Blockchain Papers

Ramesh Babu Kalathoti, Sachi Nandan Mohanty

Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by motor impairments such as tremor, rigidity, bradykinesia, and gait instability. Accurate and early detection remains challenging due to the complex temporal nature of wearable sensor signals, limited interpretability of deep learning models, and concerns regarding medical data integrity. This study proposes a novel Blockchain-Enabled Hybrid CNN–Transformer framework with Integrated Gradients for PD detection using smartwatch-based inertial sensor data. The CNN module extracts local motion features, while the Transformer captures long-range temporal dependencies within movement signals. To enhance transparency, Integrated Gradients is employed to identify the most influential signal regions contributing to model predictions. In addition, a lightweight blockchain layer is incorporated to provide tamper-resistant storage and traceability of diagnostic outcomes. Experimental evaluation on the PADS dataset achieved 97.29% accuracy, 97.14% precision, 97.29% recall, 97.12% F1-score, and an AUC of 0.9869. The results demonstrate a reliable, interpretable, and secure framework for wearable-based Parkinson’s disease detection.

Surya B, Karuppasamy L, Yuvan Sankar NKR, Prabanjan S · 6 authors

Brain–Computer Interfaces (BCIs) represent a transformative paradigm in human–machine interaction, enabling direct communication between neural signals and external devices. They hold immense promise in domains such as medical neuroprosthetics, defense communication, and immersive gaming. However, the neural data they process is highly sensitive, and current BCI frameworks that rely on centralized servers and traditional encryption are vulnerable to data breaches, manipulation, and the emerging threats of quantum decryption. These limitations highlight the urgent need for secure, privacy-preserving, and resilient architectures for BCI communication. To address these challenges, this paper introduces NeuroGuard, a blockchain-based framework enhanced with Post-Quantum Cryptography (PQC) algorithms—CRYSTALS-Kyber for secure key exchange and Dilithium for digital signatures—combined with Zero-Knowledge Proofs (ZKPs) for lightweight device authentication. Neural data packets are logged in a decentralized ledger, ensuring immutability, transparency, and tamper-proof communication. A prototype system was implemented using an EEG-based BCI headset with edge preprocessing and blockchain-secured communication. Experimental results demonstrate a 31% improvement in attack resistance, 22% reduction in latency, and complete removal of central points of failure compared to traditional BCI security models. The novelty of NeuroGuard lies in integrating PQC, blockchain, ZKPs, and edge intelligence into a unified BCI security architecture, paving the way for future quantum-resilient neural communication systems.

Gençay Sevim

Blockchain is a distributed ledger technology that allows all records in a network to be stored. Blockchain became popular with Bitcoin, a cryptocurrency created for transferring electronic money between individuals or institutions without the need for any financial institution. However, it is not limited to this; it also has significant potential in the health sector. Blockchain applications in neurological disorders and oncology can effectively ensure the security, integrity, and sharing of medical data. It can offer an effective solution for the follow-up and safety of drugs used in some diseases. It may provide secure storage and sharing of genetic data for some cancer research. This enables effective diagnosis and treatment of the disease. Also, it can accelerate innovation in treatments by increasing the efficiency of clinical trials in neurological disorders and cancers. Consequently, integrating this technology into the healthcare industry can provide more effective diagnoses and personalized treatments. In this chapter, one will discuss the potential blockchain applications in neurological disorders and oncology. First, one will briefly mention fundamentals of blockchain technology. Later, one will explain its applications in neurological disorders and oncology. Finally, one will briefly summarize.

Sibonelo Sibahle Mpanza, Rajendra Rajaram, Damilola Aboluwodi

Purpose: The primary aim of this study was to discuss the possible treatment of cryptocurrencies in the context of accounting and taxation. Design/method/approach: The study followed a qualitative approach and used paper analysis to achieve the primary objective. The paper analysis included a systematic review of papers. The study focused on the paper analysis of existing data to refine a conceptual framework. Findings: It was found that because of the volatility of cryptocurrencies, the existing measurement models which are the cost model and fair value model, do not cater to cryptocurrencies. Practical implications: This study addressed the gap between financial information and regulations. These fintech advances do not merely challenge the monetary system but also the regulation system. Thus, the importance of acknowledging the application and the implication of technology on the current regulatory system is imperative and significant. Originality/value: This study will serve as a basis for international accounting standard boards and tax authorities when modifying or developing standards and tax provisions that specifically address the treatment of cryptocurrency.

Jigna J. Hathaliya, Hetav Modi, Rajesh Gupta, Sudeep Tanwar

Essential tremor (ET) and Parkinson’s tremor (PST) are neurological movement disorders in which ET emerges with body part activation, while PST is recorded in the relaxed position of the patient. The medical symptoms of ET and PST are equivalent, including gait, anxiety, and muscular stiffness. In both disorders, doctors diagnose patients related to clinical evaluations during such hospital visits, leading to misdiagnosis. Machine Learning (ML) is being used to classify the ET and PST using human-based feature extraction to address this issue. Motivated by this, we applied Deep Learning (DL) to overcome the ML issue via automating feature extraction through the model itself. In this paper, we have used the integration of Gated recurrent unit (GRU) and Long short term memory (LSTM) algorithms to predict tremor severity. Initially, accelerometer sensors are used to record tremors in all three axial dimensions for each subject. Further, this data is pre-processed using the standard scalar function and scaled in-unit variance. Furthermore, this data first passed through the GRU model, and later it fed into the LSTM model to improve the model’s performance. Moreover, we employed the blockchain (BC) network to validate the performance of the trained model. we have used a smart contract to validate the identity of the researcher. The proposed model outperforms with 80.4% training accuracy and 74.1% testing accuracy. The total communication and computation cost of the proposed scheme is 448 bits and 0.056 ms. The integration of BC and DL makes a system more reliable, transparent, and accurate.

Min Cheol Chang, Yong Sauk Hau, Jae Chan Park, Jae Min Lee

Chang, Min Cheol MD; Hau, Yong Sauk PhD; Park, Jae Chan PhD; Lee, Jae Min MD Author Information

Alice Wexler, Edward J. Wild, Sarah J. Tabrizi

George Huntington c. 1868. (Mulfold Album, Courtesy of the East Hampton Library, Pennypacker Long Island Collection). A naturalist as well as a hunter despite his severe asthma, George Huntington also sketched and painted landscapes and local scenes all his life, a practice that no doubt contributed to his keen powers of observation. His travel reports, published in a Long Island newspaper, testify to his early skill as a writer. Map of Connecticut and environs, c. 1780. Including East Hampton (white arrow) [H. Klockhoff and B. Romans, ‘Connecticut and Parts Adjacent‘ (Amsterdam: Covens and Mortier and Covens Jur., 1780) Library of Congress, Geography and Map Division]. Phebe Hedges and her mother, also called Phebe, descended from one of the oldest and most prominent East Hampton families who had settled the town in the 17th century from New England. [They bore no known relation to the East Anglia families whom P. R. Vessie and M. Critchley later and erroneously characterized as disreputable ancestors of many Huntington’s families in the USA (Wexler, 2008)]. They were patients of George Huntington’s grandfather, known as the Honourable Abel Huntington (1777–1858), a highly respected physician who had arrived in East Hampton from Connecticut in 1797 and found the disease well established there. The Huntingtons were long considered relative newcomers but they quickly won the esteem of their neighbours and played active roles in the local community, state, and even nationally. When Abel’s political activities drew him away from East Hampton, his physician son, George Lee Huntington (1811–81), became the doctor to the descendants of Phebe and Captain David Hedges. George Huntington, the son of George Lee and his wife Mary, born in 1850 and educated in East Hampton, was thus a third generation physician in a medical family that had lived alongside families with hereditary chorea since the end of the 18th century and was well situated to observe, over multiple generations, who did and did not have the disease. In the fall of 1871, soon after graduation from medical school, George Huntington moved to Pomeroy, Ohio. His cousin had married a clergyman in Pomeroy and suggested the young George open a medical practice there. Invited to present a paper to the local Meigs and Middleport Academy of Medicine in nearby Middleport, he chose to talk ‘On Chorea’, perhaps because he had recently observed cases of childhood (Sydenham’s) chorea in the clinic as a medical student in New York City and was struck by the differences from the chorea he had observed back home. Most of the paper, in fact, described this common type of chorea but in the final paragraphs George Huntington outlined three predominant characteristics of a type of chorea he believed to be present ‘exclusively on the east end of Long Island’. First was its hereditary nature, for it was ‘confined to certain and fortunately a few families, and has been transmitted to them, an heirloom from generations away back in the dim past’. It differed, however, ‘from the general laws of so-called hereditary diseases’ in which the disease may skip a generation. ‘Unstable and whimsical as the disease may be in other respects, in this it is firm, it never skips a generation to again manifest itself in another; once having yielded its claims, it never regains them.’ Second, was the tendency to what George Huntington called, in 19th century parlance, ‘insanity, and sometimes that form of insanity which leads to suicide’. (19th century meanings of ‘insanity’ ranged from disturbances of mood to disorders of thought and behaviour as well as personality changes. Suicide typically cast the deceased as having suffered from insanity.) He also noted specifically the tendency to cognitive impairment. ‘As the disease progresses the mind becomes more or less impaired, in many amounting to insanity, while in others mind and body both gradually fail until death relieves them of their sufferings’. He further described a lack of self-awareness and loss of inhibitions on the part of sufferers, offering a far more nuanced description than had been given in earlier accounts. Finally, he noted that the symptoms generally manifested in adult life, most often between 30 and 40 years of age, increasing very gradually ‘until every muscle in the body becomes affected (excepting the involuntary ones)’. The disease progressed inexorably without any periods of remission. ‘When once it begins it clings to the bitter end.’ Huntington ended by acknowledging that he knew nothing of its pathology and offered his account, ‘not that I considered it of any great practical importance to you, but merely as a medical curiosity, and as such it may have some interest’. Pages from the ledgers and daybooks of George Huntington’s grandfather Abel (A) and father George Lee (B) who cared for the families whose illness George later described (Courtesy of the East Hampton Library, Pennypacker Long Island Collection). See Supplementary material for further references. But he also incorporated the knowledge of the East Hampton families themselves, including their recognition that this malady was hereditary. Actually many ailments were considered to be inherited in the 19th century. It is not surprising that, in an old community with memory going back many generations, the affected families—indeed the entire community—recognized that this disorder was hereditary. Nor is it surprising that they theorized about its genealogical origins and even spoke of families ‘who belonged to the disease’. What surprises is that they were expert diagnosticians who had precise ideas of who did or did not have this illness in each generation. They understood its terrors, for as George Huntington wrote, ‘it is spoken of by those in whose veins the seeds of the disease are known to exist, with a kind of horror, and not at all alluded to except through dire necessity, when it is mentioned as “that disorder”’. (According to Henry P. Hedges, a distant relative of Phebe Hedges and a historian of East Hampton, it was also called St. Vitus’s dance although ‘the subject is avoided by most people as distasteful’.) The families also understood its trajectory, for ‘its end is so well known to the sufferer and his friends, that medical advice is seldom sought’. Years after he published ‘On Chorea’, George Huntington the artist as well as the physician beautifully captured both his own childhood awe on first encountering persons with chorea and his empathy as an adult for the suffering of those who had been his family’s neighbours and friends: ‘Driving with my father through a wooded road leading from East Hampton to Amagansett, we suddenly came upon two women, mother and daughter, both tall, thin, almost cadaverous, both bowing, twisting, grimacing. I stared in wonderment, almost in fear. What could it mean? My father paused to speak with them, and we passed on. Then my Gamaliel like instruction began; my medical education had its inception. From this point my interest in the disease has never wholly ceased. Then came the hanging of D.H. in his blacksmith shop. He was a victim of incipient chorea, knew it, possibly had been waiting for it, the “Sanctus Invictus,” and well knowing the character of the foe he must meet, the so dreaded, the long expected, the conquering, he cut short the taper and his life went out. Other victims had sought the same refuge again and again by drowning. Others, of a different nervous organization perhaps, lived on if not content, still seemingly reconciled to Fate, until mind and body both exhausted they fell asleep.’ George Huntington’s 1872 paper ‘On chorea’ in the Medical and Surgical Reporter. His later talks before various medical societies on Huntington’s chorea were published, in the Brooklyn Medical Journal (1895), the Transactions of the Tri-State Medical Association (1903), and The Journal of Nervous and Mental Disease (1910). His unpublished papers are in the Special Collections of the Columbia University Health Sciences Library, New York City, and the Pennypacker Long Island Collection, East Hampton Library, New York. With the rediscovery of Mendel’s laws in 1900 and also the establishment of eugenics societies in many countries, the hereditary dimension of Huntington’s chorea—and the specific pattern of inheritance—began to draw increased attention, not only from clinicians but also from biologists studying Mendelian heredity more broadly. In addition to its interest as a case study in human Mendelian inheritance, Huntington’s chorea now appeared to some influential supporters of eugenics as a cause for public health alarm. With the resources of the Carnegie-funded Eugenics Record Office at Cold Spring Harbor, New York, the biologist and eugenics leader Charles B. Davenport in 1911 initiated the first large-scale pedigree study of families with Huntington’s chorea, creating pedigrees that included some 962 alleged cases, living and deceased, in a total of ∼4370 individuals in the northeastern USA. Davenport and Muncey’s 1916 paper ‘Huntington’s Chorea in Relation to Heredity and Eugenics’, was widely cited and largely unchallenged for decades despite Davenport’s extreme eugenic views, which helped to normalize the notion of sterilization as the recommended method of prevention, a notion that prevailed well into the 1960s (Davenport and Muncey, 1916). At that time Hans and Gilmore and later Wexler demonstrated that these pedigrees were riddled with unreliable or clearly erroneous diagnoses and gross genealogical errors, including errors that laid the foundation for subsequent claims about Huntington’s and witches, ‘criminality’, and violence (Hans and Gilmore, 1969; Wexler, 2008). Such claims, repeated even today, deepened the stigmatization of Huntington’s families while discouraging research toward effective treatment. They also gave families further incentives for maintaining secrecy and silence about this disease (Wexler and Rawlins, 2005). Reports on the neuropathology of chorea in adults appeared as early as the 1870s, with researchers generally agreed that the basic lesion was located in the basal ganglia, with the striatum, particularly the caudate nucleus, showing the greatest degree of atrophy. However, there was little agreement on its cause and relatively little progress for decades. The confluence of several developments in the 1960s radically transformed this bleak research landscape. First, the discovery of L-DOPA and its benefits for patients with Parkinson’s disease spurred an international gathering of neurologists in 1967 to organize a Research Group on Huntington’s Chorea. Second, the rise of social movements in the 1960s challenged the legacy of eugenics and encouraged members of families with Huntington’s to become active on their own behalf. Activists such as the North Americans Marjorie Guthrie, widow of the songwriter and singer Woody Guthrie who died with Huntington’s in 1967, and Milton and Nancy Wexler, husband and daughter of recently diagnosed Leonore Wexler, along with Ralph Walker in Canada, Mauveen Jones in the UK, Gerrit Dommerholt in the Netherlands, and Huntington’s family members elsewhere spearheaded efforts to improve care as well as to interest scientists in research. In the late 1960s and 1970s they formed disease advocacy associations in many countries (called self-support organizations or health voluntary agencies) which, along with revolutionary advances in molecular genetics and neuroscience, expanded biomedical interest in Huntington’s. New technologies of gene mapping opened up possibilities for identifying—and perhaps disabling—the aberrant gene. New modes of imaging offered possibilities for understanding—and potentially intervening in—the sequence of pathological changes in the brain. At a 1972 Centennial Symposium on Huntington’s disease, in Columbus Ohio, near the town where George Huntington presented his landmark paper, some 136 researchers and a few members of Huntington’s families from around the world gathered to commemorate his contribution and develop new directions for research. Out of this meeting came the impetus for a bold collaborative project focused on a unique cluster of affected families in Venezuela who had been diagnosed back in the 1950s by a local physician, Americo Negrette, author of the first monograph ever published on Huntington’s disease (Negrette, 1963). Drawing on the new somatic cell genetics for mapping genes, this project, led by Nancy Wexler, culminated in 1983 in the identification of a genetic marker for Huntington’s (Gusella et al., 1983). Besides demonstrating that the new technology could be used for mapping the human genome, the landmark marker discovery for the first time enabled those at 50% risk for Huntington’s disease to learn either that they were forever free of the disease and were not in danger of passing it on to their children or grandchildren, or that they did carry the abnormal version of the gene and would therefore develop symptoms if they lived long enough: a momentous form of new knowledge. It also inspired the formation of the legendary Huntington’s Disease Collaborative Research Group, again under the leadership of Nancy Wexler and the Hereditary Disease Foundation. After 10 agonizing years of work, the group collectively announced the identification of the abnormal Huntington’s disease gene (Huntington’s Disease Collaborative Research Group, 1993; Wexler, 2012) (Fig. 6). In a coding region of chromosome 4 initially labelled IT-15 (‘interesting transcript 15’), the Collaborative Research Group had found an expanded CAG triplet repeat that segregated completely with Huntington’s disease cases. The gene was soon renamed HTT and its protein product baptized ‘huntingtin’. So began a new age of Huntington’s disease: armed now with certainty of the cause of every past, present and future case of Huntington’s disease, researchers could focus their efforts on understanding the gene, studying the protein in its wild-type and mutant forms, elucidating the mechanisms through which mutant huntingtin (mHTT) causes disease, and working on therapies targeting the mutation and its known effects. Hopes that the gene discovery would lead overnight to a cure for Huntington’s disease quickly sublimated into a realization that a long road lay ahead—but at least, a road illuminated by the certitude conferred by the genetic basis of Huntington’s disease. At every branch-point, paths unconnected to the expanded HTT gene could be discounted. This certainty offers researchers on Huntington’s a potent advantage over those studying more common neurodegenerative diseases, which remain almost entirely idiopathic. Our understanding of the complex roles of the protein and the multiple toxicities of its mutant counterpart rapidly burgeoned, but there was solace to be drawn from knowing each was a potential new target for therapeutic development (reviewed in Wild and Tabrizi, 2014; Bate et al., 2015). The first mouse model of Huntington’s disease, the R6/2, expressing HTT exon 1 under control of the human promoter, followed rapidly in 1996 and remains a mainstay in the field thanks to its robust phenotype and rapid progression. mHTT-containing protein aggregates were soon found in its neurons and in the brains of human patients. Numerous model systems from cells to primates and everything in between are now available to elucidate aspects of pathology and explore therapeutics (reviewed in Bates et al., 2015). Huntington special issue of Neurographs. In 1908 the New York neurologist William Browning devoted an entire issue of his journal Neurographs to Huntington’s chorea, emphasizing what he called ‘the world-wide interest’ in the disease. Collectively authored paper describing the identification of the CAG triplet repeat expansion in IT15 responsible for Huntington’s disease. This discovery was considered so momentous that it appeared on the front page of The New York Times (24 March 1993). Overview of current therapeutic targets for Huntington’s disease. From Wild and Tabrizi (2014). If we could achieve in humans, using a targeted drug molecule, what was seen in Yamamoto’s conditional HTT knockout mouse, we would theoretically treat every facet of Huntington’s disease. Work on such ‘gene silencing’ or ‘huntingtin lowering’ approaches began in Huntington’s disease model animals in 2005 using RNA interference. Similar approaches using antisense oligonucleotides (ASOs)—modified single-stranded DNA—began around the same time. Each aims to reduce HTT expression by targeting its mRNA transcript for removal by the cellular mRNA degradation machinery. For the past decade these technologies have been honed and put through their paces in animal models (Wild and Tabrizi, 2014). Huntington was almost 22 when he presented his seminal work, and by coincidence it was 22 years after the discovery of the HTT gene that the first injection of an ASO therapeutic targeting huntingtin production in the brain was administered into the spinal of a with Huntington’s disease in in either or remains the of this first the of Huntington’s age of therapeutics targeting the cause and known of Huntington’s now at the ASO and its are by and established and by of Huntington’s disease family who are their time and to knowing they are not to but that many others years after George Huntington’s his disease is no the and malady that it was his Nor is it considered so New have a at in the UK, than was about although the has et al., while Huntington’s is still it is no reduce movements and and to improve of life, for family members as well as for those at risk and those living with the disease. New technologies such as in and genetic increased for those at risk who to have families without passing on the malady et al., 2015). The and of Huntington’s family the has helped reduce the and social that has long to the suffering with the disease. But all these advances are many people in Huntington’s families, not only in countries but also in not have to these it is that we to in research on it is also that therapies and be to those who them if the of is to be is by the Medical Research This was in part by the for Health University Research and the Supplementary material is available at

Bruce S. Glaeser, Wolfgang H. Vogel, D.B. Oleweiler, T.A. Hare

No abstract is available for this record.