Nanotechnology utilizes engineered materials and devices which function with biological systems at the molecular level and could transform the management of neurodegenerative diseases (NDs) by provoking, reacting to, and intermingling with target sites to stimulate physiological responses while minimizing side effects. Blood–brain barrier (BBB) protects the brain from harmful agents, and transporting drugs across the BBB is a major challenge for diagnosis, targeting, and treatment of NDs. The BBB provides severe limitations for diagnosis and treatment of Alzheimer’s disease (AD), Parkinson’s disease (PD), and various other neurological diseases. Conventional drug delivery systems generally fail to cross the BBB, thus are inefficient in treatment. Although gradual development through research is ensuring the progress of nanotheranostic approaches from animal to human modeling, aspects of translational applicability and safety are a key concern. This demands a deep understanding of the interaction of body systems with nanomaterials. There are various plant-based nanobioactive compounds which are reported to have applicability in the diagnosis and treatment of these NDs. This review article provides an overview of applications of nanotheranostics in AD and PD. The review also discusses nano-enabled drug delivery systems and their current and potential applications for the treatment of various NDs.

Pyrazinamide (PZA) is one of the main FDA approved drugs to be used as the first line of defense against Mycobacterium Tuberculosis (MTB). It is activated into pyrazinoic acid (POA) via MTB's pncA gene-encoded pyrazinamidase (PZase). Mutations are most commonly responsible for PZA-resistance in nearly 70% of the resistant samples. In the present work, MTB positive samples were chosen for PZA drug susceptibility testing (DST) against critical concentration (100 ug/ml) of PZA. The resistant samples were subjected to pncA sequencing. As a result, 36 various mutations have been observed in the PZA resistant samples, uploaded to the NCBI (GeneBank accession no. MH461111). Here we report the mechanism of PZA resistance behind the three mutants (MTs), Asp12Ala, Pro54Leu, and His57Pro in comparison with the wild type (WT) through molecular dynamics simulation to unveil how these mutations affect the overall conformational stability. The post-simulation analyses revealed notable deviations as compared to the WT structure. Molecular docking studies of PZA with MTs and WT, pocket volume inspection and overall shape complementarity analysis confirmed the deleterious nature of these mutations and gave an insight into the mechanism behind PZA-resistance. These analyses provide vital information regarding MTB drug resistance and could be extremely useful in therapy management and overcoming its global burden.