Diclofenac reduces the risk of Alzheimer’s disease: a pilot analysis of NSAIDs in two US veteran populations

Background: Our aim was to determine whether specific nonsteroidal anti-inflammatory (NSAID) agents are associated with a decreased frequency of Alzheimer’s disease (AD). Materials and methods: Days of drug exposure were determined for diclofenac, etodolac, and naproxen using US Department of Veterans Affairs (VA) pharmacy transaction records, combined from two separate VA sites. AD diagnosis was established by the International Classification of Diseases, ninth revision (ICD-9)/ICD-10 diagnostic codes and the use of AD medications. Cox regression survival analysis was used to evaluate the association between AD frequency and NSAID exposure over time. Age at the end of the study and the medication-based disease burden index (a comorbidity index) were used as covariates. Results: Frequency of AD was significantly lower in the diclofenac group (4/1431, 0.28%) compared with etodolac (328/14,646, 2.24%), and naproxen (202/12,203, 1.66%). For regression analyses, naproxen was chosen as the comparator drug, since it has been shown to have no effect on the development of AD. Compared with naproxen, etodolac had no effect on the development of AD, hazard ratio (HR) 1.00 [95% confidence interval (CI): 0.84–1.20, p = 0.95]. In contrast, diclofenac had a significantly lower HR of AD compared with naproxen, HR 0.25 (95% CI: 0.09–0.68, p <0.01). After site effects were controlled for, age at end of the study (HR = 1.08, 95% CI: 1.07–1.09, p <0.001) was also found to influence the development of AD, and the medication-based disease burden index was a strong predictor for AD, HR 5.17 (95% CI: 4.60–5.81) indicating that as comorbidities increase, the risk for AD increases very significantly. Conclusion: Diclofenac, which has been shown to have active transport into the central nervous system, and which has been shown to lower amyloid beta and interleukin 1 beta, is associated with a significantly lower frequency of AD compared with etodolac and naproxen. These results are compelling, and parallel animal studies of the closely related fenamate NSAID drug class.

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SHIFT IN HOSPITALIZATIONS FOR ALZHEIMER’S DISEASE TO RELATED DEMENTIAS IN FRANCE BETWEEN 2007 AND 2017

Journal of Prevention of Alzheimer's Disease ◽

10.14283/jpad.2019.5 ◽

2019 ◽

pp. 1-4

Author(s):

M. Rochoy ◽

E. Chazard ◽

S. Gautier ◽

R. Bordet

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

International Classification Of Diseases ◽

Principal Diagnosis ◽

Degenerative Disorders ◽

Organic Mental Disorders ◽

Classification Of Diseases ◽

Icd 10 ◽

Discharge Database

INTRODUCTION: Alzheimer’s disease (AD) is the first cause of dementia. Diagnostic criteria have evolved: proposals to revise the NINCDS–ADRDA criteria were published in 2007. Our aim was to analyze the evolution in the coding of AD in the French nationwide exhaustive hospital discharge database (PMSI) between 2007 and 2017. METHODS: We analyzed evolution of International Classification of Diseases and Related Health Problems, 10th edition (ICD-10) coding for AD and AD dementia in the PMSI database from 2008 to 2017 (285,748,938 inpatient stays). RESULTS: We observed a 44% decrease in the number of inpatient stays with a principal diagnosis of AD or AD dementia from 2007 (46,313 inpatient stays) to 2017 (25,856 inpatient stays) in France. Over the same period, we observed a 49% increase in the number of inpatient stays with a principal diagnosis of related dementias (other organic mental disorders or other degenerative disorders). Overall, the number of inpatient stays for dementia remained stable despite the increase in the total number of inpatient stays: 95,377 in 2007 (0.409% of inpatient stays) and 99,190 in 2017 (0.344%). CONCLUSION: We therefore note a shift from AD and AD dementia to other dementia diagnoses since 2007. This study suggests a more accurate use of AD related ICD-10 codes since the revised criteria in 2007.

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Predictors of the Progression of Dementia Severity in Brazilian Patients with Alzheimer's Disease and Vascular Dementia

International Journal of Alzheimer s Disease ◽

10.4061/2010/673581 ◽

2010 ◽

Vol 2010 ◽

pp. 1-7 ◽

Cited By ~ 6

Author(s):

Márcia L. Chaves ◽

Ana L. Camozzato ◽

Cristiano Köhler ◽

Jeffrey Kaye

Keyword(s):

Risk Factors ◽

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Cognitive Decline ◽

Vascular Dementia ◽

Cox Regression ◽

Strong Predictor ◽

Disease Diagnosis ◽

Vascular Risk Factors ◽

Vascular Risk

Introduction. This study evaluates the progression of dementia and identifies prognostic risk factors for dementia.Methods. A group of 80 Brazilian community residents with dementia (34 with Alzheimer's disease and 46 with vascular dementia) was assessed over the course of 2 years. Data were analyzed with Cox regression survival analysis.Results. The data showed that education predicted cognitive decline (HR=1.2;P<.05) when analyzed without controlling for vascular risk factors. After the inclusion of vascular risk factors, education (HR=1.32;P<.05) and hypertension were predictive for cognitive decline (HR=38;P<.05), and Alzheimer's disease diagnosis was borderline predictive (P=.055).Conclusion.Vascular risk factors interacted with the diagnosis of vascular dementia. Education was a strong predictor of decline.

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Dapsone is an anticatalysis for Alzheimer’s disease exacerbation

10.21203/rs.3.rs-1260878/v1 ◽

2022 ◽

Author(s):

Jong Hoon Lee ◽

Badar Kanwar ◽

Chul Joong Lee ◽

Consolato Sergi ◽

Michael Coleman

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

International Classification Of Diseases ◽

Electronic Data Interchange ◽

P Value ◽

Diaminodiphenyl Sulfone ◽

Data Interchange ◽

Classification Of Diseases ◽

Leprosy Patients ◽

Icd 10

Abstract This study investigated leprosy patients with Alzheimer's disease (AD) treated with dapsone (4,4’-diaminodiphenyl sulfone, DDS) as a cytosolic DNA sensor cyclic-GMP-AMP synthase (cGAS)/stimulator of interferon genes (STING) signaling pathway and neuroinflammasome competitor. We searched the Sorokdo National Hospital medical records and the National Health Insurance Service in South Korea with the International Classification of Diseases (ICD)-10 code and Electronic Data Interchange (EDI) from January 2005 to June 2020. Four groups were defined: Treatment (T) 1: DDS prescription (+) AD prevalence (+), T 2: DDS (+) AD nondiagnosed (-), T 3: DDS nonprescription (-) AD (+), T 4: DDS (-) AD (-). The T1:T3 tests demonstrate that the incidence of AD is significantly reduced in the presence of dapsone among AD patients. The T1:T3 tests demonstrate that the incidence of AD is significantly reduced in the presence of dapsone among AD patients. T1 (M = 0.18, SD = 0.074):T2 (M = 0.55, SD = 0.14) and T3 (M = 0.18, SD = 0.074):T4 (M = 0.55, SD = 0.14) explain that dapsone effects on AD can be clearly distinguished according to its presence or absence.The T1:T4 and the T2:T3 test demonstrate a causal relationship in which the presence or absence of dapsone determines the onset of AD. The T1:T3 test proved that the incidence of AD was significantly reduced by dapsone. (The t-value is -23.1, p-value is < .00001, significant at p < .05) The T2:T3 test proved that the prevalence of AD was significantly high without dapsone, and without AD was increased with dapsone. (The t-value is -6.38, p-value is < .00001, significant at p < .05) AD is increased in the absence of dapsone. Our study has demonstrated that dapsone has the potential for the prevention of AD. This study indicates that dapsone is a valid preventive therapeutic for AD. KEYWORD: Neuroinflmmasome, Alzheimer's disease, Dapsone

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Risk and predictors of heart failure in sarcoidosis in a population-based cohort study from Sweden

Heart ◽

10.1136/heartjnl-2021-319129 ◽

2021 ◽

pp. heartjnl-2021-319129

Author(s):

Marios Rossides ◽

Susanna Kullberg ◽

Johan Grunewald ◽

Anders Eklund ◽

Daniela Di Giuseppe ◽

...

Keyword(s):

Risk Factors ◽

Heart Failure ◽

General Population ◽

Strong Predictor ◽

Strong Association ◽

International Classification Of Diseases ◽

Population Based ◽

Clinical Predictors ◽

Cox Models ◽

Classification Of Diseases

ObjectivesPrevious studies showed a strong association between sarcoidosis and heart failure (HF) but did not consider risk stratification or risk factors to identify useful aetiological insights. We estimated overall and stratified HRs and identified risk factors for HF in sarcoidosis.MethodsSarcoidosis cases were identified from the Swedish National Patient Register (NPR; ≥2 International Classification of Diseases-coded visits, 2003–2013) and matched to general population comparators. They were followed for HF in the NPR. Treated were cases who were dispensed ≥1 immunosuppressant ±3 months from the first sarcoidosis visit (2006–2013). Using Cox models, we estimated HRs adjusted for demographics and comorbidity and identified independent risk factors of HF together with their attributable fractions (AFs).ResultsDuring follow-up, 204 of 8574 sarcoidosis cases and 721 of 84 192 comparators were diagnosed with HF (rate 2.2 vs 0.7/1000 person-years, respectively). The HR associated with sarcoidosis was 2.43 (95% CI 2.06 to 2.86) and did not vary by age, sex or treatment status. It was higher during the first 2 years after diagnosis (HR 3.7 vs 1.9) and in individuals without a history of ischaemic heart disease (IHD; HR 2.7 vs 1.7). Diabetes, atrial fibrillation and other arrhythmias were the strongest independent clinical predictors of HF (HR 2.5 each, 2-year AF 20%, 16% and 12%, respectively).ConclusionsAlthough low, the HF rate was more than twofold increased in sarcoidosis compared with the general population, particularly right after diagnosis. IHD history cannot solely explain these risks, whereas ventricular arrhythmias indicating cardiac sarcoidosis appear to be a strong predictor of HF in sarcoidosis.

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Interleukin-1 Gene –511 CT Polymorphism and the Risk of Alzheimer’s Disease in a Polish Population

Dementia and Geriatric Cognitive Disorders ◽

10.1159/000259460 ◽

2009 ◽

Vol 28 (5) ◽

pp. 461-464 ◽

Cited By ~ 12

Author(s):

A. Klimkowicz-Mrowiec ◽

M. Marona ◽

P. Wołkow ◽

A. Maruszak ◽

M. Styczynska ◽

...

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Interleukin 1 ◽

Polish Population

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Lack of Association between Interleukin-1 alpha rs1800587 Polymorphism and Alzheimer's Disease in Two Independent European Samples

Journal of Alzheimer s Disease ◽

10.3233/jad-2009-0946 ◽

2009 ◽

Vol 16 (1) ◽

pp. 181-187 ◽

Cited By ~ 16

Author(s):

Alessandro Serretti ◽

Paolo Olgiati ◽

Antonis Politis ◽

Petros Malitas ◽

Diego Albani ◽

...

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Interleukin 1

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Noise exposure accelerates the risk of cognitive impairment and Alzheimer’s disease: Adulthood, gestational, and prenatal mechanistic evidence from animal studies

Neuroscience & Biobehavioral Reviews ◽

10.1016/j.neubiorev.2019.04.001 ◽

2020 ◽

Vol 117 ◽

pp. 110-128 ◽

Cited By ~ 16

Author(s):

Zahra Jafari ◽

Bryan E. Kolb ◽

Majid H. Mohajerani

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Cognitive Impairment ◽

Animal Studies ◽

Noise Exposure

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Neurobiochemical Cross-talk Between COVID-19 and Alzheimer’s Disease

Molecular Neurobiology ◽

10.1007/s12035-020-02177-w ◽

2020 ◽

Cited By ~ 1

Author(s):

Mohammad Azizur Rahman ◽

Kamrul Islam ◽

Saidur Rahman ◽

Md Alamin

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Inflammatory Markers ◽

Interleukin 1 ◽

Therapeutic Strategies ◽

Therapeutic Approaches ◽

Angiotensin Converting Enzyme 2 ◽

Apoe4 Allele ◽

The Common ◽

Global Threat

Abstract COVID-19, the global threat to humanity, shares etiological cofactors with multiple diseases including Alzheimer’s disease (AD). Understanding the common links between COVID-19 and AD would harness strategizing therapeutic approaches against both. Considering the urgency of formulating COVID-19 medication, its AD association and manifestations have been reviewed here, putting emphasis on memory and learning disruption. COVID-19 and AD share common links with respect to angiotensin-converting enzyme 2 (ACE2) receptors and pro-inflammatory markers such as interleukin-1 (IL-1), IL-6, cytoskeleton-associated protein 4 (CKAP4), galectin-9 (GAL-9 or Gal-9), and APOE4 allele. Common etiological factors and common manifestations described in this review would aid in developing therapeutic strategies for both COVID-19 and AD and thus impact on eradicating the ongoing global threat. Thus, people suffering from COVID-19 or who have come round of it as well as people at risk of developing AD or already suffering from AD, would be benefitted.

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