Open AccessStatin therapy and risk of Alzheimer's and age‐related neurodegenerative diseases
Author(s) -
TorrandellHaro Georgina,
Branigan Gregory L.,
Vitali Francesca,
Geifman Nophar,
Zissimopoulos Julie M.,
Brinton Roberta Diaz
Publication year - 2020
Publication title -
alzheimer's and dementia: translational research and clinical interventions
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.49
H-Index - 30
ISSN - 2352-8737
DOI - 10.1002/trc2.12108
Subject(s) - medicine , statin , incidence (geometry) , dementia , medical prescription , relative risk , cohort , confidence interval , retrospective cohort study , disease , pharmacology , physics , optics
Establishing efficacy of and molecular pathways for statins has the potential to impact incidence of Alzheimer's and age‐related neurodegenerative diseases (NDD). Methods This retrospective cohort study surveyed US‐based Humana claims, which includes prescription and patient records from private‐payer and Medicare insurance. Claims from 288,515 patients, aged 45 years and older, without prior history of NDD or neurological surgery, were surveyed for a diagnosis of NDD starting 1 year following statin exposure. Patients were required to be enrolled with claims data for at least 6 months prior to first statin prescription and at least 3 years thereafter. Computational system biology analysis was conducted to determine unique target engagement for each statin. Results Of the 288,515 participants included in the study, 144,214 patients (mean [standard deviation (SD)] age, 67.22 [3.8] years) exposed to statin therapies, and 144,301 patients (65.97 [3.2] years) were not treated with statins. The mean (SD) follow‐up time was 5.1 (2.3) years. Exposure to statins was associated with a lower incidence of Alzheimer's disease (1.10% vs 2.37%; relative risk [RR], 0.4643; 95% confidence interval [CI], 0.44–0.49; P < .001), dementia 3.03% vs 5.39%; RR, 0.56; 95% CI, 0.54–0.58; P < .001), multiple sclerosis (0.08% vs 0.15%; RR, 0.52; 95% CI, 0.41–0.66; P < .001), Parkinson's disease (0.48% vs 0.92%; RR, 0.53; 95% CI, 0.48–0.58; P < .001), and amyotrophic lateral sclerosis (0.02% vs 0.05%; RR, 0.46; 95% CI, 0.30–0.69; P < .001). All NDD incidence for all statins, except for fluvastatin (RR, 0.91; 95% CI, 0.65‐1.30; P = 0.71), was reduced with variances in individual risk profiles. Pathway analysis indicated unique and common profiles associated with risk reduction efficacy. Discussion Benefits and risks of statins relative to neurological outcomes should be considered when prescribed for at‐risk NDD populations. Common statin activated pathways indicate overarching systems required for risk reduction whereas unique targets could advance a precision medicine approach to prevent neurodegenerative diseases.