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Type 2 Diabetes Tied to Subsequent Risk of PD (CME/CE)

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Type 2 Diabetes Tied to Subsequent Risk of PD

Risk of Parkinson’s later in life higher among younger T2D patients

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  • by Contributing Writer, MedPage Today
  • This article is a collaboration between MedPage Today® and:

    Medpage Today

Action Points

  • Note that this retrospective analysis leveraging hospitalization data in England suggested that those with diabetes were at increased risk of subsequently developing Parkinson’s disease.
  • Be aware that the authors did not have data on some key covariates, such as smoking, that may be related to both the exposure and outcome of interest.

People with type 2 diabetes had a higher risk for subsequent Parkinson’s disease (PD), a national retrospective analysis in England found.

A 32% higher rate of new-onset PD was seen in those with a previous type 2 diabetes diagnosis, and that rate jumped considerably if the diabetes patients were younger than 44, reported Thomas Warner, FRCP, PhD, of University College London, and co-authors in Neurology.

“Our study examined data on a large portion of the English population and found a strong link between these two seemingly different diseases,” Warner said in a statement. How the diseases are connected is unknown, but it’s possible that “restoring the brain’s ability to use insulin could potentially have a protective effect on the brain.”

Several studies have indicated that PD and diabetes may be linked, including a recent clinical trial that pointed to insulin signaling as a possible target for PD treatments. In that study, PD patients who injected themselves weekly with the glucagon-like peptide 1 receptor agonist exenatide (Byetta) performed better in movement tests than people who injected a placebo.

For this analysis, Warner and colleagues linked English national Hospital Episode Statistics and mortality data from 1999 to 2011. The team constructed a cohort of patients who were admitted for hospital care with a coded diagnosis of type 2 diabetes, comparing them with a reference group of people who did not have a diabetes diagnosis. Excluded were people diagnosed with cerebrovascular disease, vascular parkinsonism, drug-induced parkinsonism, and normal pressure hydrocephalus.

The researchers searched the records of 2,017,115 individuals in the type 2 diabetes group and 6,173,208 people in the reference group for any later hospital admission with a diagnosis of PD. Patients in the diabetes cohort were more likely to have a subsequent PD diagnosis (HR 1.32, 95% CI 1.29-1.35; P< 0.001) than patients in the reference cohort. The relative increase was greater among patients with complicated type 2 diabetes (HR 1.49, 95% CI 1.42-1.56) and rose substantially among younger people with diabetes (HR 3.81, 95% CI 2.84-5.11 for the age group 25–44).

The greater magnitude of risk in young people may occur when genetic factors might exert more of an effect, the researchers noted; more than 400 genes identified through genome-wide association studies have been linked to both conditions. The association in elderly patients may stem from disrupted insulin signaling secondary to lifestyle and environmental factors that result in cumulative pathogenic brain changes, the researchers added.

“Whether attributable to genetic predisposition, environmental factors, or both, disrupted brain insulin signaling could lead to shared dysregulated cellular pathways including neuroinflammation (microglia activation, production of pro-inflammatory cytokines), mitochondrial dysfunction, and increased oxidative stress ultimately promoting synuclein aggregation and contributing to the development of PD.”

Asked for her perspective, Stella Papa, MD, of Emory University School of Medicine in Atlanta, who was not involved in the study, told MedPage Today, “A relationship between Parkinson’s disease and type 2 diabetes has been suspected for a long time, but in spite of a number of supporting studies, we have been lacking clear, confirmatory data.”

Oxidative stress, insulin resistance, inflammation, and abnormal protein accumulation are pathogenic mechanisms the two diseases share, she noted.

“In particular, there is a growing interest around the idea that the misfolded amyloid polypeptide in the pancreatic beta islet, which can form fibrils and propagate in diabetes mellitus, could interact in a cross-seeding fashion with alpha-synuclein aggregation leading to neurodegeneration of PD. In other words, a common prion-like basis underlying both type 2 diabetes and PD may synergize to increase the risk for their association.”

There were several study limitations, Warner and colleagues noted: They were unable to adjust for medications and smoking in the analysis, and determined diabetes cases based on the first recorded hospital diagnosis, not the first point of onset. And because this was a hospital-based study, patients diagnosed with diabetes may have had a more severe form of the disease than patients diagnosed in a clinic.

The study was funded by the National Institute for Health Research Biomedical Research Centres at Oxford and University College London Hospitals in the United Kingdom.

The researchers reported relationships with Elan/Prothena Pharmaceuticals, GE Healthcare, Britannia Pharmaceuticals, and Corticobasal Degeneration Solutions.

  • Reviewed by F. Perry Wilson, MD, MSCE Assistant Professor, Section of Nephrology, Yale School of Medicine and Dorothy Caputo, MA, BSN, RN, Nurse Planner
2018-06-13T16:00:00-0400
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Accessibility Statement

At MedPage Today, we are committed to ensuring that individuals with disabilities can access all of the content offered by MedPage Today through our website and other properties. If you are having trouble accessing www.medpagetoday.com, MedPageToday's mobile apps, please email legal@ziffdavis.com for assistance. Please put "ADA Inquiry" in the subject line of your email.

Medpage Today

Type 2 Diabetes Tied to Subsequent Risk of PD

Risk of Parkinson's later in life higher among younger T2D patients

MedpageToday

  • register today

    Earn Free CME Credits by reading the latest medical news in your specialty.

    sign up

  • by Contributing Writer, MedPage Today
  • This article is a collaboration between MedPage Today® and:

    Medpage Today

Action Points

  • Note that this retrospective analysis leveraging hospitalization data in England suggested that those with diabetes were at increased risk of subsequently developing Parkinson's disease.
  • Be aware that the authors did not have data on some key covariates, such as smoking, that may be related to both the exposure and outcome of interest.

People with type 2 diabetes had a higher risk for subsequent Parkinson's disease (PD), a national retrospective analysis in England found.

A 32% higher rate of new-onset PD was seen in those with a previous type 2 diabetes diagnosis, and that rate jumped considerably if the diabetes patients were younger than 44, reported Thomas Warner, FRCP, PhD, of University College London, and co-authors in Neurology.

"Our study examined data on a large portion of the English population and found a strong link between these two seemingly different diseases," Warner said in a statement. How the diseases are connected is unknown, but it's possible that "restoring the brain's ability to use insulin could potentially have a protective effect on the brain."

Several studies have indicated that PD and diabetes may be linked, including a recent clinical trial that pointed to insulin signaling as a possible target for PD treatments. In that study, PD patients who injected themselves weekly with the glucagon-like peptide 1 receptor agonist exenatide (Byetta) performed better in movement tests than people who injected a placebo.

For this analysis, Warner and colleagues linked English national Hospital Episode Statistics and mortality data from 1999 to 2011. The team constructed a cohort of patients who were admitted for hospital care with a coded diagnosis of type 2 diabetes, comparing them with a reference group of people who did not have a diabetes diagnosis. Excluded were people diagnosed with cerebrovascular disease, vascular parkinsonism, drug-induced parkinsonism, and normal pressure hydrocephalus.

The researchers searched the records of 2,017,115 individuals in the type 2 diabetes group and 6,173,208 people in the reference group for any later hospital admission with a diagnosis of PD. Patients in the diabetes cohort were more likely to have a subsequent PD diagnosis (HR 1.32, 95% CI 1.29-1.35; P< 0.001) than patients in the reference cohort. The relative increase was greater among patients with complicated type 2 diabetes (HR 1.49, 95% CI 1.42-1.56) and rose substantially among younger people with diabetes (HR 3.81, 95% CI 2.84-5.11 for the age group 25–44).

The greater magnitude of risk in young people may occur when genetic factors might exert more of an effect, the researchers noted; more than 400 genes identified through genome-wide association studies have been linked to both conditions. The association in elderly patients may stem from disrupted insulin signaling secondary to lifestyle and environmental factors that result in cumulative pathogenic brain changes, the researchers added.

"Whether attributable to genetic predisposition, environmental factors, or both, disrupted brain insulin signaling could lead to shared dysregulated cellular pathways including neuroinflammation (microglia activation, production of pro-inflammatory cytokines), mitochondrial dysfunction, and increased oxidative stress ultimately promoting synuclein aggregation and contributing to the development of PD."

Asked for her perspective, Stella Papa, MD, of Emory University School of Medicine in Atlanta, who was not involved in the study, told MedPage Today, "A relationship between Parkinson's disease and type 2 diabetes has been suspected for a long time, but in spite of a number of supporting studies, we have been lacking clear, confirmatory data."

Oxidative stress, insulin resistance, inflammation, and abnormal protein accumulation are pathogenic mechanisms the two diseases share, she noted.

"In particular, there is a growing interest around the idea that the misfolded amyloid polypeptide in the pancreatic beta islet, which can form fibrils and propagate in diabetes mellitus, could interact in a cross-seeding fashion with alpha-synuclein aggregation leading to neurodegeneration of PD. In other words, a common prion-like basis underlying both type 2 diabetes and PD may synergize to increase the risk for their association."

There were several study limitations, Warner and colleagues noted: They were unable to adjust for medications and smoking in the analysis, and determined diabetes cases based on the first recorded hospital diagnosis, not the first point of onset. And because this was a hospital-based study, patients diagnosed with diabetes may have had a more severe form of the disease than patients diagnosed in a clinic.

The study was funded by the National Institute for Health Research Biomedical Research Centres at Oxford and University College London Hospitals in the United Kingdom.

The researchers reported relationships with Elan/Prothena Pharmaceuticals, GE Healthcare, Britannia Pharmaceuticals, and Corticobasal Degeneration Solutions.

  • Reviewed by F. Perry Wilson, MD, MSCE Assistant Professor, Section of Nephrology, Yale School of Medicine and Dorothy Caputo, MA, BSN, RN, Nurse Planner
2018-06-13T16:00:00-0400
Take Posttest Comments

Accessibility Statement

At MedPage Today, we are committed to ensuring that individuals with disabilities can access all of the content offered by MedPage Today through our website and other properties. If you are having trouble accessing www.medpagetoday.com, MedPageToday's mobile apps, please email legal@ziffdavis.com for assistance. Please put "ADA Inquiry" in the subject line of your email.



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