scholarly journals Data Clustering Improves Siamese Neural Networks Classification of Parkinson’s Disease

Complexity ◽  
2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Mohamed Shalaby ◽  
Nahla A. Belal ◽  
Yasser Omar

Parkinson’s disease (PD) is a clinical neurodegenerative disease having symptoms like tremor, rigidity, and postural disability. According to Harvard, about 60,000 of American citizens are diagnosed with PD yearly, with more than 10 million people infected worldwide. An estimate of 4% of the people have PD before they reach the age 50; however, the incident increases with age. Diagnosis of PD relies on the expertise of the physician and depends on several established clinical criteria. This makes the diagnosis subjective and inefficient. Hence, continuous efforts are being made to enhance the diagnosis of PD using deep learning approaches that rely on experienced neurologists. Siamese neural networks mainly work on two different input vectors and are used in comparison of output vectors. Moreover, clustering a dataset before applying classification enhances the distribution of similar samples among groups. In addition, applying the Siamese network can overcome the limitation of samples per class in the dataset by guiding the network to learn differences between samples rather than focusing on learning specific classes. In this paper, a Siamese neural network is applied to diagnose PD. Siamese networks predict the sample class by estimating how similar a sample is to other samples. The idea behind this work is clustering the dataset before training the network, as different pairs that belong to the same cluster are candidates to be mistaken by the network and assumed to be matched pairs. To overcome this problem, the dataset is first clustered, and then the architecture feeds the network to pairs of the same cluster. The proposed framework is concerned with comparing the performance when using clustered against unclustered data. The proposed framework outperforms the conventional framework without clustering. The accuracy achieved for classifying unclustered PD patients reached 76.75%, while it reached 84.02% for clustered data, outperforming the same technique on unclustered data. The significance of this study is in the enhanced performance achieved due to the clustering of data, which shows a promising framework to enhance the diagnostic capability of computer-aided disease diagnostic tools.

2021 ◽  
Author(s):  
Nikhil J. Dhinagar ◽  
Sophia I. Thomopoulos ◽  
Conor Owens-Walton ◽  
Dimitris Stripelis ◽  
Jose Luis Ambite ◽  
...  

2020 ◽  
Vol 13 (5) ◽  
pp. 508-523 ◽  
Author(s):  
Guan‐Hua Huang ◽  
Chih‐Hsuan Lin ◽  
Yu‐Ren Cai ◽  
Tai‐Been Chen ◽  
Shih‐Yen Hsu ◽  
...  

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Alessandro Gialluisi ◽  
Mafalda Giovanna Reccia ◽  
Nicola Modugno ◽  
Teresa Nutile ◽  
Alessia Lombardi ◽  
...  

Abstract Background Parkinson’s disease (PD) is a neurodegenerative movement disorder affecting 1–5% of the general population for which neither effective cure nor early diagnostic tools are available that could tackle the pathology in the early phase. Here we report a multi-stage procedure to identify candidate genes likely involved in the etiopathogenesis of PD. Methods The study includes a discovery stage based on the analysis of whole exome data from 26 dominant late onset PD families, a validation analysis performed on 1542 independent PD patients and 706 controls from different cohorts and the assessment of polygenic variants load in the Italian cohort (394 unrelated patients and 203 controls). Results Family-based approach identified 28 disrupting variants in 26 candidate genes for PD including PARK2, PINK1, DJ-1(PARK7), LRRK2, HTRA2, FBXO7, EIF4G1, DNAJC6, DNAJC13, SNCAIP, AIMP2, CHMP1A, GIPC1, HMOX2, HSPA8, IMMT, KIF21B, KIF24, MAN2C1, RHOT2, SLC25A39, SPTBN1, TMEM175, TOMM22, TVP23A and ZSCAN21. Sixteen of them have not been associated to PD before, were expressed in mesencephalon and were involved in pathways potentially deregulated in PD. Mutation analysis in independent cohorts disclosed a significant excess of highly deleterious variants in cases (p = 0.0001), supporting their role in PD. Moreover, we demonstrated that the co-inheritance of multiple rare variants (≥ 2) in the 26 genes may predict PD occurrence in about 20% of patients, both familial and sporadic cases, with high specificity (> 93%; p = 4.4 × 10− 5). Moreover, our data highlight the fact that the genetic landmarks of late onset PD does not systematically differ between sporadic and familial forms, especially in the case of small nuclear families and underline the importance of rare variants in the genetics of sporadic PD. Furthermore, patients carrying multiple rare variants showed higher risk of manifesting dyskinesia induced by levodopa treatment. Conclusions Besides confirming the extreme genetic heterogeneity of PD, these data provide novel insights into the genetic of the disease and may be relevant for its prediction, diagnosis and treatment.


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