CNS & neurological disorders drug targets最新文献

{"title":"Bridging Gaps in Postpartum Depression Research: Pathways to Personalized Medicine in Women's Mental Health.","authors":"Harshpreet Kaur, Neha Sharma, Joy Das, Mandeep Kaur, Navneet Khurana","doi":"10.2174/0118715273426978260515114857","DOIUrl":"https://doi.org/10.2174/0118715273426978260515114857","url":null,"abstract":"<p><p>Postpartum depression (PPD) is a prevalent and serious mental health disorder that affects nearly 15% of women after childbirth. It disrupts maternal well-being, infant development, and family relationships, and often remains underdiagnosed due to its complex biological, psychological, and social determinants. Conventional treatment strategies largely follow generalized, symptom-based approaches that fail to address the wide individual variation in hormonal sensitivity, genetic background, and psychosocial context among affected women. This review emphasizes the importance of adopting a personalized medicine framework for the management of PPD. Relevant literature was systematically reviewed from major databases, including PubMed, Scopus, Web of Science, ScienceDirect, and Google Scholar, focusing on studies published between January 2018 and September 2025. The search covered biological mechanisms, psychosocial influences, and innovative therapeutic approaches integrating pharmacogenomics, hormonal profiling, and culturally sensitive psychotherapies. The analysis highlights that personalized strategies, combining genetic testing for antidepressant response, individualized hormonal modulation, and context-based psychological interventions, offer improved therapeutic precision compared to conventional models. Emerging technologies such as digital health tools and telemedicine further enhance individualized care delivery. Clinically, the integration of personalized medicine transforms PPD management from a uniform, symptom-oriented approach to a patient-centered model that aligns biological and psychosocial dimensions. This paradigm shift has the potential to enhance treatment response, accelerate recovery, and strengthen longterm maternal and child outcomes.</p>","PeriodicalId":93947,"journal":{"name":"CNS & neurological disorders drug targets","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148145683","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bcl-2 as a Double-edged Sword for the Treatment of Multiple Sclerosis: A Systematic Review.","authors":"Naser-Aldin Lashgari, Fatemeh Badrabadi, Negar Rouhollahi, Saghar Sedigh Kheirabad, Nazanin Momeni Roudsari","doi":"10.2174/0118715273441953260516214256","DOIUrl":"https://doi.org/10.2174/0118715273441953260516214256","url":null,"abstract":"<p><strong>Introduction: </strong>Multiple sclerosis (MS) is a chronic immune-mediated neurodegenerative disease that involves inflammation, demyelination, and neuronal loss. The B-cell lymphoma 2 (Bcl-2) protein family regulates intrinsic apoptotic pathways and may impact disease progression via effects on immune cell survival and neuroprotection.</p><p><strong>Methods: </strong>To review current evidence on the role of Bcl-2 and its modulators in MS. Englishlanguage, clinical and preclinical studies (1998-October 2025) were retrieved from PubMed, Google Scholar, and other databases.</p><p><strong>Results: </strong>Clinical studies show that peripheral B lymphocytes and autoreactive T cells in relapsingremitting MS often exhibit increased Bcl-2 expression, leading to enhanced resistance to apoptosis and persistence of inflammatory immune responses. Factors such as leptin can further increase Bcl-2 levels in autoreactive T cells. In experimental studies, several interventions, including interferon-β1a, solanesol, green tea and pumpkin oils, β-hydroxybutyrate, cannabidiol, galantamine, melatonin, rifampicin, and rapamycin, were shown to modulate apoptotic pathways by increasing Bcl-2 expression or reducing the Bax/Bcl-2 ratio and caspase-3 activation in neurons. These changes were often accompanied by reduced inflammatory cytokines, decreased oxidative stress, improved neuronal survival, and attenuation of demyelination in MS models.</p><p><strong>Discussion: </strong>Overall, the collected evidence suggests that modulation of the Bcl-2 balance represents an important mechanism underlying both immune regulation and neuroprotection in MS.</p><p><strong>Conclusion: </strong>While modulating Bcl-2 pathways can be effective in MS, future research should aim to provide greater clarification and to design precision-based drugs capable of neuroprotective effects.</p>","PeriodicalId":93947,"journal":{"name":"CNS & neurological disorders drug targets","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148145666","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fisetin and Neurodegeneration: From Preclinical Studies to Potential Clinical Applications.","authors":"Md Al Amin, Mehrukh Zehravi, Sherouk Hussein Sweilam, Ronald Darwin, Jeetendra Kumar Gupta, E Bhargav, G Dharmamoorthy, Voleti Vijaya Kumar, A Anka Rao, Muath Suliman, Thirunavukkarasu Periyasamy, Talha Bin Emran","doi":"10.2174/0118715273427644251204045253","DOIUrl":"https://doi.org/10.2174/0118715273427644251204045253","url":null,"abstract":"<p><p>Neurodegenerative diseases (NDs), like Alzheimer's disease, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, and multiple sclerosis, pose significant challenges due to their gradual deterioration and limited available treatments. Fisetin, a naturally occurring flavonoid, has gained attention for its neuroprotective properties. This review explores the therapeutic potential of fisetin in NDs, focusing on its molecular processes and signaling pathways. Additionally, fisetin exhibits significant protective properties, particularly in reducing oxidative stress, neuroinflammation, and apoptosis. It enhances neuronal survival and reduces neuroinflammation by regulating key pathways, such as Nrf2/ARE, PI3K/Akt, and NF-κB. It also has anti-inflammatory, anti-apoptotic, and antioxidant actions. It stimulates autophagic processes, aiding in the removal of harmful protein aggregates, like tau tangles and amyloid plaques, which are hallmarks of NDs. Fisetin, as demonstrated through behavioral evaluations in animal models, has been found to improve motor coordination, synaptic plasticity, and cognitive function. Furthermore, fisetin's potential as a neuroprotective drug is emphasized by its role in enhancing autophagy and reducing tau and amyloid pathology. Research has shown its efficacy in enhancing neural resilience, synaptic plasticity, and cognitive function in both preclinical and in vitro settings. However, clinical translation remains limited due to challenges in pharmacokinetics and bioavailability, despite robust experimental evidence. Further clinical trials are needed to evaluate the safety and efficacy of fisetin, especially in early-stage NDs, explore potential synergistic effects, and understand the molecular interactions. The review demonstrates fisetin's therapeutic potential, recent research, and future strategies for NDs, highlighting bioavailability limitations and the need for new formulations or delivery systems.</p>","PeriodicalId":93947,"journal":{"name":"CNS & neurological disorders drug targets","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148145694","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Differential Effects of Nicotinic, Glutamatergic, and Conventional Wakefulness Agents on Cognition on a Murine Model of Acute Severe Sleep Deprivation.","authors":"Muhammed Cihan Güvel, Utku Aykan, Gökçen Paykal, Canan Uluoğlu","doi":"10.2174/0118715273471985260413210750","DOIUrl":"https://doi.org/10.2174/0118715273471985260413210750","url":null,"abstract":"<p><strong>Objective: </strong>Sleep deprivation poses critical safety risks in high-stakes professions, where traditional stimulants often fail to sustain cognitive performance. Addressing the need for novel cognitive enhancers, this study compared the effects of modafinil and caffeine with novel nicotinic (AVL-3288) and glutamatergic (CX516) positive allosteric modulators on behavior and memory in severely sleep-deprived mice.</p><p><strong>Methods: </strong>Male C57BL/6 mice underwent 48 hours of paradoxical sleep deprivation before receiving intraperitoneal doses of modafinil (300 mg/kg), caffeine (10 mg/kg), AVL-3288 (1, 2 mg/kg), CX516 (40, 80 mg/kg), or vehicle. A behavioral test series assessed locomotor activity (Open Field), anxiety (Elevated Plus Maze), reward-based working and spatial memory (Eight-Arm Radial Maze), escape-based spatial memory (Barnes Maze), and depressive mood (Tail Suspension).</p><p><strong>Results: </strong>Modafinil markedly increased locomotor activity and suppressed appetite. Caffeine, AVL-3288 (1 mg/kg), and CX516 (40 mg/kg) improved reward-based working memory (Eight- Arm Radial Maze). However, these same agents impaired performance in the escape-based spatial reference memory task (Barnes Maze). No mood-altering effects were observed. The novel modulators displayed complex, non-dose-dependent profiles.</p><p><strong>Discussion: </strong>Under severe sleep deprivation, specific wakefulness-enhancing substances can yield contrasting outcomes, enhancing reward-associated memory while negatively affecting escape-associated memory. These divergent outcomes suggest that neuromodulation during severe sleep deprivation exerts task-dependent behavioral effects, though the precise mechanisms driving the differences between the two maze paradigms remain to be elucidated.</p><p><strong>Conclusion: </strong>Pharmacological interventions under severe sleep deprivation can produce complex, bidirectional effects on cognition. This highlights that cognitive enhancement is likely task-dependent rather than global, necessitating a comprehensive assessment of diverse behavioral domains.</p>","PeriodicalId":93947,"journal":{"name":"CNS & neurological disorders drug targets","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148145730","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Effect of a Novel Antibody-based Drug, Prospekta, on Brain Electrical Activity in Mice.","authors":"Elena Kardash, Marina Kabirova, Denis Gorobets, Dilorom Begmatova, Izhak Michaelevski, Albert Pinhasov, Nataliya Petrova, Ksenia Ganina, Sergey Tarasov, Oleg Epstein","doi":"10.2174/0118715273459879260504113328","DOIUrl":"https://doi.org/10.2174/0118715273459879260504113328","url":null,"abstract":"<p><strong>Background and objective: </strong>An affinity-purified antibody to the calcium-binding protein S100B that has undergone gradual technological processing and was additionally modified with an electromagnetic signal is an active pharmaceutical ingredient of the novel neurotropic drug Prospekta. Earlier studies have shown that the drug possesses a wide range of S100B-mediated pharmacological effects. Here, we investigated Prospekta's impact on baseline brain electrical activity to deepen understanding of its mechanism of action.</p><p><strong>Methods: </strong>Extradural electrodes were surgically implanted into the skulls of adult male socially submissive mice. Animals were orally administered Prospekta for 5 days starting from the end of the recovery period. Brain baseline activity was recorded for 5 minutes after placing the mice in the arena. EEG band power (1-130 Hz, delta to high-gamma) was then analyzed quantitatively.</p><p><strong>Results: </strong>Prospekta administration reduced theta and alpha band power in the left prefrontal cortex. Additionally, the drug showed a trend toward altering electrical activity coherence between the left prefrontal cortex and the right hippocampus, manifesting as a subtle, visually present phase shift across the examined brain regions.</p><p><strong>Discussion: </strong>In a model recapitulating human cognitive and emotional impairments, Prospektainduced EEG alterations indicate a translational mechanism of neural modulation that may underlie behavioral effects, highlighting the need for future studies connecting these changes with functional outcomes.</p><p><strong>Conclusion: </strong>Our findings suggest that Prospekta modulates S100B-dependent processes, as evidenced by altered EEG oscillatory power and coherence. These effects may underlie the drug's influence on cognitive and behavioral regulation.</p>","PeriodicalId":93947,"journal":{"name":"CNS & neurological disorders drug targets","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147984374","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nanoformulations: A Progressive Strategy for Alleviating Migraine through Nasal Route.","authors":"Avinash Tekade, Snehal Kharade, Aliya Anjum Shaikh, Janhavi Nimbalkar, Rohit Shinde","doi":"10.2174/0118715273404294251129045855","DOIUrl":"https://doi.org/10.2174/0118715273404294251129045855","url":null,"abstract":"<p><strong>Introduction: </strong>Migraine is a chronic neurological disorder that can significantly interfere with day-to-day functioning. Currently, migraine is treated with various drugs administered via oral or parenteral routes; however, conventional drug delivery methods have several limitations. The blood-brain barrier (BBB) poses a major obstacle for effective drug delivery to the central nervous system. To overcome these drawbacks, the intranasal (IN) route has emerged as a preferred alternative. Intranasal delivery offers a promising approach for targeting drugs to the brain, bypassing the limitations of oral and parenteral administration. However, this route also presents challenges, such as limited nasal volume, particle size restrictions, and molecular weight constraints of drugs. Notably, nanoparticle-based technologies have shown significant potential in overcoming these challenges, enhancing drug accumulation in the brain while minimizing systemic distribution.</p><p><strong>Methods: </strong>This review article was compiled through a thorough survey of recent research and review articles focused on CNS-targeted drug delivery via the nasal route. The literature search was conducted using databases and sources including PubMed, Scopus, Google Scholar, WHO publications, and relevant books. Keywords used for the search included: Neurological disorders, Migraine, Novel approaches, Nose-to-brain delivery, Challenges, and Nanoformulations.</p><p><strong>Results: </strong>The reviewed studies demonstrate that various nanoformulations significantly enhance the brain delivery of anti-migraine drugs via the intranasal route. These delivery systems improve drug bioavailability, provide a faster onset of action, and achieve better therapeutic outcomes compared to conventional administration methods.</p><p><strong>Discussion: </strong>Intranasal nanoformulations represent a promising strategy to overcome the limitations associated with conventional oral and parenteral migraine therapies by facilitating direct nose-tobrain transport. These systems enhance brain targeting while reducing systemic exposure and adverse effects. Various nanocarriers such as SLNs, NLCs, nanoemulsions, and liposomes have demonstrated improved permeability, sustained release, and therapeutic efficacy.</p>","PeriodicalId":93947,"journal":{"name":"CNS & neurological disorders drug targets","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147984386","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MicroRNAs as Molecular Modulators in Stroke: Pathogenic Mechanisms and Therapeutic Avenues.","authors":"Hanshika Yadav, Brahma Nand Jha, Anamika Kumari, Mozammel Haque, Biplab Debnath, Joy Das","doi":"10.2174/0118715273417626251211205653","DOIUrl":"https://doi.org/10.2174/0118715273417626251211205653","url":null,"abstract":"<p><strong>Background: </strong>MicroRNAs (miRNAs) are small, non-coding RNA molecules that regulate gene expression and play crucial roles in various biological processes. Their potential as tools for disease diagnosis, prognosis, and therapeutic intervention has generated substantial interest.</p><p><strong>Objective: </strong>Although the role of miRNAs in cerebral diseases has been studied, identifying miRNAs specific to stroke remains challenging. This study focuses on understanding how miRNA profiles reflect stroke progression, differentiate between underlying causes, and serve as potential therapeutic and prognostic indicators.</p><p><strong>Methods: </strong>A literature search was conducted in PubMed, EMBASE, Web of Science, and Scopus to identify studies on miRNAs in stroke. Included studies examined miRNA roles in stroke mechanisms, neuroinflammation, oxidative stress, apoptosis, or their potential as diagnostic or therapeutic targets. Studies unrelated to miRNAs, irrelevant stroke models, or lacking molecular insights were excluded.</p><p><strong>Results: </strong>Distinct miRNA expression patterns were associated with different stages of stroke and specific etiologies. Certain miRNAs were linked to key pathophysiological mechanisms, including neuronal damage, inflammation, oxidative stress, and vascular dysfunction. These findings suggest that miRNAs could serve as biomarkers for monitoring disease progression and as targets for therapeutic interventions.</p><p><strong>Conclusion: </strong>miRNAs are integral to the molecular mechanisms underlying stroke and provide valuable information for disease characterization. Their modulation may offer new therapeutic strategies, while profiling specific miRNAs could enhance early diagnosis, prognosis, and personalized treatment approaches in stroke management.</p>","PeriodicalId":93947,"journal":{"name":"CNS & neurological disorders drug targets","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147977753","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Redefining Parkinson's Care: The Promise of Nanotechnology and Artificial Intelligence.","authors":"Yagya Dadhich, Saumya Das, Avijit Mazumder","doi":"10.2174/0118715273452060260422194722","DOIUrl":"https://doi.org/10.2174/0118715273452060260422194722","url":null,"abstract":"<p><strong>Introduction: </strong>Parkinson's Disease (PD) is a progressive neurodegenerative disorder characterized by the depletion of dopaminergic neurons and the buildup of α-synuclein aggregates, resulting in damaging motor and non-motor symptoms. Conventional therapies, comprising levodopa and dopamine agonists, give symptomatic relief but fail to terminate disease progression and are associated with long-term complications.</p><p><strong>Method and materials: </strong>Relevant review papers and articles from the past were investigated. Certain factors, including early disease diagnosis, therapeutic efficacy in PD models, and predictive modeling of drug-nanoparticle interactions, were considered during the conduct of this research. This literature review is a comprehensive narrative of research articles obtained from various platforms, namely Scopus, PubMed, Google Scholar, and Research Gate. Inclusion and exclusion criteria were applied to filter out the suitable materials.</p><p><strong>Result: </strong>Artificial intelligence (AI) is emerging as a complementary tool, facilitating design-optimized nanocarriers and predicting drug interactions while emphasizing liposomes and metallic nanoparticles as important platforms for dopamine replacement, gene therapy, and neuroinflammation modulation.</p><p><strong>Discussion: </strong>Despite the progress made so far, clinical translation still has considerable challenges to overcome, including nanoparticle toxicity, scalability, long-term safety, and variability in AI model performance. Integration of AI with biologically relevant PK/PD models and personalized nanomedicine strategies should overcome such existing gaps and enhance the therapeutic reliability of nanomedicine.</p><p><strong>Conclusion: </strong>This review summarizes current advances in nanomedicine and AI-driven approaches for PD, discussing their mechanisms, therapeutic targets, and future perspectives in achieving disease-modifying interventions.</p>","PeriodicalId":93947,"journal":{"name":"CNS & neurological disorders drug targets","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147977766","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Understanding Huntington's Disease: Epidemiology, Mechanisms, and Modeling Approaches.","authors":"Satya Prakash, Neha Kumari, Lovedeep Singh, Kamal Shah, Hitesh Kumar Dewangan, Deepika Bhatia","doi":"10.2174/0118715273413803251211091628","DOIUrl":"https://doi.org/10.2174/0118715273413803251211091628","url":null,"abstract":"<p><p>Huntington's disease (HD) is a monogenic, autosomal dominant neurodegenerative disorder. Huntington's disease is caused by a CAG trinucleotide repeat expansion in exon 1 of the huntingtin gene, which is located on the short arm of chromosome 4. Although HD has a well-defined genetic cause, the underlying molecular and cellular mechanisms remain complex and incompletely understood. This review examines the established functions of normal huntingtin protein and discusses the harmful consequences of CAG repeat expansions, which result in abnormally extended polyglutamine tracts. In this review, we offer a modern perspective on the molecular biology of HD, using it as a key example of polyglutamine disorders. We explore how mutations in the huntingtin protein disrupt its structure, leading to problems in how cells function and respond to stress, particularly in neurons that are already vulnerable. We highlight the main pathways that contribute to the disease, including issues with autophagy, mitochondrial production, lysosomal function, transport of proteins and organelles, inflammation, oxidative stress, and gene regulation by transcription factors. While much has been learned, some aspects of how the disease develops are still unclear. This concise overview summarizes what is currently known about the normal role of the huntingtin protein and the latest discoveries related to how Huntington's disease progresses at the molecular level.</p>","PeriodicalId":93947,"journal":{"name":"CNS & neurological disorders drug targets","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147977776","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanistic Insights into Terpenoid-Based Therapy for Parkinson's Disease.","authors":"Ritika Sharma, Avneet Kaur, Sonima Prasad, Divya Dhawal Bhandari, Kundan Singh Bora, Hitesh Kumar Dewangan","doi":"10.2174/0118715273396437251116214102","DOIUrl":"https://doi.org/10.2174/0118715273396437251116214102","url":null,"abstract":"<p><p>To explore the neuroprotective mechanisms of terpenoids, including their modulation of inflammation, mitigation of oxidative stress, regulation of apoptotic pathways, and promotion of neurogenesis, a wide variety of naturally occurring chemicals, known as terpenoids, have shown promise as neuroprotective agents for the treatment of Parkinson's disease (PD). In this paper, we summarize known methods, which include reducing oxidative stress, enhancing neurogenesis and neurotrophic factors, and modulating apoptotic signaling. In preclinical models of Parkinson's disease, compounds such as triptolide, andrographolide, carnosic acid, betulinic acid, and asiatic acid have demonstrated significant efficacy by modulating critical pathways, including the Nrf2/ARE, PI3K/Akt, and NF-κB pathways. In addition, terpenoids show potential as a treatment for PDrelated symptoms, such as impaired mitochondrial activity, protein misfolding, and blood-brain barrier breakdown. Although terpenoids have demonstrated some research potential, their limited target selectivity, poor solubility, and low bioavailability still hinder their clinical application. The primary objectives of future research should be to enhance formulations, explore methods for incorporating terpenoids into conventional pharmacotherapies, and investigate innovative drug delivery systems. Individualized PD therapy may be transformed by terpenoid-based personalized medicine techniques, in addition to genetics and high-throughput screening. Terpenoids should only be considered as a possible treatment option for PD after rigorous clinical trials that clarify pharmacokinetics and safety characteristics.</p>","PeriodicalId":93947,"journal":{"name":"CNS & neurological disorders drug targets","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147943958","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}