Carbon nanotubes, an emerging class of carbon nanomaterials, possess tremendous potential for application in biotechnology and biomedicine particularly in neurological disorders. Carbon nanotubes owing to their fascinating properties have the potential to revolutionize medicine and technology, particularly in the realm of drug delivery, biosensing, bioimaging, and as therapeutic agents to tackle complex neurological disorders such as Alzheimer’s and Parkinson’s disease. In this review, a summary of the use of carbon nanotubes for neuropathological outcomes such as alleviating oxidative stress and amyloid formation, which are well-studied molecular outcomes associated with Alzheimer’s and Parkinson’s disease. In the end, challenges associated with the clinical testing of carbon nanotubes and possible ways to overcome them are highlighted.

Post-translational modifications (PTMs) of alpha-synuclein (α-syn) can alter protein aggregation propensity to affect α-syn oligomer and fibril formation. The inflammatory response in Parkinson’s disease (PD) is mediated by microglia, astrocytes, T cells, B cells, macrophages, and neutrophils, which respond to α-syn aggregates in an attempt to clear synucleinopathy and restore brain homeostasis. This review focuses on the effects of PTMs on α-syn aggregation and cell-specific immune responses to α-syn aggregates in the context of PD.

Parkinson’s disease (PD) is a prevalent neurodegenerative disease (NDD) affecting millions of individuals. The pathogenesis of PD centers around α-synuclein (α-Syn), a pivotal protein whose aggregation significantly impacts disease progression. Although existing treatments mainly focus on managing motor symptoms by targeting the dopaminergic system, they frequently overlook other non-motor symptoms. The intricate nature of PD pathogenesis contributes to challenges in disease analysis and has hindered the development of effective PD treatments. In recent years, various novel therapies utilizing immunotherapy methods have exhibited promise in preclinical animal models. In NDDs, immunotherapy aims to counteract the detrimental effects of protein accumulation by neutralizing toxic species and aiding their elimination. Numerous active therapy (AI) and passive immunotherapy (PI) strategies have been devised for PD and related synucleinopathies, many of which are currently undergoing clinical trials. Despite demonstrating remarkable success in animal models, immunotherapies encountered substantial setbacks during the late stages of clinical trials, with the exception of lecanemab, which targets amyloid-β (Aβ) in Alzheimer’s disease (AD) and has recently received approval from the Food and Drug Administration (FDA). The lack of translation from experimental investigations to successful clinical outcomes, particularly in terms of cognitive and functional evaluations, highlights the limitations of relying solely on animal studies to comprehend the effects of immunotherapeutic approaches. This comprehensive review focuses on α-Syn-based immunotherapies and delves into their underlying mechanisms of action. Furthermore, Furthermore, the article discusses recent advancements and future prospects concerning the potential of immunotherapeutic strategies for PD. The focus is on highlighting the latest research in this domain to illuminate the challenges and opportunities related to the development of efficacious immunotherapies for individuals with PD.

Parkinson’s disease (PD) is a progressive neurodegenerative disorder affecting 1% of the population above sixty years. It is caused by an interaction between genetic and environmental risk factors. Loss of dopaminergic neurons in substantia nigra pars compacta (SNpc) is pathologically characterizing the disease and responsible for the cardinal motor symptoms, most notably, bradykinesia, rest tremors, rigidity, and loss of postural reflexes. Non-motor signs such as olfactory deficits, cognitive impairment, sleep behavior disorders, and gastrointestinal disturbances are reflecting disturbances in the non-dopaminergic system. They precede dopaminergic neuronal degenerations by 5–10 years and are considered the main contributors to patients’ disability, particularly after the successful implementation of levodopa (L-dopa) treatment of motor symptoms. The present general review aimed to briefly update non-motor signs and their underlying pathophysiology in PD.