scholarly journals Integration of Aluminium Interdigitated Electrodes with Zinc Oxide as Nanocomposite for Selectively Detect Alpha-Synuclein for Parkinson’s Disease Diagnosis

2021 ◽  
Vol 2129 (1) ◽  
pp. 012094
Author(s):  
Hussaini Adam ◽  
Subash C. B Gopinath ◽  
Uda Hashim

Abstract Parkinson’s disease is associated with motor and non-motor symptoms, mostly a motor symptom such as tremor is said to be an early indication for Parkinson’s disease development. Because of higher demands for faster and more precise diagnostic methods, it has sparked trends in the development of a biosensor for the diagnosis of Parkinson’s disease. Therefore, this study has fabricated a biosensor that is capable of detecting a specific Parkinson’s disease biomarker such as aggregation of alpha synuclein and this is crucial in reducing the burden of Parkinson’s disease and to be able to detect the disease at the earlier stage. Finding the inconsistent aggregation of alpha-synuclein is a promising method for the early detection of Parkinson’s disease. Using conventional photographic process, aluminium interdigitated electrodes (ALIDEs) have been fabricated and employed with sensitive electrochemical strategy for the specific detection of the Parkinson’s disease antigen (alpha synuclein). The microelectrode was developed based on aluminium electrode sputtered on silicon substrate. Further, zinc oxide (ZnO) was deposited by sputtering on the working electrode of the ALIDEs using a spin-coating method. The ZnO nanocomposite onto aluminium microelectrode surface provides a favourable platform for efficient loading of antibody via binding with antigen alpha synuclein. The effective loading of the biomolecules (antibody and antigen) on the ZnO nanocomposite surface modified aluminium microelectrode was observed by SEM, AFM and 3D Profilometer. The current flow for each concentration of alpha synuclein was observed at 7.5×10−6 A (10 fM), 8.8×10−6 A (100 fM), and 8.5×10−6 A (1 pM) respectively.

2020 ◽  
Vol 5 (4) ◽  
pp. 78
Author(s):  
Andrew E. Pechstein ◽  
Jared M. Gollie ◽  
Andrew A. Guccione

Parkinson’s disease (PD) is the second most common neurodegenerative condition after Alzheimer’s disease, affecting an estimated 160 per 100,000 people 65 years of age or older. Fatigue is a debilitating non-motor symptom frequently reported in PD, often manifesting prior to disease diagnosis, persisting over time, and negatively affecting quality of life. Fatigability, on the other hand, is distinct from fatigue and describes the magnitude or rate of change over time in the performance of activity (i.e., performance fatigability) and sensations regulating the integrity of the performer (i.e., perceived fatigability). While fatigability has been relatively understudied in PD as compared to fatigue, it has been hypothesized that the presence of elevated levels of fatigability in PD results from the interactions of homeostatic, psychological, and central factors. Evidence from exercise studies supports the premise that greater disturbances in metabolic homeostasis may underly elevated levels of fatigability in people with PD when engaging in physical activity. Cardiorespiratory impairments constraining oxygen delivery and utilization may contribute to the metabolic alterations and excessive fatigability experienced in individuals with PD. Cardiorespiratory fitness is often reduced in people with PD, likely due to the combined effects of biological aging and impairments specific to the disease. Decreases in oxygen delivery (e.g., reduced cardiac output and impaired blood pressure responses) and oxygen utilization (e.g., reduced skeletal muscle oxidative capacity) compromise skeletal muscle respiration, forcing increased reliance on anaerobic metabolism. Thus, the assessment of fatigability in people with PD may provide valuable information regarding the functional status of people with PD not obtained with measures of fatigue. Moreover, interventions that target cardiorespiratory fitness may improve fatigability, movement performance, and health outcomes in this patient population.


2020 ◽  
Vol 21 (22) ◽  
pp. 8666
Author(s):  
Dominika Fricova ◽  
Jana Harsanyiova ◽  
Alzbeta Kralova Trancikova

The primary pathogenesis associated with Parkinson’s disease (PD) occurs in peripheral tissues several years before the onset of typical motor symptoms. Early and reliable diagnosis of PD could provide new treatment options for PD patients and improve their quality of life. At present, however, diagnosis relies mainly on clinical symptoms, and definitive diagnosis is still based on postmortem pathological confirmation of dopaminergic neuronal degeneration. In addition, the similarity of the clinical, cognitive, and neuropathological features of PD with other neurodegenerative diseases calls for new biomarkers, suitable for differential diagnosis. Alpha-synuclein (α-Syn) is a potential PD biomarker, due to its close connection with the pathogenesis of the disease. Here we summarize the currently available information on the possible use of α-Syn as a biomarker of early stages of PD in gastrointestinal (GI) tissues, highlight its potential to distinguish PD and other neurodegenerative diseases, and suggest alternative methods (primarily developed for other tissue analysis) that could improve α-Syn detection procedures or diagnostic methods in general.


2022 ◽  
Vol 13 ◽  
Author(s):  
Emily M. Klann ◽  
Upuli Dissanayake ◽  
Anjela Gurrala ◽  
Matthew Farrer ◽  
Aparna Wagle Shukla ◽  
...  

Parkinson’s disease is a chronic neurodegenerative disease characterized by the accumulation of misfolded alpha-synuclein protein (Lewy bodies) in dopaminergic neurons of the substantia nigra and other related circuitry, which contribute to the development of both motor (bradykinesia, tremors, stiffness, abnormal gait) and non-motor symptoms (gastrointestinal issues, urinogenital complications, olfaction dysfunction, cognitive impairment). Despite tremendous progress in the field, the exact pathways and mechanisms responsible for the initiation and progression of this disease remain unclear. However, recent research suggests a potential relationship between the commensal gut bacteria and the brain capable of influencing neurodevelopment, brain function and health. This bidirectional communication is often referred to as the microbiome–gut–brain axis. Accumulating evidence suggests that the onset of non-motor symptoms, such as gastrointestinal manifestations, often precede the onset of motor symptoms and disease diagnosis, lending support to the potential role that the microbiome–gut–brain axis might play in the underlying pathological mechanisms of Parkinson’s disease. This review will provide an overview of and critically discuss the current knowledge of the relationship between the gut microbiota and Parkinson’s disease. We will discuss the role of α-synuclein in non-motor disease pathology, proposed pathways constituting the connection between the gut microbiome and the brain, existing evidence related to pre- and probiotic interventions. Finally, we will highlight the potential opportunity for the development of novel preventative measures and therapeutic options that could target the microbiome–gut–brain axis in the context of Parkinson’s disease.


Biomolecules ◽  
2020 ◽  
Vol 10 (6) ◽  
pp. 912 ◽  
Author(s):  
Alexia Polissidis ◽  
Lilian Petropoulou-Vathi ◽  
Modestos Nakos-Bimpos ◽  
Hardy J. Rideout

Biomarkers and disease-modifying therapies are both urgent unmet medical needs in the treatment of Parkinson’s disease (PD) and must be developed concurrently because of their interdependent relationship: biomarkers for the early detection of disease (i.e., prior to overt neurodegeneration) are necessary in order for patients to receive maximal therapeutic benefit and vice versa; disease-modifying therapies must become available for patients whose potential for disease diagnosis and prognosis can be predicted with biomarkers. This review provides an overview of the milestones achieved to date in the therapeutic strategy development of disease-modifying therapies and biomarkers for PD, with a focus on the most common and advanced genetically linked targets alpha-synuclein (SNCA), leucine-rich repeat kinase-2 (LRRK2) and glucocerebrosidase (GBA1). Furthermore, we discuss the convergence of the different pathways and the importance of patient stratification and how these advances may apply more broadly to idiopathic PD. The heterogeneity of PD poses a challenge for therapeutic and biomarker development, however, the one gene- one target approach has brought us closer than ever before to an unprecedented number of clinical trials and biomarker advancements.


2017 ◽  
Vol 2017 ◽  
pp. 1-4 ◽  
Author(s):  
Jinhua Zheng ◽  
Xinglong Yang ◽  
Quanzhen Zhao ◽  
Sijia Tian ◽  
Hongyan Huang ◽  
...  

The genetic basis of festination, a common motor symptom in Parkinson’s disease (PD), remains unclear. Since polymorphism in the alpha-synuclein (SNCA) gene is associated with PD phenotype, we examined whether such polymorphism is also associated with festination. SNCA polymorphisms rs11931074 and rs894278 were genotyped in a consecutive series of 258 patients with PD, of whom 122 (47.3%) suffered festination. Univariate analysis revealed significant differences in genotype and minor allele frequencies at rs11931074 or rs894278 between patients with festination and those without it (all p<0.05). Based on logistic regression, a GG or GT genotype at rs11931074 was associated with higher risk of festination among patients with PD (OR 2.077, 95% CI 1.111–3.883, p=0.022), as was the TT genotype at rs894278 (OR 2.271, 95% CI 1.246–4.139, p=0.007). Therefore, we conclude that festination is associated with polymorphism at rs11931074 or rs894278 among patients with PD.


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