Publications by authors named "Natalia Madetko-Alster"

Progressive supranuclear palsy (PSP) is a tauopathic atypical parkinsonian syndrome. Recent studies suggest that inflammation may play a role in PSP pathogenesis, highlighting markers like the neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and cytokines such as IL-1β and IL-6. This study aimed to assess the relationship between peripheral inflammatory markers and psychological abnormalities in PSP-RS and PSP-P patients.

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Article Synopsis
  • - Progressive supranuclear palsy (PSP) is a type of parkinsonism marked by symptoms like eye movement issues, balance problems, and cognitive decline, which complicate its diagnosis and has no effective treatments.
  • - PSP is recognized as the second most common neurodegenerative parkinsonism after Parkinson's disease (PD), with symptoms including gait instability and early cognitive changes, differing from PD presentations.
  • - The classification of PSP has evolved since its initial description in 1963, leading to better diagnostic criteria in 2017, and emphasizes the importance of assessing quality of life for patients as a basis for further research.
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  • - Atypical parkinsonisms (APs) include symptoms like motor issues, cognitive decline, and autonomic dysfunction, with olfactory loss (OL) being a unique non-motor symptom that may help differentiate APs.
  • - Research shows that olfactory loss is most severe in Dementia with Lewy Bodies (DLB), but mild OL may also occur in some patients with Progressive Supranuclear Palsy (PSP) and Corticobasal Degeneration (CBD), possibly due to abnormal protein deposits in the brain.
  • - The review emphasizes the importance of olfactory testing as a quick, non-invasive method for distinguishing APs and understanding their progression, with a call for standardized testing protocols to enhance clinical
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Introduction: Progressive supranuclear palsy (PSP) and corticobasal syndrome (CBS) are tauopathic atypical parkinsonisms. Given their overlap in terms of clinical manifestation, there is growing interest in the mechanisms leading to these entities.

Materials And Methods: In total, 71 patients were included in the study, 19 of whom were clinically diagnosed with CBS, 37 with PSP, and 15 with Parkinson's disease (PD).

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Atypical parkinsonian syndromes (APSs) are a group of neurodegenerative disorders that differ from idiopathic Parkinson's disease (IPD) in their clinical presentation, underlying pathology, and response to treatment. APSs include conditions such as multiple system atrophy (MSA), progressive supranuclear palsy (PSP), corticobasal syndrome (CBS), and dementia with Lewy bodies (DLB). These disorders are characterized by a combination of parkinsonian features and additional symptoms, such as autonomic dysfunction, supranuclear gaze palsy, and asymmetric motor symptoms.

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Article Synopsis
  • There are challenges in treating tauopathic syndromes, which are brain disorders related to a protein called tau.
  • Researchers are exploring how these brain issues might be connected to diseases like diabetes or atherosclerosis (hardening of the arteries) and how this could affect blood flow in the brain.
  • By understanding these connections better, doctors might find new ways to treat neurodegenerative diseases and help people at risk for tauopathic syndromes.
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Progressive Supranuclear Palsy is an atypical parkinsonism based on tauopathic pathology. Growing interest is associated with the pathomechanism of this disease. Among theories analyzing this issue can be mentioned the one highlighting the significance of inflammation.

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Introduction: Hepcidin is a peptide associated with controlling the distribution of iron in tissues. Growing interest is linked with its impact on neurodegenerative diseases, as disruption of the iron regulation may be considered an initiatory element of pathological protein accumulation. The possible impact of hepcidin was not previously sufficiently explored in progressive supranuclear palsy (PSP).

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Article Synopsis
  • Progressive Supranuclear Palsy (PSP) is a type of atypical parkinsonism with two main subtypes: PSP-Richardson's Syndrome and PSP Parkinsonism Predominant, each showing different clinical features.
  • This study aimed to investigate the levels of glial cell line-derived neurotrophic factor (GDNF) in the serum and cerebrospinal fluid (CSF) of PSP patients to understand its potential role in the disease.
  • The results showed increased GDNF levels in PSP-RS CSF and PSP-P serum, suggesting GDNF could help differentiate between PSP subtypes and may be relevant for future therapeutic approaches, even though it didn’t correlate with clinical symptoms.
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Multiple studies have analyzed the possible correlations between diabetes and Alzheimer's disease. Less is known about the context of cognitive deterioration among patients with atypical Parkinsonian syndromes and glucose metabolism impairment. The aim of this study was to evaluate the association between the impaired glucose metabolism and cognitive decline among patients with progressive supranuclear palsy (PSP) and corticobasal syndrome (CBS).

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Progressive supranuclear palsy (PSP) is an atypical parkinsonian syndrome based on tau pathology; its clinical phenotype differs, but PSP with Richardson's syndrome (PSP-RS) and the PSP parkinsonism predominant (PSP-P) variant remain the two most common manifestations. Neuroinflammation is involved in the course of the disease and may cause neurodegeneration. However, an up-to-date cytokine profile has not been assessed in different PSP phenotypes.

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Introduction: The pathogenesis of parkinsonisms is not fully understood. Among possible factors which may influence the course of neurodegenerative diseases, endocrine abnormalities may be interpreted as having been underevaluated.

State Of The Art: Growing interest is associated with the role of neuropeptides such as orexin.

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Misfolding protein aggregation inside or outside cells is the major pathological hallmark of several neurodegenerative diseases. Among proteinopathies are neurodegenerative diseases with atypical Parkinsonism and an accumulation of insoluble fibrillary alpha-synuclein (synucleinopathies) or hyperphosphorylated tau protein fragments (tauopathies). As there are no therapies available to slow or halt the progression of these disea ses, targeting the inflammatory process is a promising approach.

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The differential diagnosis of MSA-P and PSP-P remains a difficult issue in clinical practice due to their overlapping clinical manifestation and the lack of tools enabling a definite diagnosis ante-mortem. This paper describes the usefulness of SPECT HMPAO in MSA-P and PSP-P differentiation through the analysis of cerebellar perfusion of small ROIs. Thirty-one patients were included in the study—20 with MSA-P and 11 with PSP-P; the analysis performed indicated that the most significant difference in perfusion was observed in the anterior quadrangular lobule (H IV and V) on the left side (p < 0.

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Introduction: Corticobasal syndrome (CBS) is a specific clinical manifestation shared by multiple pathologies. The exact mechanism of this phenomenon remains unclear. Differential diagnosis of CBS in everyday clinical practice is challenging, as this syndrome can overlap with other entities, especially progressive supranuclear palsy Richardson-Steele phenotype (PSP-RS).

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Progressive Supranuclear Palsy-Parkinsonism Predominant (PSP-P) is associated with moderate responsiveness to levodopa treatment and a possible lack of typical PSP milestones. The clinical manifestation of PSP-P poses difficulties in neurological examination. In the early stages it is often misdiagnosed as Parkinson's Disease, and in the more advanced stages PSP-P shows more symptoms in common with Multiple System Atrophy-Parkinsonian type (MSA-P).

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