Classification of resting-state fMRI for olfactory dysfunction in parkinson's disease using evolutionary algorithms

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Classification of Resting-State fMRI using Evolutionary Algorithms: Towards a Brain Imaging Biomarker for Parkinson’s Disease

It is commonly accepted that accurate early diagnosis and monitoring of neurodegenerative conditions is essential for effective disease management and delivery of medication and treatment. This research develops automatic methods for detecting brain imaging preclinical biomarkers for Parkinson’s disease (PD) by considering the novel application of evolutionary algorithms. An additional novel element of this work is the use of evolutionary algorithms to both map and predict the functional connectivity in patients using rs-fMRI data. Specifically, Cartesian Genetic Programming was used to classify dynamic causal modelling data as well as timeseries data. The findings were validated using two other commonly used classification methods (Artificial Neural Networks and Support Vector Machines) and by employing k-fold cross-validation. Across dynamic causal modelling and timeseries analyses, findings revealed maximum accuracies of 75.21% for early stage (prodromal) PD patients in which patients reveal no motor symptoms versus healthy controls, 85.87% for PD patients versus prodromal PD patients, and 92.09% for PD patients versus healthy controls. Prodromal PD patients were classified from healthy controls with high accuracy – this is notable and represents the key finding since current methods of diagnosing prodromal PD have low reliability and low accuracy. Furthermore, Cartesian Genetic Programming provided comparable performance accuracy relative to Artificial Neural Networks and Support Vector Machines. Nevertheless, evolutionary algorithms enable us to decode the classifier in terms of understanding the data inputs that are used, more easily than in Artificial Neural Networks and Support Vector Machines. Hence, these findings underscore the relevance of both dynamic causal modelling analyses for classification and Cartesian Genetic Programming as a novel classification tool for brain imaging data with medical implications for disease diagnosis, particularly in early stages 5-20 years prior to motor symptoms

Towards Monitoring Parkinson's Disease Following Drug Treatment: CGP Classification of rs-MRI Data

Background and Objective: It is commonly accepted that accurate monitoring of neurodegenerative diseases is crucial for effective disease management and delivery of medication and treatment. This research develops automatic clinical monitoring techniques for PD, following treatment, using the novel application of EAs. Specifically, the research question addressed was: Can accurate monitoring of PD be achieved using EAs on rs-fMRI data for patients prescribed Modafinil (typically prescribed for PD patients to relieve physical fatigue)? Methods: This research develops novel clinical monitoring tools using data from a controlled experiment where participants were administered Modafinil versus placebo, examining the novel application of EAs to both map and predict the functional connectivity in participants using rs-fMRI data. Specifically, CGP was used to classify DCM analysis and timeseries data. Results were validated with two other commonly used classification methods (ANN and SVM) and via k-fold cross-validation. Results: Findings revealed a maximum accuracy of 74.57% for CGP. Furthermore, CGP provided comparable performance accuracy relative to ANN and SVM. Nevertheless, EAs enable us to decode the classifier, in terms of understanding the data inputs that are used, more easily than in ANN and SVM. Conclusions: These findings underscore the applicability of both DCM analyses for classification and CGP as a novel classification technique for brain imaging data with medical implications for medication monitoring. Furthermore, classification of fMRI data for research typically involves statistical modelling techniques being often hypothesis driven, whereas EAs use data-driven explanatory modelling methods resulting in numerous benefits. DCM analysis is novel for classification and advantageous as it provides information on the causal links between different brain regions.Comment: arXiv admin note: substantial text overlap with arXiv:1910.0537

Cognitive and Structural Correlates of Conversational Speech Timing in Mild Cognitive Impairment and Mild-to-Moderate Alzheimer’s Disease : Relevance for Early Detection Approaches.

FUNDING This study was supported by a Centre for Ageing Research and Development in Ireland (CARDI) Leadership Fellowship (grant number 13533).Peer reviewedPublisher PD

Characterizing the Neurobiological Mechanisms of Action of Exercise and Cognitive–Behavioral Interventions for Rheumatoid Arthritis Fatigue : a magnetic resonance imaging brain study

Open Access via the Wiley/JISC agreement Acknowledgements We would like to thank all the investigators from the original LIFT study, including Kathryn Martin, Lorna Aucott, Neeraj Dhaun, Emma Dures, Stuart R. Gray, Elizabeth Kidd, Vinod Kumar, Karina Lovell, Graeme MacLennan, Paul McNamee, John Norrie, Lorna Paul, Jon Packham, Stefan Siebert, Alison Wearden, and Gary Macfarlane, without whose work this research would not be possible. Furthermore, we thank all the participants who generously supported the LIFT trial. We also acknowledge the contribution of the Trial Steering Committee and Data Monitoring Committee, and Brian Taylor and Mark Forrest (Centre for Healthcare Randomised Trials [CHaRT], University of Aberdeen, Aberdeen, UK) for their technical assistance Funding This study was funded by the Chief Scientist Office (TCS/17/14) and Versus Arthritis (22092).Peer reviewe

Elevated CSF GAP-43 is associated with accelerated tau accumulation and spread in Alzheimer's disease

In Alzheimer's disease, amyloid-beta (A beta) triggers the trans-synaptic spread of tau pathology, and aberrant synaptic activity has been shown to promote tau spreading. A beta induces aberrant synaptic activity, manifesting in increases in the presynaptic growth-associated protein 43 (GAP-43), which is closely involved in synaptic activity and plasticity. We therefore tested whether A beta-related GAP-43 increases, as a marker of synaptic changes, drive tau spreading in 93 patients across the aging and Alzheimer's spectrum with available CSF GAP-43, amyloid-PET and longitudinal tau-PET assessments. We found that (1) higher GAP-43 was associated with faster A beta-related tau accumulation, specifically in brain regions connected closest to subject-specific tau epicenters and (2) that higher GAP-43 strengthened the association between A beta and connectivity-associated tau spread. This suggests that GAP-43-related synaptic changes are linked to faster A beta-related tau spread across connected regions and that synapses could be key targets for preventing tau spreading in Alzheimer's disease. Trans-synaptic tau spread drives neurodegeneration in Alzheimer's disease. This study shows that GAP-43, a marker of synaptic abnormality, is linked to faster tau spread, showing that synaptic changes may contribute to tau spreading in Alzheimer's disease

Characterising the neurobiological mechanisms of action of exercise and cognitive behavioural interventions for rheumatoid arthritis fatigue: an MRI brain study

Objective: Chronic fatigue is a major clinical unmet need among patients with rheumatoid arthritis (RA). Current therapies are limited to nonpharmacological interventions, such as personalized exercise programs (PEPs) and cognitive–behavioral approaches (CBAs); however, most patients still continue to report severe fatigue. To inform more effective therapies, we conducted a magnetic resonance imaging (MRI) brain study of PEPs and CBAs, nested within a randomized controlled trial (RCT), to identify their neurobiological mechanisms of fatigue reduction in RA. Methods: A subgroup of patients with RA (n = 90), participating in an RCT of PEPs and CBAs for fatigue, undertook a multimodal MRI brain scan following randomization to either usual care (UC) alone or in addition to PEPs and CBAs and again after the intervention (six months). Brain regional volumetric, functional, and structural connectivity indices were curated and then computed employing a causal analysis framework. The primary outcome was fatigue improvement (Chalder fatigue scale). Results: Several structural and functional connections were identified as mediators of fatigue improvement in both PEPs and CBAs compared to UC. PEPs had a more pronounced effect on functional connectivity than CBAs; however, structural connectivity between the left isthmus cingulate cortex (L-ICC) and left paracentral lobule (L-PCL) was shared, and the size of mediation effect ranked highly for both PEPs and CBAs (ßAverage = −0.46, SD 0.61; ßAverage = −0.32, SD 0.47, respectively). Conclusion: The structural connection between the L-ICC and L-PCL appears to be a dominant mechanism for how both PEPs and CBAs reduce fatigue among patients with RA. This supports its potential as a substrate of fatigue neurobiology and a putative candidate for future targeting

Elevated CSF GAP-43 is associated with accelerated tau accumulation and spread in Alzheimer's disease

In Alzheimer's disease, amyloid-beta (Aβ) triggers the trans-synaptic spread of tau pathology, and aberrant synaptic activity has been shown to promote tau spreading. Aβ induces aberrant synaptic activity, manifesting in increases in the presynaptic growth-associated protein 43 (GAP-43), which is closely involved in synaptic activity and plasticity. We therefore tested whether Aβ-related GAP-43 increases, as a marker of synaptic changes, drive tau spreading in 93 patients across the aging and Alzheimer's spectrum with available CSF GAP-43, amyloid-PET and longitudinal tau-PET assessments. We found that (1) higher GAP-43 was associated with faster Aβ-related tau accumulation, specifically in brain regions connected closest to subject-specific tau epicenters and (2) that higher GAP-43 strengthened the association between Aβ and connectivity-associated tau spread. This suggests that GAP-43-related synaptic changes are linked to faster Aβ-related tau spread across connected regions and that synapses could be key targets for preventing tau spreading in Alzheimer's disease

Artificial intelligence for dementia research methods optimization

Artificial intelligence (AI) and machine learning (ML) approaches are increasingly being used in dementia research. However, several methodological challenges exist that may limit the insights we can obtain from high-dimensional data and our ability to translate these findings into improved patient outcomes. To improve reproducibility and replicability, researchers should make their well-documented code and modeling pipelines openly available. Data should also be shared where appropriate. To enhance the acceptability of models and AI-enabled systems to users, researchers should prioritize interpretable methods that provide insights into how decisions are generated. Models should be developed using multiple, diverse datasets to improve robustness, generalizability, and reduce potentially harmful bias. To improve clarity and reproducibility, researchers should adhere to reporting guidelines that are co-produced with multiple stakeholders. If these methodological challenges are overcome, AI and ML hold enormous promise for changing the landscape of dementia research and care. HIGHLIGHTS: Machine learning (ML) can improve diagnosis, prevention, and management of dementia. Inadequate reporting of ML procedures affects reproduction/replication of results. ML models built on unrepresentative datasets do not generalize to new datasets. Obligatory metrics for certain model structures and use cases have not been defined. Interpretability and trust in ML predictions are barriers to clinical translation

Classification of Resting-State fMRI using Evolutionary Algorithms : Towards a Brain Imaging Biomarker for Parkinson's Disease

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