Neuroprotective Potential of Semaglutide in Parkinson’s Disease: Mechanisms, Preclinical Evidence, and Clinical Perspectives

Semaglutide as a potential neuroprotective agent for neurological and neurodegenerative disorders: Mechanisms, preclinical evidence, and translational challenges and opportunities

Targeting Neuroinflammation and Neurodegeneration in Parkinson's Disease: Emerging Natural and Synthetic Therapeutic Strategies.

Natural bioactive compounds, gene-based therapies, stem cell-based therapies, stem cell-based therapies, and nanotechnology-assisted drug delivery systems are promising alternatives as suggested by recent advances and could help to more effectively and permanently manage PD.

Targeting Neurodegeneration With Naringenin: Mechanistic Perspectives and Therapeutic Implications

NAR has demonstrated the ability to reduce amyloid-β plaque deposition, inhibit α-synuclein aggregation, preserve dopaminergic neurons, modulate immune responses in multiple sclerosis, and improve functional recovery after spinal cord injury.

Hesperidin as a Neuroprotective Agent in Parkinson’s Disease: Mechanistic Insights and In Silico Validation

Combined in silico and experimental findings highlight hesperidin’s strong binding to key molecular targets, whereas experimental evidence also confirms its antioxidant, anti-inflammatory, and anti-apoptotic effects, supporting its potential as a disease-modifying candidate in PD therapy.

Nanotechnology-enabled delivery of bioactive compounds for neuroprotection in Parkinson's disease: mechanisms and future directions.

Parkinson's disease (PD) is a neurodegenerative disorder marked by the progressive loss of dopaminergic neurons in the substantia nigra. Its clinical features include motor symptoms such as tremor, bradykinesia, rigidity, and postural instability. The pathophysiology of PD involves oxidative stress, mitochondrial impairment, neuroinflammation, protein misfolding, and aberrant alpha-synuclein aggregation, which disrupt dopaminergic signaling pathways. Biomarkers such as α-synuclein, DJ-1, neurofilament light chain, and imaging biomarkers such as DAT-SPECT are being studied for early diagnosis, evaluation of disease progression, and therapy monitoring. Although advancements have been made, current options-such as dopamine replacement therapy, deep brain stimulation, and physiotherapy-remain largely symptomatic, carry long-term side effects, and fail to halt disease progression. Nanotechnology advancements have brought a major paradigm shift in the management of PD. Curcumin, Resveratrol, and EGCG are bioactive compounds with antioxidant, anti-inflammatory, and neuroprotective properties. However, their clinical use is limited because of poor bioavailability and stability. Nanocarrier systems such as liposomes, dendrimers, and polymeric nanoparticles improve targeted delivery through the blood-brain barrier. This helps in reducing systemic toxicity and enhancing therapeutic effectiveness. The therapeutic mechanism of these nanoformulations mainly involves free radical scavenging, modulation of mitochondrial function, inhibition of α-synuclein fibril formation, and regulation of cell signal transduction pathways such as Nrf2/ARE and NF-κB. The major challenges include large-scale production, long-term safety assessment, regulatory challenges, and site-specific delivery. Future research is moving toward the convergence of gene therapy, nanomedicine, and precision targeting to develop disease-modifying therapy. This approach aims not only to control symptoms but also to potentially control neurodegeneration in PD.

Neuropharmacological Interventions in Alzheimer’s Disease: Current and Emerging Approaches

Alzheimer’s Disease (AD) is a neurodegenerative disorder with progressive cognitive decline, β-amyloid plaques, neurofibrillary tangles, oxidative stress, and neuroinflammatory responses. So far, the pathogenesis of AD has been explained by the cholinergic hypothesis, amyloid cascade hypothesis, and tau protein dysfunction. However, the current pharmacological treatment of AD with cholinesterase inhibitors and NMDA receptor antagonists provides only symptomatic relief and cannot prevent the progression of the disease. This review article discusses the recent developments in neuropharmacology in the treatment of AD with a focus on the discovery of novel therapeutic targets and innovative therapeutic strategies with multi-target pharmacology involving protein–protein interaction inhibitors, allosteric modulators, selective enzyme inhibitors, and proteolysistargeting chimeras (PROTACs), and the discovery of novel drug delivery systems to overcome the blood–brain barrier. Current preclinical and emerging evidence indicate that the modulation of interconnected pathological pathways, including mitochondrial dysfunction, insulin resistance, and neuroinflammation, may lead to improved therapeutic outcomes. Dual inhibitors of tau hyperphosphorylation and Aβ aggregation have been shown to improve therapeutic efficacy, while modulation of neurotrophic signaling pathways, including BDNF, has been shown to possess neuroprotective effects. Moreover, improved drug delivery systems across the BBB will enhance drug bioavailability, thereby increasing therapeutic efficiency. Despite the promising preclinical data, there are several challenges in translating these therapeutic interventions into clinical success in AD treatment due to the complexity of the disease, delayed diagnosis, and lack of predictive markers. The incorporation of early diagnostic biomarkers in conjunction with the use of multi-target therapy will improve therapeutic efficacy in the treatment of AD. Neuropharmacological approaches, where various mechanisms of pathology are targeted, hold promise for developing disease-modifying treatments for AD. Further research in this area, incorporating innovative drug development techniques, drug delivery systems, and early intervention techniques, is crucial for better patient outcomes and slower disease progression.