to 950 (2.4%) PD cases in those not treated with DCCB, during a median follow-up duration of 8.3 years and 6.2 years, respectively. The risk of PD in the DCCB-treated group (hazard ratio [HR] = 0.50) was significantly lower than that in the group without DCCB treatment. DCCB reduced the risk of PD in a dose-dependent manner, with HRs ranging from 0.61 to 0.37 for DDDs of 90-180 to >720.

Conclusions: DCCB treatment was associated with a significantly reduced risk of PD in patients with newly diagnosed hypertension. Further clinical trials are needed to confirm the proposed neuroprotective effects of DCCB in PD.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.jns.2021.117412DOI Listing

Publication Analysis

Top Keywords

reduced risk
12
patients newly
12
newly diagnosed
12
calcium channel
8
channel blockers
8
associated reduced
8
risk
8
risk parkinson's
8
parkinson's disease
8
patients hypertension
8

Similar Publications

Drug Development.

Alzheimers Dement

December 2024

GSK R&D, Stevenage, Hertfordshire, United Kingdom.

Background: Genetic variants in GRN, the gene encoding progranulin, are causal for or are associated with the risk of multiple neurodegenerative diseases. Modulating progranulin has been considered as a therapeutic strategy for neurodegenerative diseases including Frontotemporal Dementia (FTD) and Alzheimer's Disease (AD). Here, we integrated genetics with proteomic data to determine the causal human evidence for the therapeutic benefit of modulating progranulin in AD.

View Article and Find Full Text PDF

Background: Traumatic Brain Injury (TBI) is one of the most common nonheritable causes of Alzheimer's disease (AD). However, there is lack of effective treatment for both AD and TBI. We posit that network-based integration of multi-omics and endophenotype disease module coupled with large real-world patient data analysis of electronic health records (EHR) can help identify repurposable drug candidates for the treatment of TBI and AD.

View Article and Find Full Text PDF

Drug Development.

Alzheimers Dement

December 2024

MEPSGEN, Seoul, Korea, Republic of (South).

Background: Impaired Aβ clearance plays a key role in the common, late-onset AD. Anti-Aβ immunotherapies are controversial, in part because of high rates of serious side effects including edema, microhemorrhages, and siderosis, highlighting the importance of the development of alternative Aβ clearance strategy. Here, we introduce a bioinspired nanoparticle named MG-PE3 crossing the human blood-brain barrier (BBB) and clearing Aβ with no adverse effect.

View Article and Find Full Text PDF

Background: Although investment in biomedical and pharmaceutical research has increased significantly over the past two decades, there are no oral disease-modifying treatments for Alzheimer's disease (AD).

Method: We performed comprehensive human genetic and multi-omics data analyses to test likely causal relationship between EPHX2 (encoding soluble epoxide hydrolase [sEH]) and risk of AD. Next, we tested the effect of the oral administration of EC5026 (a first-in-class, picomolar sEH inhibitor) in a transgenic mouse model of AD-5xFAD and mechanistic pathways of EC5026 in patient induced Pluripotent Stem Cells (iPSC) derived neurons.

View Article and Find Full Text PDF

Background: Epidemiological studies report an elevated risk of neurodegenerative disorders, particularly Parkinson's disease (PD), in patients with type 2 diabetes mellitus (T2DM) that is mitigated in those prescribed incretin mimetics or dipeptidyl peptidase 4 inhibitors (DPP-4Is). Incretin mimetic repurposing appears promising in human PD and Alzheimer's disease (AD) clinical trials. DPP-4Is are yet to be evaluated in PD or AD human studies.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!