Arterial Blood Pressure Variability and Other Vascular Factors Contribution to the Cognitive Decline in Parkinson’s Disease

Pierzchlińska, Anna; Kwaśniak-Butowska, Magdalena; Sławek, Jarosław; Droździk, Marek; Białecka, Monika

doi:10.3390/molecules26061523

Cited by 9 publications

(9 citation statements)

References 132 publications

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“…Comorbidity of AD pathology is common in PD and affects the clinical phenotype of patients ( 100 – 102 ). Moreover, vascular factors contribute to both AD and PD pathology ( 58 , 103 ). Consideration of these overlapping and interacting pathologies during the prodromal stages is essential for developing disease-modifying therapeutic and/or preventive methods for PD ( 104 ).…”

Section: Discussionmentioning

confidence: 99%

Bidirectional Relationship Between Sleep Disturbances and Parkinson's Disease

Minakawa

2022

Front. Neurol.

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Parkinson's disease (PD) is the second most common neurodegenerative disease after Alzheimer's disease (AD). Both diseases share common clinical and pathological features: the gradual progression of neurological and psychiatric symptoms caused by neuronal dysfunction and neuronal cell death due to the accumulation of misfolded and neurotoxic proteins. Furthermore, both of them are multifactorial diseases in which both genetic and non-genetic factors contribute to the disease course. Non-genetic factors are of particular interest for the development of preventive and therapeutic approaches for these diseases because they are modifiable; of these, sleep is a particularly intriguing factor. Sleep disturbances are highly prevalent among both patients with AD and PD. To date, research has suggested that sleep disturbances are a consequence as well as a risk factor for the onset and progression of AD, which implies a bidirectional relationship between sleep and AD. Whether such a relationship exists in PD is less certain, albeit highly plausible given the shared pathomechanisms. This review examines the current evidence for the bidirectional relationship between sleep and PD. It includes research in both humans and animal models, followed by a discussion of the current understanding of the mechanisms underlying this relationship. Finally, potential avenues of research toward achieving disease modification to treat or prevent PD are proposed. Although further efforts are crucial for preventing the onset and slowing the progress of PD, it is evident that sleep is a valuable candidate target for future interventions to improve the outcomes of PD patients.

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Section: Discussionmentioning

confidence: 99%

Bidirectional Relationship Between Sleep Disturbances and Parkinson's Disease

Minakawa

2022

Front. Neurol.

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“…In fact, this may not be a reason but a result. According to Pierzchlinska et al, variability in hemodynamic parameters initiates the occurrence of dementia, causing white matter hyperintensity and microvascular damage [ 26 ]. The results in these subgroups with psychosis and dementia should be interpreted with caution because of the small number of patients included.…”

Section: Discussionmentioning

confidence: 99%

“…The sympathetic noradrenergic denervation observed in patients with PD seems to occur independently of striatal dopaminergic denervation [ 15 , 26 – 28 ]. Our data confirm that neither the duration nor the severity of disease had any effect on cardiac hemodynamic parameters, suggesting that cardiac autonomic disorders are caused by mechanisms other than central causes.…”

Section: Discussionmentioning

confidence: 99%

Central Aortic Pressure and Arterial Stiffness in Parkinson’s Disease: A Comparative Study

Balal

Demirkıran

Paydaş

2022

Parkinson's Disease

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Background. Cardiovascular autonomic dysfunction, which leads to hemodynamic disorders, is commonly observed in patients with Parkinson’s disease (PD). Central aortic pressure (CAP) is the systolic blood pressure (SBP) at the root of the aorta. In young people, CAP is lower than peripheral arterial blood pressure. In older people, the difference between CAP and peripheral arterial blood pressure decreases depending on the extent of arterial stiffness (AS). In patients with AS, CAP increases. CAP is thus regarded as an indicator of AS. Objective. To compare CAP and other hemodynamic parameters for AS between patients with Parkinson’s disease and control group. We also aimed to evaluate changes in these hemodynamic parameters after the levodopa (LD) intake. Methods. We included 82 patients with PD and 76 healthy controls. Age, sex, disease duration, disease subtype, Hoehn–Yahr stage (H&Y), and nonmotor symptoms (NMS) were documented. TensioMed Software v.3.0.0.1 was used to measure CAP, peripheral arterial blood pressure, pulse pressure (PP), heart rate (HR), mean arterial pressure (MAP), augmentation index (AI), pulse wave velocity, and ejection time. All patients were being treated with LD, and measurements were performed 1 h before and 1 h after LD intake. Results. Baseline peripheral arterial blood pressure and CAP values were significantly higher in the PD group than in the control group ( p < 0.001 and p = 0.02 , respectively). Most cardiac hemodynamic parameters, including peripheral arterial blood pressure and CAP, decreased significantly ( p < 0.02 and p < 0.001 , respectively) after LD intake in the PD group. Disease subtype, duration, and severity did not affect any of the hemodynamic parameters. When NMS were evaluated, patients with psychosis and dementia showed higher baseline parameters. Conclusion. Loss of postganglionic noradrenergic innervation is well-known with PD. Several cardiac hemodynamic parameters were affected, suggesting cardiac autonomic dysfunction in these patients. The data obtained were independent of disease severity, duration, and subtype. After LD intake, most of these parameters decreased, which might have a positive effect on the vascular burden.

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“…Neurodegeneration in patients with AD and other neuropathies is associated with peripheral changes including metabolic disturbances, hypertension, alterations of body weight and fat metabolism (Lee 2011;McGuire and Ishii 2016;Mogi 2019;den Brok et al 2021;Pierzchlinska et al 2021;Ungvari et al 2021). These disorders are generally considered risk factors for the development of neurodegeneration, but it is difficult to study in humans whether or not they may also be the consequences of neuropathology.…”

Section: Discussionmentioning

confidence: 99%

Hypertension does not alter disturbances in leptin signalling observed in experimental model of tauopathy

Cente¹,

Smolek²,

Zórad³

et al. 2021

gpb

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Neurodegeneration is associated with hypertension and disturbance in fat metabolism. The complex interaction of neurodegenerative processes with both metabolic changes and blood pressure is still not fully elucidated. Here we demonstrate that the experimentally induced tauopathy in hypertensive transgenic animals causes significant downregulation of plasma leptin (53% of control), reduction of body weight by 11%, a 1.2-fold drop of adiposity index, and decrease in HDL cholesterol level, while the fasting glucose and insulin concentration remain unchanged. Despite of these alterations we found the leptin projection circuit including the arcuate nucleus, paraventricular nucleus in hypothalamus, and nucleus tractus solitarius in the brainstem not affected by neurofibrillary pathology. Furthermore, hypertension does not alter disturbances in leptin signalling. The presented data provide further insight into neurodegeneration-induced metabolic alterations relevant for human tauopathies.

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Arterial Blood Pressure Variability and Other Vascular Factors Contribution to the Cognitive Decline in Parkinson’s Disease

Cited by 9 publications

References 132 publications

Bidirectional Relationship Between Sleep Disturbances and Parkinson's Disease

Bidirectional Relationship Between Sleep Disturbances and Parkinson's Disease

Central Aortic Pressure and Arterial Stiffness in Parkinson’s Disease: A Comparative Study

Hypertension does not alter disturbances in leptin signalling observed in experimental model of tauopathy

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