Background: Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by the degeneration of dopaminergic neurons in the substantia nigra, resulting in dopamine deficiency and motor dysfunction. While levodopa (L‐DOPA) remains the gold standard for symptomatic treatment, its long‐term administration is associated with complications such as motor fluctuations, dyskinesia, and oxidative stress. Given these limitations, interest has grown in plant‐derived bioactive compounds for their potential neuroprotective and disease‐modifying effects.Methods: A systematic literature review was conducted across PubMed, Scopus, Google Scholar, and Web of Science, focusing on peer‐reviewed studies published between 2023 and March 2025. The inclusion criteria targeted in vitro and in vivo preclinical studies as well as clinical trials that directly compared levodopa with plant‐derived compounds in the context of PD. Key search terms included “Parkinson's disease,” “levodopa,” “phytochemicals,” and “plant‐based neuroprotection”.Results: Recent studies have highlighted several classes of plant‐based compounds—including polyphenols (resveratrol, curcumin, EGCG), flavonoids (quercetin, apigenin, naringenin), alkaloids (berberine, caffeine, L‐DOPA derived from Mucuna pruriens), and terpenoids (ginkgolide B, celastrol)—as potential neuroprotective agents. These compounds exert multiple actions, such as reducing oxidative stress, blocking neuroinflammation, preventing α‐synuclein aggregation, and protecting mitochondria. Although levodopa effectively addresses motor symptoms, these phytochemicals may complement conventional therapy by targeting underlying disease processes.Conclusions: Although levodopa is indispensable for the symptomatic management of PD, emerging evidence supports the integration of plant‐derived bioactive compounds as adjunct therapies with disease‐modifying potential. Future research should prioritize improving bioavailability, developing standardized formulations, and conducting long‐term clinical trials to evaluate the translational applicability of these natural agents in Parkinson's disease therapy.

There are certain mutations related to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). In addition to these known mutations, other new mutations have been found across regions in this study. Based on the results, in which 4,326 SARS-CoV-2 whole sequences were used, some mutations are found to be peculiar with certain regions, while some other mutations are found in all regions. In Asia, mutations (3 different mutations in QLA46612 isolated from South Korea) were found in the same sequence. Although huge number of mutations are detected (more than 70 in Asia) by regions, according to bioinformatics tools, some of them which are G75V (isolated from North America), T95I (isolated from South Korea), G143V (isolated from North America), M177I (isolated from Asia), L293M (isolated from Asia), P295H (isolated from Asia), T393P (isolated from Europe), P507S (isolated from Asia), and D614G (isolated from all regions) (These color used only make correct) predicted a damage to spike’ protein structure. Furthermore, this study also aimed to reveal how binding sites of ligands change if the spike protein structure is damaged, and whether more than one mutation affects ligand binding. Mutations that were predicted to damage the structure did not affect the ligand-binding sites, whereas ligands’ binding sites were affected in those with multiple mutations. It is thought that this study will give a different perspective to both the vaccine SARS-CoV studies and the change in the structure of the spike protein belonging to this virus against mutations.

The ACE2 receptor plays a vital role not only in the SARS-CoV-induced epidemic but also in various other diseases, including cardiovascular diseases and ARDS. While studies have explored the interactions between ACE2 and SARS-CoV proteins, comprehensive research utilizing bioinformatic tools on the ACE2 protein has been lacking. The one aim of present study was to extensively analyze the regions of the ACE2 protein. After utilizing all bioinformatics tools especially G104 and L108 regions on ACE2 were come forward. The results of our analysis revealed that possible mutations or deletions in the G104 and L108 regions play a critical role in both the biological functioning and the determination of the chemical-physical properties of ACE2. Additionally, these regions were found to be more susceptible to mutations or deletions compared to other regions of the ACE2 protein. Notably, the randomly selected peptide, LQQNGSSVLS (100-109), which includes G104 and L108, exhibited a crucial role in binding the RBD of the spike protein, as supported by docking scores. Furthermore, both MDs and iMODs results provided evidence that G104 and L108 influence the dynamics of ACE2-spike complexes. This study is expected to offer a new perspective on the ACE2-SARS-CoV interaction and other research areas where ACE2 plays a significant role, such as biotechnology (protein engineering, enzyme optimization), medicine (RAS, pulmonary and cardiac diseases), and basic research (structural motifs, stabilizing protein folds, or facilitating important inter molecular contacts, protein's proper structure and function).Communicated by Ramaswamy H. Sarma.

Alzheimer's disease (AD) is the leading cause of dementia, characterized by irreversible neuronal loss and progressive cognitive decline. The disease is driven by complex and interconnected pathological processes, including amyloid‐β plaque deposition and tau neurofibrillary tangle formation, which converge on neuroinflammation, oxidative stress, synaptic dysfunction, and widespread neuronal network failure. Although recently approved antibody‐based therapies such as lecanemab and donanemab effectively reduce cerebral amyloid burden, their clinical benefits remain modest and are accompanied by significant safety concerns, including amyloid‐related imaging abnormalities (ARIA). Current pharmacological strategies predominantly rely on single‐target mechanisms, an approach increasingly recognized as insufficient to address the multifactorial neurobiology of AD. This review critically evaluates the limitations of conventional amyloid‐centric therapeutic strategies and contrasts them with emerging multi‐target approaches based on phytochemicals. We synthesize current experimental and translational evidence to present a mechanistic framework illustrating how plant‐derived bioactive compounds, including flavonoids and polyphenols, function as systems‐level modulators of AD pathology rather than purely symptomatic agents. Particular emphasis is placed on their coordinated actions on amyloid processing via BACE1 inhibition, restoration of tau homeostasis through GSK‐3β/PP2A regulation, attenuation of neuroinflammatory signaling, enhancement of endogenous antioxidant defenses through Nrf2 activation, and preservation of synaptic integrity. When considered collectively, the available evidence supports the concept that multi‐target phytochemical strategies represent a biologically congruent and neurologically relevant paradigm for Alzheimer's disease therapy. Future progress will likely depend on integrating these compounds into broader polypharmacological and multidomain intervention frameworks, together with lifestyle‐based strategies, repurposed drugs, anti‐amyloid therapies, and rigorous translational validation. image

This study explores the impact of juglone on cucumber (Cucumis sativus cv. Beith Alpha), scrutinizing its effects on seed germination, growth, and the polyphenol oxidase (PPO) enzyme's activity and gene expression. Employing concentrations ranging from 0.01 to 0.5 mM, we found juglone's effects to be concentration‐dependent. At lower concentrations (0.01 and 0.1 mM), juglone promoted root and shoot growth along with germination, whereas higher concentrations (0.25 and 0.5 mM) exerted inhibitory effects, delineating a threshold for its allelopathic influence. Notably, PPO activity surged, especially at 0.5 mM in roots, hinting at oxidative stress involvement. Real‐time PCR unveiled that juglone modulates PPO gene expression in cotyledons, peaking at 0.1 mM and diminishing at elevated levels. Correlation analyses elucidated a positive link between juglone‐induced root growth and cotyledon PPO gene expression but a negative correlation with heightened root enzyme activity. Additionally, germination percentage inversely correlated with root PPO activity, while PPO activities positively associated with dopa and catechol substrates in both roots and cotyledons. Molecular docking studies revealed juglone's selective interactions with PPO's B chain, suggesting regulatory impacts. Protein interaction assessments highlighted juglone's influence on amino acid metabolism, and molecular dynamics indicated juglone's stronger, more stable binding to PPO, inferring potential alterations in enzyme function and stability. Conclusively, our findings elucidate juglone's dose‐dependent physiological and biochemical shifts in cucumber plants, offering insights into its role in plant growth, stress response, and metabolic modulation.