Body-first Parkinson’s disease and variant Creutzfeldt–Jakob disease – similar or different?

Woerman, Amanda L.; Tamgüney, Gültekin

doi:10.1016/j.nbd.2022.105625

Cited by 6 publications

(9 citation statements)

References 159 publications

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“…The incidence rate of PD was 2.8 cases per 1,000 person-years (95% confidence interval: [ 2.8–2.9 ]) in people who never had a colonoscopy, whereas the incidence was significantly lower in people who had a CRC screening (2.3 [ 2.0–2.5 ]), as the confidence intervals did not overlap ( Table 1 ). The incidence rate with additional BDE (2.5 [ 1.9–3.2 ]) was also lower, but not significantly.…”

Section: Resultsmentioning

confidence: 99%

“…monomers into growing α-synuclein aggregates [2]. Postmortem studies in PD patients revealed that pathologic α-synuclein propagates along relatively large distances within the central nervous system [3], and, surprisingly, also between the enteric and central nervous system along the vagal nerve, the so-called neural gut-brain-axis [4].…”

Section: Introductionmentioning

confidence: 99%

“…Parkinson’s disease (PD) is the second most frequent neurodegenerative disease after Alzheimer’s disease and one of the central events in its pathogenesis is the misfolding and aggregation of α-synuclein, a protein that is expressed in neurons of the central and peripheral nervous system [ 1 ]. Pathologic α-synuclein aggregates have prion-like properties and can spread within the nervous system by transmission from diseased to healthy neurons, where they seed de novo aggregation by recruiting α-synuclein monomers into growing α-synuclein aggregates [ 2 ]. Postmortem studies in PD patients revealed that pathologic α-synuclein propagates along relatively large distances within the central nervous system [ 3 ], and, surprisingly, also between the enteric and central nervous system along the vagal nerve, the so-called neural gut-brain-axis [ 4 ].…”

Section: Introductionmentioning

confidence: 99%

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Colonoscopy and Subsequent Risk of Parkinson’s Disease

Holtz,

Fink,

Tamgüney

et al. 2024

Journal of Parkinson’s Disease

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Background: Parkinson’s disease (PD) is caused by the misfolding and aggregation of α-synuclein in neurons into toxic oligomers and fibrils that have prion-like properties allowing them to infect healthy neurons and to be transmitted to animal models of PD by injection or oral exposure. Given α-synuclein fibrils’ potential transmission on the gut-brain axis, α-synuclein may be transmitted through colonoscopy procedures. Objective: This study examines a possible association between colonoscopy and PD. Methods: Longitudinal health insurance data of 250,000 individuals aged 50+ from 2004–2019 was analyzed. Cox proportional hazard and competing risk models with death as a competing event were estimated to calculate the risk of PD. Colonoscopy was categorized as never receiving colonoscopy, colorectal cancer (CRC) screening without or with biopsy, destruction or excision (BDE), and diagnostic colonoscopy without or with BDE. Results: We identified 6,422 new cases of PD among 221,582 individuals. The Cox model revealed a significantly increased risk of PD for patients who ever had a diagnostic colonoscopy without or with BDE (HR = 1.31; 95% CI: [1.23–1.40]; HR = 1.32 [1.22–1.42]) after adjustment for age and sex. After controlling for covariates and death, persons who ever underwent CRC screening had a 40% reduced risk of PD (CRHR = 0.60 [0.54–0.67]), while persons who underwent diagnostic colonoscopy had a 20% reduced risk of PD (CRHR = 0.81 [0.75–0.88]). Conclusions: Colonoscopy does not increase the risk of PD, after adjusting for death and covariates. Individuals who underwent only CRC screening had the lowest risk of PD, which may be a result of a more health-conscious lifestyle.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Colonoscopy and Subsequent Risk of Parkinson’s Disease

Holtz,

Fink,

Tamgüney

et al. 2024

Journal of Parkinson’s Disease

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“…Together with findings of pathological α-synuclein in the enteric nervous system (ENS) and the dorsal motor nucleus of the vagus nerve and the anterior olfactory bulb as the earliest lesion sites in PD, Braak and colleagues postulated the dual-hit hypothesis suggesting that α-synuclein pathology spreads from the olfactory bulb to the temporal lobes, and from the ENS via the vagus nerve to the CNS 30,31 . Further, several studies suggest that pathologic αsynuclein assemblies have prion-like properties, allowing them to multiply and propagate between neurons in the nervous system and to spread across large distances in the brain and body, including from the ENS to the CNS and vice versa [32][33][34][35] .…”

Section: Introductionmentioning

confidence: 99%

Patients with isolated REM-sleep behavior disorder have elevated levels of alpha-synuclein aggregates in stool

Schaffrath

Schleyken

Seger

et al. 2023

npj Parkinsons Dis.

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Misfolded and aggregated α-synuclein is a neuropathological hallmark of Parkinson’s disease (PD). Thus, α-synuclein aggregates are regarded as a biomarker for the development of diagnostic assays. Quantification of α-synuclein aggregates in body fluids is challenging, and requires highly sensitive and specific assays. Recent studies suggest that α-synuclein aggregates may be shed into stool. We used surface-based fluorescence intensity distribution analysis (sFIDA) to detect and quantify single particles of α-synuclein aggregates in stool of 94 PD patients, 72 isolated rapid eye movement sleep behavior disorder (iRBD) patients, and 51 healthy controls. We measured significantly elevated concentrations of α-synuclein aggregates in stool of iRBD patients versus those of controls (p = 0.024) or PD patients (p < 0.001). Our results show that α-synuclein aggregates are excreted in stool and can be measured using the sFIDA assay, which could support the diagnosis of prodromal synucleinopathies.

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“…Parkinson's disease (PD) is the second most frequent neurodegenerative disease after Alzheimer's disease and is caused by the misfolding and aggregation of α-synuclein, a protein that is expressed in neurons of the central and peripheral nervous system 1 . Pathologic α-synuclein aggregates have prionlike properties and can spread within the nervous system by transmission from diseased to healthy neurons, where they seed de novo aggregation by recruiting α-synuclein monomers into growing αsynuclein aggregates 2 . Post mortem studies in PD patients revealed that pathologic α-synuclein propagates along relatively large distances within the central nervous system 3 , and, surprisingly, also between the enteric and central nervous system along the vagal nerve, the so-called neural gut-brainaxis 4 .…”

Section: Introductionmentioning

confidence: 99%

Colonoscopy does not increase the risk of Parkinson’s disease

Holtz,

Fink,

Tamgüney

et al. 2023

Preprint

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Parkinson's disease (PD) is caused by the misfolding and aggregation of α-synuclein in neurons into toxic oligomers and fibrils that have prion-like properties allowing them to infect healthy neurons and to be transmitted to animal models of PD by injection or oral exposure. Considering that α-synuclein fibrils can also propagate from the enteric to the central nervous system, α-synuclein may be transmitted through colonoscopy procedures. This study examines a possible association between colonoscopy and PD. We used longitudinal data of 250,000 individuals aged 50+ from 2004-2019 from Germany's largest health insurer. Cox proportional hazard and competing risk models with death as a competing event were estimated to calculate the risk of PD. Models were adjusted for age, sex, reason for colonoscopy and co-morbidities of PD. Colonoscopy was categorized as never receiving colonoscopy, colorectal cancer (CRC) screening without or with biopsy, destruction, excision, laser vaporization or argon plasma coagulation (BDE), and diagnostic colonoscopy without or with BDE. We identified 6,422 new cases of PD among 221,582 individuals. The Cox model revealed a significantly increased risk of PD for patients who ever had a diagnostic colonoscopy without or with BDE (HR=1.31; 95% confidence interval: [1.23-1.40]; HR=1.32 [1.22-1.42]) after adjustment for age and sex. After controlling for covariates and death, persons who ever underwent CRC screening had a 40% reduced risk of PD (HR=0.60 [0.53-0.66]), while persons who underwent diagnostic colonoscopy had a 20% reduced risk of PD (HR=0.80 [0.74-0.87]). Individuals who ever had any type of colonoscopy had a lower risk of PD compared to those who never had a colonoscopy, after adjusting for death and covariates. Individuals who underwent only CRC screening had the lowest risk of PD, which may be a result of a more health-conscious lifestyle.

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Body-first Parkinson’s disease and variant Creutzfeldt–Jakob disease – similar or different?

Cited by 6 publications

References 159 publications

Colonoscopy and Subsequent Risk of Parkinson’s Disease

Colonoscopy and Subsequent Risk of Parkinson’s Disease

Patients with isolated REM-sleep behavior disorder have elevated levels of alpha-synuclein aggregates in stool

Colonoscopy does not increase the risk of Parkinson’s disease

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