Background: Parkinson’s disease (PD) is a multifactorial, progressive neurodegenerative disorder that primarily affects dopaminergic neurons in the substantia nigra. In addition to hallmark motor symptoms, it manifests a wide range of nonmotor complications, including cognitive decline, neuropsychiatric symptoms, autonomic dysfunction, and comorbid metabolic and infectious diseases.Objectives: This review aims to elucidate the molecular and cellular mechanisms underlying PD, explore the influence of genetic and environmental factors, evaluate current treatment limitations, and assess the clinical and socioeconomic burden globally. Emphasis is placed on emerging therapeutic avenues and innovative research directions.Methods: A structured literature review was conducted using PubMed, Scopus, and Web of Science databases. The search included articles published between 2010 and 2025, using keywords: “Parkinson’s disease,” “α-synuclein,” “dopaminergic degeneration,” “ferroptosis,” “deep brain stimulation,” “stem cell therapy,” and “AI in PD diagnosis.”Results: The review highlights a multifactorial etiology involving α-synuclein pathology, oxidative stress, mitochondrial dysfunction, genetic mutations (SNCA, LRRK2, VPS35), environmental toxins, and gut dysbiosis. Comorbidities such as HIV, diabetes, and cardiovascular disorders exacerbate disease burden. While Levodopa remains the gold standard, its limitations necessitate combination therapy and adjunct modalities such as deep brain stimulation and nanocarrier-based drug delivery. Emerging approaches—stem cell therapy, CRISPR-Cas9, and AI-enhanced diagnostics—show promise.Conclusion: PD management requires a paradigm shift toward precision medicine. Advancing research into biomarkers, immunotherapy, and systems biology, coupled with equitable access to care and early diagnosis tools, is critical to mitigating the global impact of PD.

Advancements in medicine have increased the longevity of humans, resulting in a higher incidence of chronic diseases. Due to the rise in the elderly population, age-dependent neurodegenerative disorders are becoming increasingly prevalent. The available treatment options only provide symptomatic relief and do not cure the underlying cause of the disease. Therefore, it has become imperative to discover new markers and therapies to modulate the course of disease progression and develop better treatment options for the affected individuals. Growing evidence indicates that neuroinflammation is a common factor and one of the main inducers of neuronal damage and degeneration. Galectins (Gals) are a class of β-galactoside-binding proteins (lectins) ubiquitously expressed in almost all vital organs. Gals modulate various cellular responses and regulate significant biological functions, including immune response, proliferation, differentiation, migration, and cell growth, through their interaction with glycoproteins and glycolipids. In recent years, extensive research has been conducted on the Gal superfamily, with Gal-1, Gal-3, and Gal-9 in prime focus. Their roles have been described in modulating neuroinflammation and neurodegenerative processes. In this review, we discuss the role of Gals in the causation and progression of neurodegenerative disorders. We describe the role of Gals in microglia and astrocyte modulation, along with their pro- and anti-inflammatory functions. In addition, we discuss the potential use of Gals as a novel therapeutic target for neuroinflammation and restoring tissue damage in neurodegenerative diseases.

Rhizoctonia solani is a soil-borne fungus causing sheath blight disease in cereal crops including rice. Genetic resistance to sheath blight disease in cereal crops is not well understood in most of the host(s). Aside from this, a comparative study on the different hosts at the biochemical and proteomic level upon R. solani infection was not reported earlier. Here, we performed proteomic based analysis and studied defense pathways among cultivated rice (cv. Pusa Basmati-1), wild rice accession (Oryza grandiglumis), and barley (cv. NDB-1445) after inoculation with R. solani. Increased levels of phenol, peroxidase, and β-1, 3-glucanase were observed in infected tissue as compared to the control in all of the hosts. Wild rice accession O. grandiglumis showed a higher level of biochemical signals than barley cv. NDB 1445 and cultivated rice cv. Pusa Basmati-1. Using two-dimensional polyacrylamide gel electrophoresis (2D-PAGE) and mass spectrometry (MS), differently expressed proteins were also studied in control and after inoculation with R. solani. Wild rice accession O. grandiglumis induced a cysteine protease inhibitor and zinc finger proteins, which have defense functions and resistance against fungal pathogens. On the other hand, barley cv. NDB-1445 and cultivated rice cv. Pusa Basmati-1 mainly induce energy metabolism-related proteins/signals after inoculation with R. solani in comparison to wild rice accession O. grandiglumis. The present comprehensive study of R. solani interaction using three hosts, namely, Pusa Basmati-1 (cultivated rice), O. grandiglumis (wild rice), and NDB-1445 (barley) would interpret wider possibilities in the dissection of the protein(s) induced during the infection process. These proteins may further be correlated to the gene(s) and other related molecular tools that will help for the marker-assisted breeding and/or gene editing for this distressing disease among the major cereal crops.

The COVID19, a fatal disease by coronavirus (SARS-CoV-2) in late 2019 in China is now pandemic caused severe acute respiratory syndrome. The pandemic of COVID-19 has reached almost all regions of the world including territories with the death toll of more than 35,000. It has been estimated that one out every six-person affected by COVID-19 developed life-threatening conditions. The difficulty is that there are no vaccines or no specific treatment modalities for the management of COVID-19, apart from symptomatic treatments. Efforts for the development of vaccines and other specific treatment modalities are co-ordinated by the World Health Organisation (WHO), with many clinical trials ongoing with modern and traditional medicines. In this regard, various Phyto-actives from the plants are getting analyzed, which has earlier shown to be effective in various viral infections. Therefore, keeping the world scenario and due to the lack of vaccine, we have in silico studied the activity of tetrahydrocurcumin, a major metabolite of curcumin, a household spice, matairesinol, a major compound in wheat bran or flaxseed and vitamin K2-7 against both SARS-CoV's main peptide and COVID-19 M^pro.

Covid-19, a SARS-CoV virus-based disease, was identified in Wuhan, China, in December 2019. Initially, it was considered just an infection of the respiratory system, but due to its transmittable nature, it was declared a pandemic. A variety of treatment options were implemented, including antivirals like remdesvir, favipiravir along with vitamins and antioxidants. Further investigations revealed that the Covid-19 infection results in thrombotic cardiovascular complications, which are the major concern for the increased mortality associated with this disease. This study investigates the in Silico design of hybrid molecules with antiviral and an-tithrombotic properties. A docking study was performed using Autodock Vina software, and binding energies of the designed compounds were determined for papain-like protease (PDB: 3E9S) and 3-chymotrypsin-like cysteine protease (PDB: 6LU7). The docked poses and amino acids interactions were verified using Biovia Discovery studio 4.5. The binding energies of all designed compounds were compared with the standards, Compound RL1 (2-(5-(3-carbamoyl-1H-1,2,4-triazol-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methoxy)-carbonyl)amino)(hydroxy)methyl)carbamoyl)phenyl acetate) and Compound FL2 (8-hydroxy-2-(3-hydroxy-4-methoxyphenyl)-4-oxochroman-6-yl(2-(6-flouro-3-oxo-3,4-dihydropyrazine-2-carboxamido)-1-hydroxy-3-phenylpropyl)carbamate) proved to be promising agents with strong binding interactions. Hybrid molecules that inhibit viral replication, possibly as transition state inhibitors, can be investigated further for use in the treatment of SARS-Co-V infection and its associated complications.