Parkinson's Disease (PD) is a progressive neurodegenerative disease, which is mainly characterised by the selective depletion of dopaminergic neurons in the substantia nigra and deposition of misfolded aggregates of α-synuclein. It is increasingly being observed that neuroinflammation, mitochondrial dysfunction, and lost neurotrophic support are interacting factors that drive disease progression. The aggregated 1-synuclein triggers an anti-inflammatory phenotype and pro-inflammatory phenotypes in activated microglia, which produce cytokines and reactive oxygen species, aggravating stress in neurons. At the same time, mitochondrial dynamic dysfunction increases oxidative injury, which makes neurons sensitive to degeneration. The low concentration of neurotrophic factors, especially the brain-derived neurotrophic factor (BDNF), impairs the innate ability of the brain to repair itself and maintain its synapses. These pathological processes gradually create a loop of self-feeding, which results in prolonged inflammation, loss of proteostasis, and gradual loss of dopaminergic neurons. This network is interconnected, and understanding it is crucial in the creation of therapies that attempt to restore proteostasis, inhibit inflammation, and increase neurotrophic signalling to delay or prevent PD progression.

Glutamate is known as the most important excitatory neurotransmitter in brain. Glutamate and glutamine recycling is very essential to maintain the nitrogen metabolism. Despite of its major functions, its dysregulation is a basic pathology which is common to neurodegenerative diseases such as Parkinson's disease (PD), Alzheimer's disease (AD), and Amyotrophic lateral sclerosis (ALS). Amyloid-β and Tau in AD disrupt glutamate uptake and the glutamate-glutamine cycle, accelerating synaptic failure, whereas loss of astrocytic EAAT2 in ALS generates unrelenting excitotoxicity and motor neuron demise. Toxic α-synuclein aggregation in PD exacerbates dopamine-glutamate imbalance through destabilizing corticostriatal transmission. This review explores on the key mechanisms by which glutamate impairment leads to the pathogenies of neurogenerative disorders and also about current medications like amantadine, memantine, and riluzole which are glutamate antagonists, are shown to partially alleviative but cannot halt the advancement of the disease. One of the potential targets for disease-modifying treatments could be the receptor modulation, astrocytic function, and elimination of excess glutamate.

AimThis study aimed to characterise the resistome of Acinetobacter isolates from pharmaceutical effluents and assess its association with phylogeny.MethodologyIn this study, Whole-genome sequences were assembled and screened for Antimicrobial Resistance (AMR) genes using CARD. Core and accessory resistomes were defined, and phylogeny was inferred using 16S rRNA analysis.ResultsIsolates carried 13–35 AMR genes despite shared origin. Efflux systems (AdeIJK, AdeABC) formed a conserved intrinsic core, while accessory genes, including OXA-type carbapenemases, ESBLs, aminoglycoside- and sulfonamide-resistance genes, and qacEΔ1, were variably distributed. Resistome patterns did not strictly follow phylogeny.InterpretationPharmaceutical effluents select for a conserved efflux-based resistance backbone while enabling dynamic acquisition of accessory genes via Horizontal Gene Transfer, highlighting the role of environmental pressure in multidrug resistance evolution.

Zinc is an essential trace element that plays a critical role in synaptic transmission, neuronal survival, gene regulation, and antioxidant defence in the brain. Hence, one of the central contributors to Alzheimer’s disease (AD) pathology is the disruption of zinc homeostasis. Recent studies suggest that an interconnected regulatory network maintains neuronal stability, comprising zinc-binding proteins, such as metallothioneins, zinc-dependent enzymes, zinc finger transcription factors, and zinc transporters. The accumulation of amyloid-β, Tau hyperphosphorylation, mitochondrial dysfunction, oxidative stress, and chronic neuroinflammation are the underlying causes of the mislocalization of zinc in AD. Also, the involvement of zinc-associated enzymes influences the amyloid clearance, as well as transcriptional regulation, which disrupts neuronal proteostasis. Hence, the therapeutic strategies usually aim at restoring the zinc balance, which involves the small-molecule metal modulators, natural phytochemicals with zinc-interacting properties and gene-based approaches. Hence, understanding zinc-binding protein networks provides a system-level framework for developing multi-target therapeutic interventions that could slow rapid progression, as well as might increase neuronal resilience in AD.

Alzheimer's disease (AD) is increasingly recognised as a multifactorial disorder driven by metabolic, microbial, and neuroinflammatory imbalances. The study of the research results proposes that gut dysbiosis and impaired brain glucose metabolism are closely interrelated through the gut-brain metabolism axis. Changes in the intestinal microbiome may disrupt insulin sensitivity, cause systemic inflammation, and disrupt the blood-brain barrier, worsening neuronal glucose deficits and facilitating amyloid-β (Aβ) aggregation and tau phosphorylation. Alongside, neurodegenerative cascades are further enhanced by neuronal metabolic reprogramming, characterised by decreased glucose uptake, dysfunctional glycolytic enzymes, and oxidative stress. Short-chain fatty acids (SCFAs) are mainly butyrate, which have a neuroprotective effect in regulating inflammation and gut integrity, and dysbiosis causes increased pro-inflammatory cytokines and endotoxin leakage. This two-way communication network provides new therapeutic opportunities, such as probiotics, prebiotics, nutritional control, and metabolic reprogramming interventions, to regain homeostasis and prevent the advancement of AD.

Optimal proportions of plasticizers, crosslinkers, and hydrophobicity modifiers are essential for biopolymer film formulations. In this study, Cellulose acetate bioplastic films were prepared with varying concentrations of polyethylene glycol (PEG), malic acid (MA), and hexadecanoic acid (HAD). The resulting films were characterized for thickness (TH), water absorbency (WA), transparency (TP), and equilibrium moisture content (MC). Each of these attributes was modeled using artificial neural networks (ANN) and an ensemble regression tree. The ANN models offered an excellent fit to these responses (R2: 0.981-0.999, R2CV: 0.928-0.978). The models were assessed using partial dependency, Local Interpretable Model-Agnostic Explanations, and Shapley explanation. Individual optimization projected a minimum TH of 0.03 mm, maximum TP of 43.14 % with WA, and MC below the detection limit. Multi-objective optimization suggested a blend containing 299.78 mg g-1 PEG, 7.51 mg g-1 MA, and 44.00 mg g-1 of HAD while maintaining TH (0.06 mm), MC (0.05 %), and TP (42.83 %).

Chilling injury severely threatens postharvest produce; integrating physical, chemical, biological, and genetic strategies with advanced diagnostics offers sustainable solutions to enhance cold tolerance, extend shelf life and ensure food security. Chilling injury, caused by exposure to suboptimal temperatures, leads to membrane damage, oxidative stress, and metabolic disruptions resulting in visible symptoms such as discoloration, pitting, and spoilage. This condition severely affects the quality, shelf life, and marketability of tropical and subtropical produce, posing significant challenges during storage and transportation. This review examines the underlying mechanisms of chilling injury, along with advancements in diagnosis and mitigation strategies. Diagnostic methods range from traditional visual inspections to modern tools such as spectroscopy, molecular biomarkers, and thermal imaging, enabling early detection of chilling injury. Mitigation strategies are classified into physical approaches (controlled storage conditions, preconditioning), chemical treatments (antioxidants, phytohormones), and biological interventions (genetic engineering, biostimulants). While these methods show promise, challenges such as scalability, crop-specific applicability, and universal effectiveness persist. Emerging molecular and genetic techniques offer potential solutions but require further validation and careful consideration of ecological and regulatory implications. By addressing existing gaps in research and practice, this review details the above stated approaches and emphasizes the importance of integrative approaches that combine physical, chemical, and biological strategies. Such comprehensive efforts are crucial for reducing postharvest losses, enhancing produce resilience, and promoting food security through sustainable agricultural practices.

Neurodegenerative diseases such as Alzheimer's, Parkinson's, Huntington's, and amyotrophic lateral sclerosis disease are characterized by progressive neuronal loss, protein aggregation, and synaptic dysfunction. These diseases share common pathological mechanisms including oxidative stress, mitochondrial impairment, chronic neuroinflammation, protein misfolding, and epigenetic dysregulation. Current therapies offer only symptomatic relief and fail to halt disease progression. Recent advances in transcriptomics and proteomics have enabled the identification of shared molecular pathways and druggable targets across multiple neurodegenerative diseases. The key targets, such as BDNF-TrkB, TREM2, SIRT1, PINK1-Parkin, GSK-3β, NLRP3, and mTOR have shown promise in preclinical models, offering opportunities for broad-spectrum therapeutic development. Importantly, blood-brain barrier disruption and neuroinflammatory crosstalk exacerbate disease pathology and hinder drug delivery. Innovative strategies involving nanocarriers, gene therapy, and epigenetic modulation are emerging to overcome these barriers. This review highlights the convergence of disease mechanisms, discusses common molecular signatures and therapeutic vulnerabilities, and explores novel small molecular interventions targeting shared pathways mainly in AD and PD. A deeper understanding of aging-associated molecular dysfunction is essential to design sustainable, disease-modifying therapeutics with cross-disease relevance.

Microbiome-based dietary supplements have gained attention for their role in enhancing brain development and cognitive health. The gut microbiome influences neurological functions through the gut-brain axis, impacting neurotransmitter production, immune regulation, and metabolic pathways. Dysbiosis is linked to neurological disorders such as Alzheimer's, Parkinson's, and autism spectrum disorders. This chapter explores dietary interventions targeting the microbiome, emphasising probiotics, prebiotics, and postbiotics. Additionally, AI and machine learning are transforming microbiome research by enabling personalised supplementation strategies tailored to individual gut profiles. Ethical challenges, including data privacy and algorithmic bias, are also discussed. Advances in big data analytics and predictive modelling are paving the way for precision-targeted interventions to optimise brain health. While microbiome-based therapies hold great promise, further clinical validation and regulatory frameworks are needed to ensure their efficacy and accessibility. This chapter highlights the future potential of microbiome-targeted strategies in neuroprotection and cognitive well-being.

Parkinson's disease (PD) and melanoma are considered high risk in affecting an individual's health. The association between PD and melanoma has been reported with consistent results by various epidemiological studies. The identification of differentially expressed genes (DEGs) and pathways between the two diseases can support the findings of the epidemiological studies. Transcriptomics studies play a vital role in investigating DEGs with better specificity and sensitivity. Hence, we have performed transcriptomic data analysis to discover the gene expression profiles and significant pathways and provide insights into the relationship between PD and melanoma. The DEG analysis revealed that genes, such as CLU, glial fibrillary acidic protein (GFAP), and bone morphogenetic protein 6 (BMP6), highly expressed in melanoma, were associated with the progression of PD and genes such as BAG6, heat shock protein family A member 1B (HSPA1B), and ubiquitin-conjugating enzyme E2C (UBE2C), highly expressed in PD, were associated with the progression of melanoma based on evidence from previous studies. Out of the significant common KEGG pathways observed between PD and melanoma, tryptophan metabolism, steroid biosynthesis, peroxisome proliferator-activated receptor (PPAR) signaling and arginine biosynthesis were directly related to the pathogenesis and progression of the two diseases. Therefore, these findings have elucidated the involvement of multiple genes and pathways in the association of PD and melanoma.

Human health and neurological functions are significantly impacted by lipids, the fundamental building block of cell membranes. The central nervous system is rich in lipids, and they are evidently disturbed in neurological conditions and neurodegenerative diseases like Alzheimer's disease (AD). Alteration in lipid profile is highly linked with aging. During early onset of AD, there is a noted lipid peroxidation and modifications of fatty acids at the level of lipid rafts in the neuronal cells. AD is an age-linked neurodegenerative condition with multifaceted etiology, with combining genetic and environmental risk factors, which lacks disease-modifying therapies. While the aberrant deposition of lipids was shown in the initial studies of AD neuropathology. Clinically, lipidomic and metabolomic research have constantly exposed the changes in the levels of various lipid classes emerging in early onset of AD individuals. Also, decades of investigations have discovered multifactorial link between lipid metabolism and key AD pathogenic pathway such as amyloidogenesis, bioenergetic deficit, oxidative stress, neuroinflammation, and myelin degeneration. Herewith, we highlighted the features that impact lipid composition in neuronal cells, and the association of different lipids with known aspects of AD pathogenesis, and potential therapeutics that aim lipid crossroads.

Nanobiotechnology is primarily driving the reshaping of food geography, distribution, and consumption. These factors investigate the far-reaching effects of nanobiotechnology on the quality and composition of food, providing insight into its role. Additionally, it is transforming food supply chains from farm to plate, streamlining products, distribution processes, and reducing waste. Furthermore, nanobiotechnology has the potential to extend shelf life and reduce food waste. Nanoclay and nanobiosensors play an important role in food quality preservation by detecting food toxins and pollutants in real-time. The struggle against foodborne illnesses takes center stage, demonstrating how nanoparticles can be used as powerful pathogen bombs. The ethical constraints and safety implications of adopting nanobiotechnology into our food system are promoted, as well as a focus on food nanotechnology norms. Finally, this review concluded by projecting unborn developments, stressing nanobiotechnology’s undiscovered potential in influencing the food attention. In substance, it offers a taste of the continuing nanobiotechnological food revolution, applying revolutionary power, promising results to major difficulties in food production and consumption. HIGHLIGHTS This paper explains about the usage of nanobiotechnology in food, which makes a massive revolution in food sectors. The paper focuses on the nanomaterials such as nanoclays and nanobiosensors that may be utilized in food to improve its nutritional value and shelf life. The development of food packaging methods using nanobiotechnology have also been explained in this paper. It also explains about the ethics and safety issues in food nanobiotechnology. GRAPHICAL ABSTRACT

Widespread adoption of lithium-ion batteries in electronic products, electric cars, and renewable energy systems has raised severe worries about the environmental consequences of spent lithium batteries. Because of its mobility and possible toxicity to aquatic and terrestrial ecosystems, lithium, as a vital component of battery technology, has inherent environmental problems. Leaching of lithium from discharged batteries, as well as its subsequent migration through soil and water, represents serious environmental hazards, since it accumulates in the food chain, impacting ecosystems and human health. This study thoroughly analyses the effects of lithium on plants, including its absorption, transportation, and toxicity. An attempt has been made to examine how lithium moves throughout plants through symplastic and apoplastic pathways and the factors that affect lithium accumulation in plant tissues, such as soil pH and calcium. This review focuses on the possible toxicity of lithium and its impact on ecosystems and human health. Aside from examining the environmental impacts, this review also emphasizes the significance of proper disposal and recycling measures in order to offset the negative effects of used lithium batteries. The paper also highlights the need for ongoing research to develop innovative and sustainable techniques for lithium recovery and remediation.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) has a direct impact on the dopaminergic neurons in the substantia nigra pars compacta (SNpc), dopamine in the striatum (ST), homovanillic acid (HVA), neurotrophic factors of the SNpc, and ST regions leading to Parkinson's disease (PD). Dopaminergic neuron atrophy in the SNpc and dopamine degradation in the ST have an explicit link to disrupted homeostasis of the neurotrophic factor brain-derived neurotrophic factor (BDNF) of the SNpc and ST regions. Chrysin is a flavonoid with a pharmacological potential that directly influences neurotrophic levels as well as neurotransmitters. As a result, analysis of the altering levels of neurotransmitters such as dopamine and its metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), are observed via high-performance liquid chromatography (HPLC) and the confirmation of the influential role of BDNF and glial-derived neurotrophic factor (GDNF) in the homeostasis of dopamine, DOPAC, and HAV via examination of gene expression. The observation confirmed that chrysin balances the altering levels of neurotransmitters as well as neurotrophic factors. The protocols for reverse transcription-polymerase chain reaction (RT-PCR) and HPLC analysis for neurotransmitter levels from the SNpc and ST regions of acute PD mice brain-induced MPTP are described in this chapter.

Traumatic brain injury (TBI) is caused by the disruption in the brain's normal function due to some external forces like jolt or blow to the head. While, Parkinson's disease (PD) is a neurodegenerative disorder which starts with tremor in one hand and gradually worsens over time. The connection between these two important diseases is not yet fully understood. Thus, we have proposed a transcriptome-based approach to identify the interrelation between TBI and PD. Determining the common over-or under gene expression pattern could reveal common pathobiological pathways that may explain the linkage between these two diseases. A total of 609 differentially expressed genes were discovered as commonly expressed genes for both TBI and PD. Further, the pathway studies reveal that nine genes such as NDUFA6, SLC17A7, EMXI, PLPPR1, FEZF2 and DUSP14, SERF1B, HBB and ABR made a significant impact on the disease progression of TBI and PD. In particular, SERF1B and HBB and ABR were considered as the top-ranked genes based on the pathway analysis and functional enrichment calculations. We believe that in-depth study on the identified biomarkers will provide possible treatments strategies to overcome TBI and PD.